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| - | [[Image:3rqg.png|left|200px]] | |
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| - | <!-- | + | ==Cerebral cavernous malformation 3 (CCM3) in complex with paxillin LD4== |
| - | The line below this paragraph, containing "STRUCTURE_3rqg", creates the "Structure Box" on the page.
| + | <StructureSection load='3rqg' size='340' side='right'caption='[[3rqg]], [[Resolution|resolution]] 2.50Å' scene=''> |
| - | You may change the PDB parameter (which sets the PDB file loaded into the applet)
| + | == Structural highlights == |
| - | or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
| + | <table><tr><td colspan='2'>[[3rqg]] is a 5 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=3RQG OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3RQG FirstGlance]. <br> |
| - | or leave the SCENE parameter empty for the default display.
| + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.5Å</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=3rqg FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3rqg OCA], [https://pdbe.org/3rqg PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3rqg RCSB], [https://www.ebi.ac.uk/pdbsum/3rqg PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3rqg ProSAT]</span></td></tr> |
| - | {{STRUCTURE_3rqg| PDB=3rqg | SCENE= }}
| + | </table> |
| | + | == Disease == |
| | + | [https://www.uniprot.org/uniprot/PDC10_HUMAN PDC10_HUMAN] Hereditary cerebral cavernous malformation. Defects in PDCD10 are the cause of cerebral cavernous malformations type 3 (CCM3) [MIM:[https://omim.org/entry/603285 603285]. Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and usually present clinically during the 3rd to 5th decade of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters.<ref>PMID:15543491</ref> |
| | + | == 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> |
| | | | |
| - | ===Cerebral cavernous malformation 3 (CCM3) in complex with paxillin LD4=== | + | ==See Also== |
| - | | + | *[[Cell death protein 3D structures|Cell death protein 3D structures]] |
| - | | + | *[[Paxillin|Paxillin]] |
| - | <!--
| + | == References == |
| - | The line below this paragraph, {{ABSTRACT_PUBMED_21632544}}, adds the Publication Abstract to the page
| + | <references/> |
| - | (as it appears on PubMed at http://www.pubmed.gov), where 21632544 is the PubMed ID number.
| + | __TOC__ |
| - | -->
| + | </StructureSection> |
| - | {{ABSTRACT_PUBMED_21632544}}
| + | |
| - | | + | |
| - | ==About this Structure==
| + | |
| - | [[3rqg]] is a 5 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3RQG OCA]. | + | |
| - | | + | |
| - | ==Reference== | + | |
| - | <ref group="xtra">PMID:021632544</ref><references group="xtra"/> | + | |
| | [[Category: Homo sapiens]] | | [[Category: Homo sapiens]] |
| - | [[Category: Boggon, T J.]] | + | [[Category: Large Structures]] |
| - | [[Category: Li, X.]] | + | [[Category: Boggon TJ]] |
| - | [[Category: Zhang, R.]] | + | [[Category: Li X]] |
| - | [[Category: Cerebral cavernous malformation]] | + | [[Category: Zhang R]] |
| - | [[Category: Dimerization]]
| + | |
| - | [[Category: Fat domain]]
| + | |
| - | [[Category: Protein binding]]
| + | |
| - | [[Category: Protein-peptide complex]]
| + | |
| Structural highlights
Disease
PDC10_HUMAN Hereditary cerebral cavernous malformation. Defects in PDCD10 are the cause of cerebral cavernous malformations type 3 (CCM3) [MIM:603285. Cerebral cavernous malformations (CCMs) are congenital vascular anomalies of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. CCMs have an incidence of 0.1%-0.5% in the general population and usually present clinically during the 3rd to 5th decade of life. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters.[1]
Function
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).[2] [3] [4]
See Also
References
- ↑ Bergametti F, Denier C, Labauge P, Arnoult M, Boetto S, Clanet M, Coubes P, Echenne B, Ibrahim R, Irthum B, Jacquet G, Lonjon M, Moreau JJ, Neau JP, Parker F, Tremoulet M, Tournier-Lasserve E. Mutations within the programmed cell death 10 gene cause cerebral cavernous malformations. Am J Hum Genet. 2005 Jan;76(1):42-51. Epub 2004 Nov 12. PMID:15543491 doi:10.1086/426952
- ↑ Bergametti F, Denier C, Labauge P, Arnoult M, Boetto S, Clanet M, Coubes P, Echenne B, Ibrahim R, Irthum B, Jacquet G, Lonjon M, Moreau JJ, Neau JP, Parker F, Tremoulet M, Tournier-Lasserve E. Mutations within the programmed cell death 10 gene cause cerebral cavernous malformations. Am J Hum Genet. 2005 Jan;76(1):42-51. Epub 2004 Nov 12. PMID:15543491 doi:10.1086/426952
- ↑ Ma X, Zhao H, Shan J, Long F, Chen Y, Chen Y, Zhang Y, Han X, Ma D. PDCD10 interacts with Ste20-related kinase MST4 to promote cell growth and transformation via modulation of the ERK pathway. Mol Biol Cell. 2007 Jun;18(6):1965-78. Epub 2007 Mar 14. PMID:17360971 doi:10.1091/mbc.E06-07-0608
- ↑ Fidalgo M, Fraile M, Pires A, Force T, Pombo C, Zalvide J. CCM3/PDCD10 stabilizes GCKIII proteins to promote Golgi assembly and cell orientation. J Cell Sci. 2010 Apr 15;123(Pt 8):1274-84. doi: 10.1242/jcs.061341. Epub 2010 Mar, 23. PMID:20332113 doi:10.1242/jcs.061341
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