4o1v

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'''Unreleased structure'''
 
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The entry 4o1v is ON HOLD
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==SPOP Promotes Tumorigenesis by Acting as a Key Regulatory Hub in Kidney Cancer==
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<StructureSection load='4o1v' size='340' side='right'caption='[[4o1v]], [[Resolution|resolution]] 2.00&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>[[4o1v]] 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=4O1V OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4O1V FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2&#8491;</td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=4o1v FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4o1v OCA], [https://pdbe.org/4o1v PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4o1v RCSB], [https://www.ebi.ac.uk/pdbsum/4o1v PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4o1v ProSAT]</span></td></tr>
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</table>
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== Function ==
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[https://www.uniprot.org/uniprot/SPOP_HUMAN SPOP_HUMAN] Inhibits IPF1/PDX1 transactivation of established target promoters, such as insulin, may be by recruiting a repressor complex (By similarity). In complex with CUL3, involved in ubiquitination of BMI1, H2AFY and DAXX, and probably also in ubiquitination and proteasomal degradation of Gli2 or Gli3.<ref>PMID:14528312</ref> <ref>PMID:15897469</ref> <ref>PMID:16524876</ref>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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Hypoxic stress and hypoxia-inducible factors (HIFs) play important roles in a wide range of tumors. We demonstrate that SPOP, which encodes an E3 ubiquitin ligase component, is a direct transcriptional target of HIFs in clear cell renal cell carcinoma (ccRCC). Furthermore, hypoxia results in cytoplasmic accumulation of SPOP, which is sufficient to induce tumorigenesis. This tumorigenic activity occurs through the ubiquitination and degradation of multiple regulators of cellular proliferation and apoptosis, including the tumor suppressor PTEN, ERK phosphatases, the proapoptotic molecule Daxx, and the Hedgehog pathway transcription factor Gli2. Knockdown of SPOP specifically kills ccRCC cells, indicating that it may be a promising therapeutic target. Collectively, our results indicate that SPOP serves as a regulatory hub to promote ccRCC tumorigenesis.
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Authors: Calabrese, M.F., Watson, E.R., Schulman, B.A.
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SPOP Promotes Tumorigenesis by Acting as a Key Regulatory Hub in Kidney Cancer.,Li G, Ci W, Karmakar S, Chen K, Dhar R, Fan Z, Guo Z, Zhang J, Ke Y, Wang L, Zhuang M, Hu S, Li X, Zhou L, Li X, Calabrese MF, Watson ER, Prasad SM, Rinker-Schaeffer C, Eggener SE, Stricker T, Tian Y, Schulman BA, Liu J, White KP Cancer Cell. 2014 Apr 14;25(4):455-68. doi: 10.1016/j.ccr.2014.02.007. Epub 2014 , Mar 20. PMID:24656772<ref>PMID:24656772</ref>
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Description: E3-substrate
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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</div>
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<div class="pdbe-citations 4o1v" style="background-color:#fffaf0;"></div>
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==See Also==
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*[[Speckle-type POZ protein 3D structures|Speckle-type POZ protein 3D structures]]
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Homo sapiens]]
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[[Category: Large Structures]]
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[[Category: Calabrese MF]]
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[[Category: Schulman BA]]
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[[Category: Watson ER]]

Current revision

SPOP Promotes Tumorigenesis by Acting as a Key Regulatory Hub in Kidney Cancer

PDB ID 4o1v

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