3w8h - Revision history

OCA at 12:58, 8 November 2023

OCA — Wed, 08 Nov 2023 12:58:19 GMT

←Older revision		Revision as of 12:58, 8 November 2023
Line 3:		Line 3:
	<StructureSection load='3w8h' size='340' side='right'caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>		<StructureSection load='3w8h' size='340' side='right'caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3w8h]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3W8H OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3W8H FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3w8h]] 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=3W8H OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3W8H FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></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]] 2.426Å</td></tr>
-	~~<tr id='related'><td class="sblockLbl"><b>~~[[~~Related_structure~~\|~~Related:~~]]~~</b></td><td class="sblockDat"><div style='overflow: auto~~; ~~max-height: 3em;'>[[3w8i\|3w8i]]</div>~~</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	<tr id='~~gene~~'><td class="sblockLbl"><b>[[~~Gene~~\|~~Gene~~:]]</b></td><td class="sblockDat"~~>CCM3, PDCD10, TFAR15 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&~~id=~~9606 HUMAN]), SOK1, STK25, YSK1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td~~><~~/tr>~~	+
-	~~<tr id~~='~~activity'><td class~~=~~"sblockLbl"><b>Activity~~:~~</b></td><td class="sblockDat"><span class='plainlinks~~'>[https://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </~~span~~></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=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [https://pdbe.org/3w8h PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [https://www.ebi.ac.uk/pdbsum/3w8h PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3w8h ProSAT]</span></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=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [https://pdbe.org/3w8h PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [https://www.ebi.ac.uk/pdbsum/3w8h PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3w8h ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== 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>	+	[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 ==		== 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> [[https://www.uniprot.org/uniprot/STK25_HUMAN STK25_HUMAN]] Oxidant stress-activated serine/threonine kinase that may play a role in the response to environmental stress. Targets to the Golgi apparatus where it appears to regulate protein transport events, cell adhesion, and polarity complexes important for cell migration.<ref>PMID:15037601</ref>	+	[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;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 31:		Line 29:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	~~[[Category: Non-specific serine/threonine protein kinase]]~~	+	[[Category: Ding J]]
-	[[Category: Ding, J]]	+	[[Category: Wang DC]]
-	[[Category: Wang~~, D C~~]]	+	[[Category: Xu X]]
-	[[Category: Xu, X]]	+
-	~~[[Category: Protein binding-transferase complex~~]]	+

OCA at 05:27, 3 August 2022

OCA — Wed, 03 Aug 2022 05:27:12 GMT

←Older revision		Revision as of 05:27, 3 August 2022
Line 1:		Line 1:

	==Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25==		==Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25==
-	<StructureSection load='3w8h' size='340' side='right' caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>	+	<StructureSection load='3w8h' size='340' side='right'caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3w8h]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3W8H OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3W8H FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3w8h]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3W8H OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3W8H FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3w8i\|3w8i]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3w8i\|3w8i]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CCM3, PDCD10, TFAR15 ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), SOK1, STK25, YSK1 ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CCM3, PDCD10, TFAR15 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), SOK1, STK25, YSK1 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [~~http~~://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>	+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [~~http~~://pdbe.org/3w8h PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3w8h PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3w8h ProSAT]</span></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=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [https://pdbe.org/3w8h PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [https://www.ebi.ac.uk/pdbsum/3w8h PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3w8h ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://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:[~~http~~://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>	+	[[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 ==		== Function ==
-	[[~~http~~://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> [[~~http~~://www.uniprot.org/uniprot/STK25_HUMAN STK25_HUMAN]] Oxidant stress-activated serine/threonine kinase that may play a role in the response to environmental stress. Targets to the Golgi apparatus where it appears to regulate protein transport events, cell adhesion, and polarity complexes important for cell migration.<ref>PMID:15037601</ref>	+	[[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> [[https://www.uniprot.org/uniprot/STK25_HUMAN STK25_HUMAN]] Oxidant stress-activated serine/threonine kinase that may play a role in the response to environmental stress. Targets to the Golgi apparatus where it appears to regulate protein transport events, cell adhesion, and polarity complexes important for cell migration.<ref>PMID:15037601</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
Line 25:		Line 25:

