1fu2: Difference between revisions

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{{Seed}}
[[Image:1fu2.png|left|200px]]


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==FIRST PROTEIN STRUCTURE DETERMINED FROM X-RAY POWDER DIFFRACTION DATA==
The line below this paragraph, containing "STRUCTURE_1fu2", creates the "Structure Box" on the page.
<StructureSection load='1fu2' size='340' side='right'caption='[[1fu2]]' scene=''>
You may change the PDB parameter (which sets the PDB file loaded into the applet)  
== Structural highlights ==
or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
<table><tr><td colspan='2'>[[1fu2]] is a 8 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1FU2 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1FU2 FirstGlance]. <br>
or leave the SCENE parameter empty for the default display.
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray powder diffraction</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CL:CHLORIDE+ION'>CL</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene>, <scene name='pdbligand=ZN:ZINC+ION'>ZN</scene></td></tr>
{{STRUCTURE_1fu2| PDB=1fu2 |  SCENE= }}
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=1fu2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1fu2 OCA], [https://pdbe.org/1fu2 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1fu2 RCSB], [https://www.ebi.ac.uk/pdbsum/1fu2 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1fu2 ProSAT]</span></td></tr>
</table>
== Disease ==
[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN] Defects in INS are the cause of familial hyperproinsulinemia (FHPRI) [MIM:[https://omim.org/entry/176730 176730].<ref>PMID:3470784</ref> <ref>PMID:2196279</ref> <ref>PMID:4019786</ref> <ref>PMID:1601997</ref>  Defects in INS are a cause of diabetes mellitus insulin-dependent type 2 (IDDM2) [MIM:[https://omim.org/entry/125852 125852]. IDDM2 is a multifactorial disorder of glucose homeostasis that is characterized by susceptibility to ketoacidosis in the absence of insulin therapy. Clinical fetaures are polydipsia, polyphagia and polyuria which result from hyperglycemia-induced osmotic diuresis and secondary thirst. These derangements result in long-term complications that affect the eyes, kidneys, nerves, and blood vessels.<ref>PMID:18192540</ref>  Defects in INS are a cause of diabetes mellitus permanent neonatal (PNDM) [MIM:[https://omim.org/entry/606176 606176]. PNDM is a rare form of diabetes distinct from childhood-onset autoimmune diabetes mellitus type 1. It is characterized by insulin-requiring hyperglycemia that is diagnosed within the first months of life. Permanent neonatal diabetes requires lifelong therapy.<ref>PMID:17855560</ref> <ref>PMID:18162506</ref>  Defects in INS are a cause of maturity-onset diabetes of the young type 10 (MODY10) [MIM:[https://omim.org/entry/613370 613370]. MODY10 is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:18192540</ref> <ref>PMID:18162506</ref> <ref>PMID:20226046</ref>
== Function ==
[https://www.uniprot.org/uniprot/INS_HUMAN INS_HUMAN] Insulin decreases blood glucose concentration. It increases cell permeability to monosaccharides, amino acids and fatty acids. It accelerates glycolysis, the pentose phosphate cycle, and glycogen synthesis in liver.
== 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/fu/1fu2_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]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1fu2 ConSurf].
<div style="clear:both"></div>


===FIRST PROTEIN STRUCTURE DETERMINED FROM X-RAY POWDER DIFFRACTION DATA===
==See Also==
 
*[[Insulin 3D Structures|Insulin 3D Structures]]
 
== References ==
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The line below this paragraph, {{ABSTRACT_PUBMED_11092920}}, adds the Publication Abstract to the page
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(as it appears on PubMed at http://www.pubmed.gov), where 11092920 is the PubMed ID number.
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[[Category: Homo sapiens]]
{{ABSTRACT_PUBMED_11092920}}
[[Category: Large Structures]]
 
[[Category: Blessing RH]]
==About this Structure==
[[Category: Smith GD]]
1FU2 is a [[Protein complex]] structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1FU2 OCA].
[[Category: Stephens PW]]
 
[[Category: Von Dreele RB]]
==Reference==
The first protein crystal structure determined from high-resolution X-ray powder diffraction data: a variant of T3R3 human insulin-zinc complex produced by grinding., Von Dreele RB, Stephens PW, Smith GD, Blessing RH, Acta Crystallogr D Biol Crystallogr. 2000 Dec;56(Pt 12):1549-53. PMID:[http://www.ncbi.nlm.nih.gov/pubmed/11092920 11092920]
[[Category: Protein complex]]
[[Category: Blessing, R H.]]
[[Category: Dreele, R B.Von.]]
[[Category: Smith, G D.]]
[[Category: Stephens, P W.]]
[[Category: Insulin]]
[[Category: Powder diffraction]]
[[Category: Rietveld refinement]]
 
''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Tue Jul  1 03:56:56 2008''
Retrieved from "https://proteopedia.org/1fu2"