Proteopedia - User contributions [en]

Monocyte chemoattractant protein

2016-01-30T17:17:44Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
The structure of the monomer is made of <scene name='72/721520/Ligand_binding_on_ccl2/2'>3 Beta sheets and 1 alpha helix</scene>.
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>. The potassium binds to the S33 and S34 of the monomer and PO4 binds to F15 and N17.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Image:chaine.png]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Sandbox Reserved 1134

2016-01-30T17:14:21Z

Alexane Caignard:

{{Sandbox_Reserved_ESBS_2015}}
<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. On chromosome 17 in region 17q11.2-q12 is the gene MCP1. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The MCP1<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or: 
- CCL2 
- small inducible cytokine A2 (SCYA2) 
- MCAF 
- GDCF-2 
- SMC-CF 
- HSMCR30 
- MGC9434 
- GDCF-2 
- HC11 

It exists as a monomer or a dimer, even though the homodimer form is preferred.
The structure of the monomer is made of <scene name='72/721520/Ligand_binding_on_ccl2/2'>3 Beta sheets and 1 alpha helix</scene>.

== Action principle ==

MCP1 is secreted thanks to variety of cells including endothelial cells, fibroblasts, epithelial, and smooth muscle. It acts by attracting some of the immune cells like monocytes and lymphocytes. These cells are equipped with a CCR2 receptor coupled with a G protein that can recuits MCP1.
MCP1 apply its chemotaxis power thanks to a concentration gradient : immune cells move from region with low concentration of MCP1 to region where a lot of MCP1 is secreted. Monocytes will then themselves be matured in macrophages that are able to secrete MCP1 in order to recruit more immune cells on the damage tissue.

== Ligands ==
To see the ligands it binds to, please show the <scene name='72/721520/Ligand_binding_on_ccl2/1'>monomer structure</scene> and then show the binding sites for <scene name='pdbligand=K:POTASSIUM+ION'>potassium</scene> and <scene name='pdbligand=PO4:PHOSPHATE+ION'>phosphate</scene> ions. The PO4 binds to the K35, S33 and S34 of the monomer and K binds to F15, N14 and N17.

== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
<jmolCheckbox>
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/if/3ifd_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
</jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB].
<div style="clear:both"></div>
<div style="background-color:#fffaf0;">

== Diseases ==

MCP1 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
MCP1 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

MCP1 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.

== Synthesis ==

Thanks to a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL), MCP1 was synthesized. Its thioester-peptide segment was made by using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS and that is probably one of the first crystal structures prepared using these techniques. To facilitate the synthesis of both MCP1 fragments, pseudoproline dipeptides were used. Then, NCL was used to assembly the all chain and MCP1 was folded and oxidized by a glutathione redox buffer.
MCP1 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution.

</StructureSection>

[[Image:chaine.png]]

== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Sandbox Reserved 1134

2016-01-30T17:06:45Z

Alexane Caignard:

{{Sandbox_Reserved_ESBS_2015}}
<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. On chromosome 17 in region 17q11.2-q12 is the gene MCP1. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The MCP1<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or: 
- CCL2 
- small inducible cytokine A2 (SCYA2) 
- MCAF 
- GDCF-2 
- SMC-CF 
- HSMCR30 
- MGC9434 
- GDCF-2 
- HC11 

It exists as a monomer or a dimer, even though the homodimer form is preferred.
The structure of the monomer is made of <scene name='72/721520/Ligand_binding_on_ccl2/2'>3 Beta sheets and 1 alpha helix</scene>.

== Action principle ==

MCP1 is secreted thanks to variety of cells including endothelial cells, fibroblasts, epithelial, and smooth muscle. It acts by attracting some of the immune cells like monocytes and lymphocytes. Theses cells are equipped with a CCR2 receptor coupled with a G protein which can recuits MCP1.
MCP1 apply its chemotaxis power thanks to a concentration gradient : immune cells move from region with low concentration of MCP1 to region where a lot of MCP1 is secreted. Monocytes will then themselves be matured in macrophage which are able to secrete MCP1 in order to recruit more immune cells on the damage tissue.

== Ligands ==
To see the ligands it binds to, please show the <scene name='72/721520/Ligand_binding_on_ccl2/1'>monomer structure</scene> and then show the binding sites for <scene name='pdbligand=K:POTASSIUM+ION'>potassium</scene> and <scene name='pdbligand=PO4:PHOSPHATE+ION'>phosphate</scene> ions. The PO4 binds to the K35, S33 and S34 of the monomer and K binds to F15, N14 and N17.

== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
<jmolCheckbox>
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/if/3ifd_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
</jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB].
<div style="clear:both"></div>
<div style="background-color:#fffaf0;">

== Diseases ==

MCP1 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
MCP1 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

MCP1 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.

