|
|
| Line 1: |
Line 1: |
| | | | |
| | ==PTPRZ CNTN1 complex== | | ==PTPRZ CNTN1 complex== |
| - | <StructureSection load='3s97' size='340' side='right' caption='[[3s97]], [[Resolution|resolution]] 2.30Å' scene=''> | + | <StructureSection load='3s97' size='340' side='right'caption='[[3s97]], [[Resolution|resolution]] 2.30Å' 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). |
| | <div style="background-color:#fffaf0;"> | | <div style="background-color:#fffaf0;"> |
| | == Publication Abstract from PubMed == | | == Publication Abstract from PubMed == |
| Line 24: |
Line 24: |
| | | | |
| | ==See Also== | | ==See Also== |
| - | *[[Contactin|Contactin]] | + | *[[Tyrosine phosphatase 3D structures|Tyrosine phosphatase 3D structures]] |
| | == References == | | == References == |
| | <references/> | | <references/> |
| Line 30: |
Line 30: |
| | </StructureSection> | | </StructureSection> |
| | [[Category: Human]] | | [[Category: Human]] |
| | + | [[Category: Large Structures]] |
| | [[Category: Protein-tyrosine-phosphatase]] | | [[Category: Protein-tyrosine-phosphatase]] |
| | [[Category: Bouyain, S]] | | [[Category: Bouyain, S]] |
| Structural highlights
3s97 is a 4 chain structure with sequence from Human. Full crystallographic information is available from OCA. For a guided tour on the structure components use FirstGlance.
| | Ligands: | |
| Gene: | HTPZP2, PTPRZ, PTPRZ1, PTPRZ2, PTPZ (HUMAN), CNTN1 (HUMAN) |
| Activity: | Protein-tyrosine-phosphatase, with EC number 3.1.3.48 |
| Resources: | FirstGlance, OCA, PDBe, RCSB, PDBsum, ProSAT |
Disease
[CNTN1_HUMAN] Defects in CNTN1 are the cause of Compton-North congenital myopathy (CNCM) [MIM: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.[1]
Function
[PTPRZ_HUMAN] May be involved in the regulation of specific developmental processes in the CNS. [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).
Publication Abstract from PubMed
The six members of the contactin (CNTN) family of neural cell adhesion molecules are involved in the formation and maintenance of the central nervous system (CNS) and have been linked to mental retardation and neuropsychiatric disorders such as autism. Five of the six CNTNs bind to the homologous receptor protein tyrosine phosphatases gamma (PTPRG) and zeta (PTPRZ), but the biological roles of these interactions remain unclear. We report here the cocrystal structure of the carbonic anhydrase-like domain of PTPRZ bound to tandem Ig repeats of CNTN1 and combine these structural data with binding assays to show that PTPRZ binds specifically to CNTN1 expressed at the surface of oligodendrocyte precursor cells. Furthermore, analyses of glial cell populations in wild-type and PTPRZ-deficient mice show that the binding of PTPRZ to CNTN1 expressed at the surface of oligodendrocyte precursor cells inhibits their proliferation and promotes their development into mature oligodendrocytes. Overall, these results implicate the PTPRZ/CNTN1 complex as a previously unknown modulator of oligodendrogenesis.
A complex between contactin-1 and the protein tyrosine phosphatase PTPRZ controls the development of oligodendrocyte precursor cells.,Lamprianou S, Chatzopoulou E, Thomas JL, Bouyain S, Harroch S Proc Natl Acad Sci U S A. 2011 Oct 18;108(42):17498-503. Epub 2011 Oct 3. PMID:21969550[2]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
See Also
References
- ↑ Compton AG, Albrecht DE, Seto JT, Cooper ST, Ilkovski B, Jones KJ, Challis D, Mowat D, Ranscht B, Bahlo M, Froehner SC, North KN. Mutations in contactin-1, a neural adhesion and neuromuscular junction protein, cause a familial form of lethal congenital myopathy. Am J Hum Genet. 2008 Dec;83(6):714-24. doi: 10.1016/j.ajhg.2008.10.022. Epub 2008, Nov 20. PMID:19026398 doi:10.1016/j.ajhg.2008.10.022
- ↑ Lamprianou S, Chatzopoulou E, Thomas JL, Bouyain S, Harroch S. A complex between contactin-1 and the protein tyrosine phosphatase PTPRZ controls the development of oligodendrocyte precursor cells. Proc Natl Acad Sci U S A. 2011 Oct 18;108(42):17498-503. Epub 2011 Oct 3. PMID:21969550 doi:10.1073/pnas.1108774108
|
