1g3j
From Proteopedia
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<StructureSection load='1g3j' size='340' side='right'caption='[[1g3j]], [[Resolution|resolution]] 2.10Å' scene=''> | <StructureSection load='1g3j' size='340' side='right'caption='[[1g3j]], [[Resolution|resolution]] 2.10Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
| - | <table><tr><td colspan='2'>[[1g3j]] is a 4 chain structure with sequence from [ | + | <table><tr><td colspan='2'>[[1g3j]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/African_clawed_frog African clawed frog] and [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1G3J OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1G3J FirstGlance]. <br> |
| - | </td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | + | </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=1g3j FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1g3j OCA], [https://pdbe.org/1g3j PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1g3j RCSB], [https://www.ebi.ac.uk/pdbsum/1g3j PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1g3j ProSAT]</span></td></tr> |
</table> | </table> | ||
== Disease == | == Disease == | ||
| - | [[ | + | [[https://www.uniprot.org/uniprot/CTNB1_HUMAN CTNB1_HUMAN]] Defects in CTNNB1 are associated with colorectal cancer (CRC) [MIM:[https://omim.org/entry/114500 114500]]. Note=Activating mutations in CTNNB1 have oncogenic activity resulting in tumor development. Somatic mutations are found in various tumor types, including colon cancers, ovarian and prostate carcinomas, hepatoblastoma (HB), hepatocellular carcinoma (HCC). HBs are malignant embryonal tumors mainly affecting young children in the first three years of life. Defects in CTNNB1 are a cause of pilomatrixoma (PTR) [MIM:[https://omim.org/entry/132600 132600]]; a common benign skin tumor.<ref>PMID:11703283</ref> <ref>PMID:12027456</ref> <ref>PMID:10192393</ref> Defects in CTNNB1 are a cause of medulloblastoma (MDB) [MIM:[https://omim.org/entry/155255 155255]]. MDB is a malignant, invasive embryonal tumor of the cerebellum with a preferential manifestation in children.<ref>PMID:12027456</ref> <ref>PMID:10666372</ref> Defects in CTNNB1 are a cause of susceptibility to ovarian cancer (OC) [MIM:[https://omim.org/entry/167000 167000]]. Ovarian cancer common malignancy originating from ovarian tissue. Although many histologic types of ovarian neoplasms have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Note=A chromosomal aberration involving CTNNB1 is found in salivary gland pleiomorphic adenomas, the most common benign epithelial tumors of the salivary gland. Translocation t(3;8)(p21;q12) with PLAG1. Defects in CTNNB1 may be a cause of mesothelioma malignant (MESOM) [MIM:[https://omim.org/entry/156240 156240]]. An aggressive neoplasm of the serosal lining of the chest. It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos.<ref>PMID:11464291</ref> |
== Function == | == Function == | ||
| - | [[ | + | [[https://www.uniprot.org/uniprot/CTNB1_HUMAN CTNB1_HUMAN]] Key downstream component of the canonical Wnt signaling pathway. In the absence of Wnt, forms a complex with AXIN1, AXIN2, APC, CSNK1A1 and GSK3B that promotes phosphorylation on N-terminal Ser and Thr residues and ubiquitination of CTNNB1 via BTRC and its subsequent degradation by the proteasome. In the presence of Wnt ligand, CTNNB1 is not ubiquitinated and accumulates in the nucleus, where it acts as a coactivator for transcription factors of the TCF/LEF family, leading to activate Wnt responsive genes. Involved in the regulation of cell adhesion. Acts as a negative regulator of centrosome cohesion. Involved in the CDK2/PTPN6/CTNNB1/CEACAM1 pathway of insulin internalization. Blocks anoikis of malignant kidney and intestinal epithelial cells and promotes their anchorage-independent growth by down-regulating DAPK2.<ref>PMID:17524503</ref> <ref>PMID:18086858</ref> <ref>PMID:18957423</ref> <ref>PMID:21262353</ref> [[https://www.uniprot.org/uniprot/T7L1A_XENLA T7L1A_XENLA]] Participates in the Wnt signaling pathway. Binds to DNA and acts as a repressor in the absence of ctnnb1-A and possibly ctnnb1-B, and as an activator in the presence of these proteins. Required early in development for the establishment of the dorsal body axis in response to maternal Wnt signaling. Also required during development of the CNS for the establishment of dorsal-ventral patterning in the prospective diencephalon.<ref>PMID:8756721</ref> <ref>PMID:9308964</ref> <ref>PMID:9783587</ref> <ref>PMID:10375506</ref> <ref>PMID:10495268</ref> <ref>PMID:10559484</ref> <ref>PMID:11493528</ref> <ref>PMID:11356018</ref> <ref>PMID:11524435</ref> <ref>PMID:11238923</ref> <ref>PMID:12445388</ref> <ref>PMID:12163405</ref> <ref>PMID:11934150</ref> <ref>PMID:14568102</ref> <ref>PMID:15329348</ref> <ref>PMID:15747128</ref> <ref>PMID:15923623</ref> |
== Evolutionary Conservation == | == Evolutionary Conservation == | ||
[[Image:Consurf_key_small.gif|200px|right]] | [[Image:Consurf_key_small.gif|200px|right]] | ||
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==See Also== | ==See Also== | ||
*[[Catenin 3D structures|Catenin 3D structures]] | *[[Catenin 3D structures|Catenin 3D structures]] | ||
| - | *[[Intrinsically Disordered Protein|Intrinsically Disordered Protein]] | ||
== References == | == References == | ||
<references/> | <references/> | ||
Revision as of 11:18, 28 July 2021
CRYSTAL STRUCTURE OF THE XTCF3-CBD/BETA-CATENIN ARMADILLO REPEAT COMPLEX
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