	==See Also==		==See Also==
-	*[[Cell death protein\|Cell death protein]]	+	*[[Cell death protein 3D structures\|Cell death protein 3D structures]]
-	*[[Serine/threonine protein kinase\|Serine/threonine protein kinase]]	+	*[[Serine/threonine protein kinase 3D structures\|Serine/threonine protein kinase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
Line 32:		Line 32:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Non-specific serine/threonine protein kinase]]		[[Category: Non-specific serine/threonine protein kinase]]
	[[Category: Ding, J]]		[[Category: Ding, J]]

OCA at 18:38, 11 August 2016

OCA — Thu, 11 Aug 2016 18:38:11 GMT

←Older revision		Revision as of 18:38, 11 August 2016
Line 1:		Line 1:
		+
	==Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25==		==Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25==
	<StructureSection load='3w8h' size='340' side='right' caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>		<StructureSection load='3w8h' size='340' side='right' caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3w8h]] is a 2 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=3W8H OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3W8H FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3w8h]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3W8H OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3W8H FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3w8i\|3w8i]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3w8i\|3w8i]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CCM3, PDCD10, TFAR15 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), SOK1, STK25, YSK1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~])</td></tr>	+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CCM3, PDCD10, TFAR15 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), SOK1, STK25, YSK1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>		<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [http://www.ebi.ac.uk/pdbsum/3w8h PDBsum]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [http://pdbe.org/3w8h PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [http://www.ebi.ac.uk/pdbsum/3w8h PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3w8h ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 21:		Line 22:
	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>		From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
	</div>		</div>
		+	<div class="pdbe-citations 3w8h" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 29:		Line 31:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Non-specific serine/threonine protein kinase]]		[[Category: Non-specific serine/threonine protein kinase]]
	[[Category: Ding, J]]		[[Category: Ding, J]]

OCA at 10:14, 4 January 2015

OCA — Sun, 04 Jan 2015 10:14:18 GMT

←Older revision		Revision as of 10:14, 4 January 2015
Line 1:		Line 1:
-	~~{{STRUCTURE_3w8h\| PDB=3w8h \| SCENE= }}~~	+	==Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25==
-	===Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25===	+	<StructureSection load='3w8h' size='340' side='right' caption='[[3w8h]], [[Resolution\|resolution]] 2.43Å' scene=''>
-	~~{{ABSTRACT_PUBMED_23665169}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[3w8h]] is a 2 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=3W8H OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3W8H FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[3w8i\|3w8i]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">CCM3, PDCD10, TFAR15 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), SOK1, STK25, YSK1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Non-specific_serine/threonine_protein_kinase Non-specific serine/threonine protein kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.11.1 2.7.11.1] </span></td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3w8h FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3w8h OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3w8h RCSB], [http://www.ebi.ac.uk/pdbsum/3w8h PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
	[[http://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:[http://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>		[[http://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:[http://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 ==
		+	[[http://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> [[http://www.uniprot.org/uniprot/STK25_HUMAN STK25_HUMAN]] Oxidant stress-activated serine/threonine kinase that may play a role in the response to environmental stress. Targets to the Golgi apparatus where it appears to regulate protein transport events, cell adhesion, and polarity complexes important for cell migration.<ref>PMID:15037601</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Defects in cerebral cavernous malformation protein CCM3 result in cerebral cavernous malformation (CCM), a common vascular lesion of the human CNS. CCM3 functions as an adaptor protein that interacts with various signal proteins. Among these partner proteins, germinal center kinase III (GCKIII) proteins have attracted significant interest because GCKIII-CCM3 interactions play essential roles in vascular physiology. Here, we report the crystal structures of CCM3 in complex with the C-terminal regulatory domains of GCKIII (GCKIIIct) at 2.4 A resolution. Our results reveal that GCKIIIct adopts a fold closely resembling that of the CCM3 N-terminal dimeric domain. GCKIIIct heterodimerizes with CCM3 in a manner analogous to CCM3 homodimerization. The remarkable structural rearrangement of CCM3 induced by GCKIIIct binding and the ensuing interactions within CCM3 are characterized as the structural determinants for GCKIIIct-CCM3 heterodimerization. Taken together, these findings provide a precise structural basis for GCKIIIct-CCM3 heterodimerization and the functional performance of GCKIII mediated by CCM3.

