4geh: Difference between revisions

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 == Structural highlights ==
 <table><tr><td colspan='2'>[[4geh]] is a 4 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=4GEH OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=4GEH FirstGlance]. <br>
-</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=4geh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4geh OCA], [https://pdbe.org/4geh PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4geh RCSB], [https://www.ebi.ac.uk/pdbsum/4geh PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4geh ProSAT]</span></td></tr>
+</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 1.95&#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=4geh FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4geh OCA], [https://pdbe.org/4geh PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=4geh RCSB], [https://www.ebi.ac.uk/pdbsum/4geh PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=4geh ProSAT]</span></td></tr>
 </table>
 == Disease ==
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 == Function ==
 [https://www.uniprot.org/uniprot/PDC10_HUMAN PDC10_HUMAN] Promotes cell proliferation. Modulates apoptotic pathways. Increases mitogen-activated protein kinase activity and MST4 activity. Important for cell migration, and for normal structure and assembly of the Golgi complex. Important for KDR/VEGFR2 signaling. Increases the stability of KDR/VEGFR2 and prevents its breakdown. Required for normal cardiovascular development. Required for normal angiogenesis, vasculogenesis and hematopoiesis during embryonic development (By similarity).<ref>PMID:15543491</ref> <ref>PMID:17360971</ref> <ref>PMID:20332113</ref>
-<div style="background-color:#fffaf0;">
-== Publication Abstract from PubMed ==
-Mutation of CCM3 causes cerebral cavernous malformations of the vasculature, leading to focal neurological deficits, seizures, and hemorrhagic stroke. CCM3 can heterodimerize with GCKIII kinases (MST3, MST4, and STK25) to regulate cardiovascular development. Here, we provide direct experimental evidence to prove that CCM3 heterodimerizes with GCKIII in a manner structurally resembling the CCM3 homodimerization. Structural comparison revealed the mechanism and critical residues that drive CCM3-GCKIII heterodimerization versus homodimerization. A flexible linker was identified for CCM3, which mediates a large-scale conformational rotation of the FAT domain relative to the dimerization domain. The conformational flipover of FAT domain removes steric locking in the CCM3 homodimer and allows its disassembly and subsequent heterodimerization with GCKIII. CCM3 forms a stable complex with MST4 in vivo to promote cell proliferation and migration synergistically in a manner dependent on MST4 kinase activity. Collectively, our work offers a structural basis for further functional study.
-Structural Mechanism of CCM3 Heterodimerization with GCKIII Kinases.,Zhang M, Dong L, Shi Z, Jiao S, Zhang Z, Zhang W, Liu G, Chen C, Feng M, Hao Q, Wang W, Yin M, Zhao Y, Zhang L, Zhou Z Structure. 2013 Mar 26. pii: S0969-2126(13)00055-5. doi:, 10.1016/j.str.2013.02.015. PMID:23541896<ref>PMID:23541896</ref>
-From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-</div>
-<div class="pdbe-citations 4geh" style="background-color:#fffaf0;"></div>
 ==See Also==