== Synthesis ==

Thanks to a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL), MCP1 was synthesized. Its thioester-peptide segment was made using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS and that is probably one of the first crystal structures prepared using these techniques. To facilitate the synthesis of both MCP1 fragments, pseudoproline dipeptides were used. Then, NCL was used to assembly the all chain and MCP1 was folded and oxidized by a glutathione redox buffer.
MCP1 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution.

</StructureSection>

[[Image:chaine.png]]

== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Sandbox Reserved 1134

2016-01-30T17:06:19Z

Alexane Caignard:

{{Sandbox_Reserved_ESBS_2015}}
<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. On chromosome 17 in region 17q11.2-q12 is the gene MCP1. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The MCP1<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or: 
- CCL2 
- small inducible cytokine A2 (SCYA2) 
- MCAF 
- GDCF-2 
- SMC-CF 
- HSMCR30 
- MGC9434 
- GDCF-2 
- HC11 

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
The structure of the monomer is made of <scene name='72/721520/Ligand_binding_on_ccl2/2'>3 Beta sheets and 1 alpha helix</scene>.

== Action principle ==

MCP1 is secreted thanks to variety of cells including endothelial cells, fibroblasts, epithelial, and smooth muscle. It acts by attracting some of the immune cells like monocytes and lymphocytes. Theses cells are equipped with a CCR2 receptor coupled with a G protein which can recuits MCP1.
MCP1 apply its chemotaxis power thanks to a concentration gradient : immune cells move from region with low concentration of MCP1 to region where a lot of MCP1 is secreted. Monocytes will then themselves be matured in macrophage which are able to secrete MCP1 in order to recruit more immune cells on the damage tissue.

== Ligands ==
To see the ligands it binds to, please show the <scene name='72/721520/Ligand_binding_on_ccl2/1'>monomer structure</scene> and then show the binding sites for <scene name='pdbligand=K:POTASSIUM+ION'>potassium</scene> and <scene name='pdbligand=PO4:PHOSPHATE+ION'>phosphate</scene> ions. The PO4 binds to the K35, S33 and S34 of the monomer and K binds to F15, N14 and N17.

== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
<jmolCheckbox>
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/if/3ifd_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
</jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB].
<div style="clear:both"></div>
<div style="background-color:#fffaf0;">

== Diseases ==

MCP1 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
MCP1 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

MCP1 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.

== Synthesis ==

Thanks to a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL), MCP1 was synthesized. Its thioester-peptide segment was made using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS and that is probably one of the first crystal structures prepared using these techniques. To facilitate the synthesis of both MCP1 fragments, pseudoproline dipeptides were used. Then, NCL was used to assembly the all chain and MCP1 was folded and oxidized by a glutathione redox buffer.
MCP1 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution.

</StructureSection>

[[Image:chaine.png]]

== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Sandbox Reserved 1134

2016-01-27T12:56:14Z

Alexane Caignard:

{{Sandbox_Reserved_ESBS_2015}}
<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. On chromosome 17 in region 17q11.2-q12 is the gene MCP1. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The MCP1<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or: 
- MCP1 
- small inducible cytokine A2 (SCYA2) 
- MCAF 
- GDCF-2 
- SMC-CF 
- HSMCR30 
- MGC9434 
- GDCF-2 
- HC11 

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
The structure of the monomer is made of <scene name='72/721520/Ligand_binding_on_ccl2/2'>3 Beta sheets and 1 alpha helix</scene>.

== Action principle ==

MCP1 is secreted thanks to variety of cells including endothelial cells, fibroblasts, epithelial, and smooth muscle. It acts by attracting some of the immune cells like monocytes and lymphocytes. Theses cells are equipped with a CCR2 receptor coupled with a G protein which can recuits MCP1.
MCP1 apply its chemotaxis power thanks to a concentration gradient : immune cells move from region with low concentration of MCP1 to region where a lot of MCP1 is secreted. Monocytes will then themselves be matured in macrophage which are able to secrete MCP1 in order to recruit more immune cells on the damage tissue.

== Ligands ==
To see the ligands it binds to, please show the <scene name='72/721520/Ligand_binding_on_ccl2/1'>monomer structure</scene> and then show the binding sites for <scene name='pdbligand=K:POTASSIUM+ION'>potassium</scene> and <scene name='pdbligand=PO4:PHOSPHATE+ION'>phosphate</scene> ions. The PO4 binds to the K35, S33 and S34 of the monomer and K binds to F15, N14 and N17.

== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
<jmolCheckbox>
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/if/3ifd_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
</jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB].
<div style="clear:both"></div>
<div style="background-color:#fffaf0;">

== Diseases ==

MCP1 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
MCP1 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

MCP1 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.