-	~~==Function==~~	+	Structural Basis for the Unique Heterodimeric Assembly between Cerebral Cavernous Malformation 3 and Germinal Center Kinase III.,Xu X, Wang X, Zhang Y, Wang DC, Ding J Structure. 2013 Jun 4;21(6):1059-66. doi: 10.1016/j.str.2013.04.007. Epub 2013, May 9. PMID:23665169<ref>PMID:23665169</ref>
-	~~[[http://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> [[http://www~~.~~uniprot~~.~~org/uniprot/STK25_HUMAN STK25_HUMAN]] Oxidant stress-activated serine/threonine kinase that may play a role in the response to environmental stress~~. ~~Targets to the Golgi apparatus where it appears to regulate protein transport events~~, ~~cell adhesion, and polarity complexes important for cell migration~~.<ref>PMID:~~15037601~~</ref>	+

-	~~==About this Structure==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[3w8h]] is~~ a ~~2 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=3W8H OCA].~~	+	</div>

-	==~~Reference~~==	+	==See Also==
-	~~<ref group~~=~~"xtra">PMID:023665169</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	*[[Cell death protein\|Cell death protein]]
		+	*[[Serine/threonine protein kinase\|Serine/threonine protein kinase]]
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Non-specific serine/threonine protein kinase]]		[[Category: Non-specific serine/threonine protein kinase]]
-	[[Category: Ding, J.]]	+	[[Category: Ding, J]]
-	[[Category: Wang, D C.]]	+	[[Category: Wang, D C]]
-	[[Category: Xu, X.]]	+	[[Category: Xu, X]]
	[[Category: Protein binding-transferase complex]]		[[Category: Protein binding-transferase complex]]

OCA at 14:00, 3 July 2013

OCA — Wed, 03 Jul 2013 14:00:51 GMT

←Older revision		Revision as of 14:00, 3 July 2013
Line 1:		Line 1:
-	~~'''Unreleased~~ structure~~'''~~	+	{{STRUCTURE_3w8h\| PDB=3w8h \| SCENE= }}
		+	===Crystal structure of CCM3 in complex with the C-terminal regulatory domain of STK25===
		+	{{ABSTRACT_PUBMED_23665169}}

-	~~The~~ entry ~~3w8h is ON HOLD~~ ~~until Paper Publication~~	+	==Disease==
		+	[[http://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:[http://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>

-	~~Authors~~: Xu, X., ~~Wang, D~~.C., ~~Ding~~, J.	+	==Function==
		+	[[http://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> [[http://www.uniprot.org/uniprot/STK25_HUMAN STK25_HUMAN]] Oxidant stress-activated serine/threonine kinase that may play a role in the response to environmental stress. Targets to the Golgi apparatus where it appears to regulate protein transport events, cell adhesion, and polarity complexes important for cell migration.<ref>PMID:15037601</ref>

-	~~Description: Crystal~~ Structure ~~of Complex AB~~	+	==About this Structure==
		+	[[3w8h]] is a 2 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=3W8H OCA].
		+
		+	==Reference==
		+	<ref group="xtra">PMID:023665169</ref><references group="xtra"/><references/>
		+	[[Category: Homo sapiens]]
		+	[[Category: Non-specific serine/threonine protein kinase]]
		+	[[Category: Ding, J.]]
		+	[[Category: Wang, D C.]]
		+	[[Category: Xu, X.]]
		+	[[Category: Protein binding-transferase complex]]

OCA at 19:37, 17 April 2013

OCA — Wed, 17 Apr 2013 19:37:48 GMT

←Older revision		Revision as of 19:37, 17 April 2013
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 3w8h is ON HOLD	+	The entry 3w8h is ON HOLD until Paper Publication

	Authors: Xu, X., Wang, D.C., Ding, J.		Authors: Xu, X., Wang, D.C., Ding, J.

	Description: Crystal Structure of Complex AB		Description: Crystal Structure of Complex AB

OCA: Protected "3w8h" [edit=sysop:move=sysop]

OCA — Wed, 20 Mar 2013 16:02:21 GMT

Protected "3w8h" [edit=sysop:move=sysop]

←Older revision

Revision as of 16:02, 20 March 2013

OCA: New page: '''Unreleased structure''' The entry 3w8h is ON HOLD Authors: Xu, X., Wang, D.C., Ding, J. Description: Crystal Structure of Complex AB

OCA — Wed, 20 Mar 2013 16:02:20 GMT

New page: '''Unreleased structure''' The entry 3w8h is ON HOLD Authors: Xu, X., Wang, D.C., Ding, J. Description: Crystal Structure of Complex AB

New page

'''Unreleased structure'''

The entry 3w8h is ON HOLD

Authors: Xu, X., Wang, D.C., Ding, J.

Description: Crystal Structure of Complex AB