4kmh: Difference between revisions

<StructureSection load='4kmh' size='340' side='right'caption='[[4kmh]], [[Resolution|resolution]] 3.04&Aring;' scene=''>

<table><tr><td colspan='2'>[[4kmh]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4KMH OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4KMH FirstGlance]. <br>

</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.04&#8491;</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=4kmh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4kmh OCA], [https://pdbe.org/4kmh PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4kmh RCSB], [https://www.ebi.ac.uk/pdbsum/4kmh PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4kmh ProSAT]</span></td></tr>

[https://www.uniprot.org/uniprot/SUFU_HUMAN SUFU_HUMAN] Defects in SUFU 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. Defects in SUFU play a role in predisposition to desmoplastic MDB. These tumors make up about 20 to 30% of medulloblastomas, have a more nodular architecture than 'classical' medulloblastoma, and may have a better prognosis.

[https://www.uniprot.org/uniprot/SUFU_HUMAN SUFU_HUMAN] Negative regulator in the hedgehog signaling pathway. Down-regulates GLI1-mediated transactivation of target genes. Part of a corepressor complex that acts on DNA-bound GLI1. May also act by linking GLI1 to BTRC and thereby targeting GLI1 to degradation by the proteasome. Sequesters GLI1, GLI2 and GLI3 in the cytoplasm, this effect is overcome by binding of STK36 to both SUFU and a GLI protein. Negative regulator of beta-catenin signaling. Regulates the formation of either the repressor form (GLI3R) or the activator form (GLI3A) of the full length form of GLI3 (GLI3FL). GLI3FL is complexed with SUFU in the cytoplasm and is maintained in a neutral state. Without the Hh signal, the SUFU-GLI3 complex is recruited to cilia, leading to the efficient processing of GLI3FL into GLI3R. When Hh signaling is initiated, SUFU dissociates from GLI3FL and the latter translocates to the nucleus, where it is phosphorylated, destabilized, and converted to a transcriptional activator (GLI3A).<ref>PMID:10564661</ref> <ref>PMID:10559945</ref> <ref>PMID:12068298</ref> <ref>PMID:10806483</ref> <ref>PMID:22365972</ref>  

[[Category: Homo sapiens]]

[[Category: Large Structures]]

[[Category: Qi X]]

[[Category: Wu G]]

[[Category: Zhang Y]]

[[Category: Zhang Z]]