== Synthesis ==

Thanks to a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL), MCP1 was synthesized. Its thioester-peptide segment was made using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS and that is probably one of the first crystal structures prepared using these techniques. To facilitate the synthesis of both MCP1 fragments, pseudoproline dipeptides were used. Then, NCL was used to assembly the all chain and MCP1 was folded and oxidized by a glutathione redox buffer.
MCP1 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution.

</StructureSection>

[[Image:chaine.png]]

== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Sandbox Reserved 1134

2016-01-27T12:55:02Z

Alexane Caignard:

{{Sandbox_Reserved_ESBS_2015}}
<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. On chromosome 17 in region 17q11.2-q12 is the gene MCP1. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The MCP1<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or: 
- MCP1 
- small inducible cytokine A2 (SCYA2) 
- MCAF 
- GDCF-2 
- SMC-CF 
- HSMCR30 
- MGC9434 
- GDCF-2 
- HC11 

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
The structure of the monomer is made of <scene name='72/721520/Ligand_binding_on_ccl2/2'>3 Beta sheets and 1 alpha helix</scene>.

== Action principle ==

MCP1 is secreted thanks to variety of cells including endothelial cells, fibroblasts, epithelial, and smooth muscle. It acts by attracting some of the immune cells like monocytes and lymphocytes. Theses cells are equipped with a CCR2 receptor coupled with a G protein which can recuits MCP1.
MCP1 apply its chemotaxis power thanks to a concentration gradient : immune cells move from region with low concentration of MCP1 to region where a lot of MCP1 is secreted. Monocytes will then themselves be matured in macrophage which are able to secrete MCP1 in order to recruit more immune cells on the damage tissue.

== Ligands ==
To see the ligands it binds to, please show the <scene name='72/721520/Ligand_binding_on_ccl2/1'>monomer structure</scene> and then show the binding sites for <scene name='pdbligand=K:POTASSIUM+ION'>potassium</scene> and <scene name='pdbligand=PO4:PHOSPHATE+ION'>phosphate</scene> ions. The PO4 binds to the K35, S33 and S34 of the monomer and K binds to F15, N14 and N17.

== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
Check<jmol>
<jmolCheckbox>
<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/if/3ifd_consurf.spt"</scriptWhenChecked>
<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
<text>to colour the structure by Evolutionary Conservation</text>
</jmolCheckbox>
</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB].
<div style="clear:both"></div>
<div style="background-color:#fffaf0;">

== Diseases ==

MCP1 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
MCP1 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

MCP1 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Image:chaine.png]]

== Synthesis ==

Thanks to a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL), MCP1 was synthesized. Its thioester-peptide segment was made using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS and that is probably one of the first crystal structures prepared using these techniques. To facilitate the synthesis of both MCP1 fragments, pseudoproline dipeptides were used. Then, NCL was used to assembly the all chain and MCP1 was folded and oxidized by a glutathione redox buffer.
MCP1 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution.

== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

File:Chaine.png

2016-01-26T18:45:46Z

Alexane Caignard:

Monocyte chemoattractant protein

2016-01-26T18:45:20Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Image:chaine.png]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T18:41:06Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Image:getimg.gif]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T18:38:39Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Image:chain.png]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T18:35:56Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Media:http://www.rcsb.org/pdb/explore/remediatedChain.do?structureId=3IFD&chainId=A.ogg]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T18:33:56Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Image:chain.jpg]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T18:28:00Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Media:chain.jpg]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T13:59:47Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function and Structure ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.

<scene name='72/721520/Ligand_binding_on_ccl2/2'>Beta sheets and alpha helix on monomer</scene>
== Ligands ==
The known ligands for CCL2 are <scene name='72/721520/Ligand_binding_on_ccl2/1'>Potassium and PO4</scene>.

== Diseases ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall as well as in prostate cancer<ref>PMID:25917126</ref>.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Media:proteopedia.odg]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T13:29:52Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
-> Binds to CCR2 and CCR4. Is tethered on endothelial cells by glycosaminoglycan (GAG) side chains of proteoglycans.
== Ligands ==
K and PO4

== Disease ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

[[Media:http://www.rcsb.org/pdb/protein/P13500]]

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T13:18:56Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
-> Binds to CCR2 and CCR4. Is tethered on endothelial cells by glycosaminoglycan (GAG) side chains of proteoglycans.
== Ligands ==
K and PO4

== Disease ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

== Synthesis ==

The protein human CCL2 has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein.
CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. This is probably one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T13:13:44Z

Alexane Caignard:

<StructureSection load='1dok' size='350' side='right' caption='Monocyte chemoattractant protein 1 (PDB code [[3idf]])' scene='72/721520/Cv/2'>
== Function ==

'''Human synthetic monocyte chemoattractant protein 1 (MCP)''' belongs to the superfamily of chemokines, which are proteins involved in immunoregulatory and inflammatory processes. The gene for CCL2 is on chromosome 17 in region 17q11.2-q12. The superfamily can be subdivided into 4 smaller groups, depending on the N-ter arangment of the cysteines. The CCL2<ref>PMID:8170963</ref> is also known as '''chemokine (C-C motif) ligand''' or:
- MCP1
- small inducible cytokine A2 (SCYA2)
- MCAF
- GDCF-2
- SMC-CF
- HSMCR30
- MGC9434
- GDCF-2
- HC11.

