2jng: Difference between revisions
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{{STRUCTURE_2jng| PDB=2jng | SCENE= }} | {{STRUCTURE_2jng| PDB=2jng | SCENE= }} | ||
===Solution structure of the CUL7-CPH domain from Homo Sapiens; Northeast Structural Genomics Consortium target HT1.=== | |||
{{ABSTRACT_PUBMED_17298945}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/CUL7_HUMAN CUL7_HUMAN]] Defects in CUL7 are the cause of 3M syndrome type 1 (3M1) [MIM:[http://omim.org/entry/273750 273750]]. An autosomal recessive disorder characterized by severe pre- and postnatal growth retardation, facial dysmorphism, large head circumference, and normal intelligence and endocrine function. Skeletal changes include long slender tubular bones and tall vertebral bodies.<ref>PMID:16142236</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/CUL7_HUMAN CUL7_HUMAN]] Component of a probable SCF-like E3 ubiquitin-protein ligase complex, which mediates the ubiquitination and subsequent proteasomal degradation of target proteins. Probably plays a role in the degradation of proteins involved in endothelial proliferation and/or differentiation (By similarity). Seems not to promote polyubiquitination and proteasomal degradation of TP53. In vitro, complexes of CUL7 with either CUL9 or FBXW8 or TP53 contain E3 ubiquitin-protein ligase activity.<ref>PMID:16547496</ref><ref>PMID:17332328</ref> | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:017298945</ref><references group="xtra"/> | <ref group="xtra">PMID:017298945</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Arrowsmith, C H.]] | [[Category: Arrowsmith, C H.]] | ||
