3s97: Difference between revisions

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==PTPRZ CNTN1 complex==
==PTPRZ CNTN1 complex==
<StructureSection load='3s97' size='340' side='right' caption='[[3s97]], [[Resolution|resolution]] 2.30&Aring;' scene=''>
<StructureSection load='3s97' size='340' side='right'caption='[[3s97]], [[Resolution|resolution]] 2.30&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[3s97]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3S97 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3S97 FirstGlance]. <br>
<table><tr><td colspan='2'>[[3s97]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3S97 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3S97 FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">HTPZP2, PTPRZ, PTPRZ1, PTPRZ2, PTPZ ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), CNTN1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">HTPZP2, PTPRZ, PTPRZ1, PTPRZ2, PTPZ ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), CNTN1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Protein-tyrosine-phosphatase Protein-tyrosine-phosphatase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.48 3.1.3.48] </span></td></tr>
<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Protein-tyrosine-phosphatase Protein-tyrosine-phosphatase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.1.3.48 3.1.3.48] </span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3s97 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3s97 OCA], [http://pdbe.org/3s97 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3s97 RCSB], [http://www.ebi.ac.uk/pdbsum/3s97 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3s97 ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3s97 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3s97 OCA], [https://pdbe.org/3s97 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3s97 RCSB], [https://www.ebi.ac.uk/pdbsum/3s97 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3s97 ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/CNTN1_HUMAN CNTN1_HUMAN]] Defects in CNTN1 are the cause of Compton-North congenital myopathy (CNCM) [MIM:[http://omim.org/entry/612540 612540]]. CNCM is a familial lethal form of congenital onset muscle weakness, inherited in an autosomal-recessive fashion and characterized by a secondary loss of beta2-syntrophin and alpha-dystrobrevin from the muscle sarcolemma, central nervous system involvement, and fetal akinesia.<ref>PMID:19026398</ref>   
[[https://www.uniprot.org/uniprot/CNTN1_HUMAN CNTN1_HUMAN]] Defects in CNTN1 are the cause of Compton-North congenital myopathy (CNCM) [MIM:[https://omim.org/entry/612540 612540]]. CNCM is a familial lethal form of congenital onset muscle weakness, inherited in an autosomal-recessive fashion and characterized by a secondary loss of beta2-syntrophin and alpha-dystrobrevin from the muscle sarcolemma, central nervous system involvement, and fetal akinesia.<ref>PMID:19026398</ref>   
== Function ==
== Function ==
[[http://www.uniprot.org/uniprot/PTPRZ_HUMAN PTPRZ_HUMAN]] May be involved in the regulation of specific developmental processes in the CNS. [[http://www.uniprot.org/uniprot/CNTN1_HUMAN CNTN1_HUMAN]] Contactins mediate cell surface interactions during nervous system development. Involved in the formation of paranodal axo-glial junctions in myelinated peripheral nerves and in the signaling between axons and myelinating glial cells via its association with CNTNAP1. Participates in oligodendrocytes generation by acting as a ligand of NOTCH1. Its association with NOTCH1 promotes NOTCH1 activation through the released notch intracellular domain (NICD) and subsequent translocation to the nucleus. Interaction with TNR induces a repulsion of neurons and an inhibition of neurite outgrowth (By similarity).  
[[https://www.uniprot.org/uniprot/PTPRZ_HUMAN PTPRZ_HUMAN]] May be involved in the regulation of specific developmental processes in the CNS. [[https://www.uniprot.org/uniprot/CNTN1_HUMAN CNTN1_HUMAN]] Contactins mediate cell surface interactions during nervous system development. Involved in the formation of paranodal axo-glial junctions in myelinated peripheral nerves and in the signaling between axons and myelinating glial cells via its association with CNTNAP1. Participates in oligodendrocytes generation by acting as a ligand of NOTCH1. Its association with NOTCH1 promotes NOTCH1 activation through the released notch intracellular domain (NICD) and subsequent translocation to the nucleus. Interaction with TNR induces a repulsion of neurons and an inhibition of neurite outgrowth (By similarity).  
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== Publication Abstract from PubMed ==
== Publication Abstract from PubMed ==
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==See Also==
==See Also==
*[[Contactin|Contactin]]
*[[Tyrosine phosphatase 3D structures|Tyrosine phosphatase 3D structures]]
== References ==
== References ==
<references/>
<references/>
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</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Human]]
[[Category: Large Structures]]
[[Category: Protein-tyrosine-phosphatase]]
[[Category: Protein-tyrosine-phosphatase]]
[[Category: Bouyain, S]]
[[Category: Bouyain, S]]