It exists as a monomer or a dimer, eventhough the homodimer form is preferred.
-> Binds to CCR2 and CCR4. Is tethered on endothelial cells by glycosaminoglycan (GAG) side chains of proteoglycans.
== Ligands ==
K and PO4

== Disease ==

CCL2 is implicated in several diseases like psoriasis and rheumatoid arthritis where the appear to recruit macrophages, therefore bolstering the inflammation on joints.
It is thought to be involved in atherosclerosis in the recruitment of monocytes into the arterial wall.
It has also been found elevated in the urine of people with lupus as a sign warning of inflammation of the kidney.
CCL2 is overexpressed in epilepsy, brain ischemia, Alzheimer's disease, EAE and traumatic brain injury.

== Structural highlights ==

CCL2 is part of the C-C motif group because of the covalent bond made between <scene name='72/721520/Cv/4'>2 of the 4 cysteines of the N terminal domain</scene>.<ref>PMID:8989326</ref>
Post translational modifications at the N-terminus can regulate receptor and target cell selectivity. Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant.
</StructureSection>

== Synthesis ==

The protein human CC chemokine ligand 2 (CCL2, also known as monocyte chemoattractant protein 1 or MCP-1) has been synthesized using a combination of solid phase peptide synthesis (SPPS) and native chemical ligation (NCL). The thioester-peptide segment was synthesized using the sulfonamide safety-catch linker and 9-fluorenylmethoxycarbonyl (Fmoc) SPPS, and pseudoproline dipeptides were used to facilitate the synthesis of both CCL2 fragments. After assembly of the full-length peptide chain by NCL, a glutathione redox buffer was used to fold and oxidize the CCL2 protein. Synthetic human CCL2 binds to and activates the CCR2 receptor on THP-1 cells, as expected. CCL2 was crystallized and the structure was determined by X-ray diffraction at 1.9-A resolution. The structure of the synthetic protein is very similar to that of a previously reported structure of recombinant human CCL2, although the crystal form is different. The functional CCL2 dimer for the crystal structure reported here is formed around a crystallographic twofold axis. The dimer interface involves residues Val9-Thr10-Cys11, which form an intersubunit antiparallel beta-sheet. Comparison of the CCL2 dimers in different crystal forms indicates a significant flexibility of the quaternary structure. To our knowledge, this is one of the first crystal structures of a protein prepared using the sulfonamide safety-catch linker and NCL.

==3D structures of Monocyte chemoattractant protein==
Updated on {{REVISIONDAY2}}-{{MONTHNAME|{{REVISIONMONTH}}}}-{{REVISIONYEAR}}
{{#tree:id=OrganizedByTopic|openlevels=0|

* Monocyte chemoattractant protein 1

**[[1dok]], [[1dol]] – hMCP-1 (mutant) - human 
**[[3ifd]] – hMCP-1 
**[[1dom]], [[1don]] – hMCP-1 - NMR 
**[[1ml0]], [[2nz1]] – hMCP-1 (mutant) + M3 protein 
**[[2bdn]] – hMCP-1 + antibody 
**[[4dn4]] – hMCP-1 (mutant) + antibody 
**[[4zk9]] – hMCP-1 + chemokine binding protein 
**[[4r8i]] – hMCP-1 + RNA 

* Monocyte chemoattractant protein 2

**[[1esr]] – hMCP-2 (mutant) 

* Monocyte chemoattractant protein 3

**[[1ncv]], [[1bo0]] – hMCP-3 - NMR 
**[[4zkc]] – hMCP-3 + chemokine binding protein 

* Monocyte chemoattractant protein 4

**[[2ra4]] – hMCP-4 
}}
== References ==
https://fr.wikipedia.org/wiki/CCL2
http://www.ebi.ac.uk/thornton-srv/databases/cgi-bin/pdbsum/GetPage.pl?pdbcode=1DOK
http://www.uniprot.org/uniprot/P13500#interaction
http://www.rcsb.org/pdb/explore/explore.do?structureId=3IFD
<references/>

Monocyte chemoattractant protein

2016-01-26T12:58:38Z

Alexane Caignard:

Monocyte chemoattractant protein

2016-01-26T12:57:10Z

Alexane Caignard:

Monocyte chemoattractant protein

2016-01-26T12:56:42Z

Alexane Caignard: