3s97: Difference between revisions

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~~[[Image:3s97.png|left|200px]]~~

===PTPRZ CNTN1 complex===

===~~PTPRZ~~ CNTN1 ~~complex===~~

==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>

~~{{ABSTRACT_PUBMED_21969550}}~~

==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).

==About this Structure==

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==Reference==

[[Category: Homo sapiens]]

[[Category: Protein-tyrosine-phosphatase]]

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-[[Image:3s97.png|left|200px]]
 {{STRUCTURE_3s97|  PDB=3s97  |  SCENE=  }}
+===PTPRZ CNTN1 complex===
+{{ABSTRACT_PUBMED_21969550}}
-===PTPRZ CNTN1 complex===
+==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>
-{{ABSTRACT_PUBMED_21969550}}
+==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).
 ==About this Structure==
@@ Line 14: / Line 16: @@
 ==Reference==
-<ref group="xtra">PMID:021969550</ref><references group="xtra"/>
+<ref group="xtra">PMID:021969550</ref><references group="xtra"/><references/>
 [[Category: Homo sapiens]]
 [[Category: Protein-tyrosine-phosphatase]]