5swt - Revision history

OCA at 12:49, 4 October 2023

2023-10-04T12:49:43Z

← Older revision		Revision as of 12:49, 4 October 2023
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	<StructureSection load='5swt' size='340' side='right'caption='[[5swt]], [[Resolution\|resolution]] 3.49Å' scene=''>		<StructureSection load='5swt' size='340' side='right'caption='[[5swt]], [[Resolution\|resolution]] 3.49Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5swt]] 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=5SWT OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5SWT FirstGlance]. <br>		<table><tr><td colspan='2'>[[5swt]] 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=5SWT OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5SWT FirstGlance]. <br>
	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat">~~<scene name='pdbligand=71A:PYRIDIN~~-~~3-OL'>71A</scene>~~, ~~<scene name='pdbligand=71B:~~3~~-FLUORO-4-METHOXYANILINE'>71B</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]] 3.49Å</td></tr>
	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=~~SEP~~:~~PHOSPHOSERINE~~'>~~SEP~~</scene><~~/td></tr>~~		<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=71A:PYRIDIN-3-OL'>71A</scene>, <scene name='pdbligand=71B:3-FLUORO-4-METHOXYANILINE'>71B</scene>, <scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
	~~<tr id~~='~~related'><td class~~=~~"sblockLbl"><b>[[Related_structure\|Related~~:~~]]</b~~></~~td><td class="sblockDat"~~>[[5sw8\|5sw8]], [[5swg\|5swg]], [[5swo\|5swo]], [[5swp\|5swp]], [[5swr\|5swr]], [[5sx8\|5sx8]], [[5sx9\|5sx9]], [[5sxa\|5sxa]], [[5sxb\|5sxb]], [[5sxc\|5sxc]], [[5sxd\|5sxd]], [[5sxe\|5sxe]], [[5sxf\|5sxf]], [[5sxi\|5sxi]], [[5sxj\|5sxj]], ~~[[5sxk\|5sxk]]~~<~~/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=5swt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5swt OCA], [https://pdbe.org/5swt PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5swt RCSB], [https://www.ebi.ac.uk/pdbsum/5swt PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5swt ProSAT]</span></td></tr>
	~~<tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b~~></td><td class="sblockDat">PIK3CA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), PIK3R1, GRB1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=5swt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5swt OCA], [~~http~~://pdbe.org/5swt PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5swt RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5swt PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5swt ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
	[~~[http~~://www.uniprot.org/uniprot/PK3CA_HUMAN PK3CA_HUMAN]] Note=Most of the cancer-derived mutations are missense mutations and map to one of the three hotspots: Glu-542; Glu-545 and His-1047. Mutated isoforms participate in cellular transformation and tumorigenesis induced by oncogenic receptor tyrosine kinases (RTKs) and HRAS1/KRAS. Interaction with HRAS1/KRAS is required for Ras-driven tumor formation. Mutations increasing the lipid kinase activity are required for oncogenic signaling. The protein kinase activity may not be required for tumorigenesis. Defects in PIK3CA are associated with colorectal cancer (CRC) [MIM:[~~http~~://omim.org/entry/114500 114500]]. Defects in PIK3CA are a cause of susceptibility to breast cancer (BC) [MIM:[~~http~~://omim.org/entry/114480 114480]]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Defects in PIK3CA are a cause of susceptibility to ovarian cancer (OC) [MIM:[~~http~~://omim.org/entry/167000 167000]]. Ovarian cancer common malignancy originating from ovarian tissue. Although many histologic types of ovarian neoplasms have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in PIK3CA may underlie hepatocellular carcinoma (HCC) [MIM:[~~http~~://omim.org/entry/114550 114550]].<ref>PMID:15608678</ref> Defects in PIK3CA are a cause of keratosis seborrheic (KERSEB) [MIM:[~~http~~://omim.org/entry/182000 182000]]. A common benign skin tumor. Seborrheic keratoses usually begin with the appearance of one or more sharply defined, light brown, flat macules. The lesions may be sparse or numerous. As they initially grow, they develop a velvety to finely verrucous surface, followed by an uneven warty surface with multiple plugged follicles and a dull or lackluster appearance.<ref>PMID:17673550</ref> Defects in PIK3CA are the cause of congenital lipomatous overgrowth, vascular malformations, and epidermal nevi (CLOVE) [MIM:[~~http~~://omim.org/entry/612918 612918]]. CLOVE is a sporadically occurring, non-hereditary disorder characterized by asymmetric somatic hypertrophy and anomalies in multiple organs. It is defined by four main clinical findings: congenital lipomatous overgrowth, vascular malformations, epidermal nevi, and skeletal/spinal abnormalities. The presence of truncal overgrowth and characteristic patterned macrodactyly at birth differentiates CLOVE from other syndromic forms of overgrowth.<ref>PMID:22658544</ref>		[https://www.uniprot.org/uniprot/PK3CA_HUMAN PK3CA_HUMAN] Note=Most of the cancer-derived mutations are missense mutations and map to one of the three hotspots: Glu-542; Glu-545 and His-1047. Mutated isoforms participate in cellular transformation and tumorigenesis induced by oncogenic receptor tyrosine kinases (RTKs) and HRAS1/KRAS. Interaction with HRAS1/KRAS is required for Ras-driven tumor formation. Mutations increasing the lipid kinase activity are required for oncogenic signaling. The protein kinase activity may not be required for tumorigenesis. Defects in PIK3CA are associated with colorectal cancer (CRC) [MIM:[https://omim.org/entry/114500 114500]. Defects in PIK3CA are a cause of susceptibility to breast cancer (BC) [MIM:[https://omim.org/entry/114480 114480]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case. Defects in PIK3CA are a cause of susceptibility to ovarian cancer (OC) [MIM:[https://omim.org/entry/167000 167000]. Ovarian cancer common malignancy originating from ovarian tissue. Although many histologic types of ovarian neoplasms have been described, epithelial ovarian carcinoma is the most common form. Ovarian cancers are often asymptomatic and the recognized signs and symptoms, even of late-stage disease, are vague. Consequently, most patients are diagnosed with advanced disease. Defects in PIK3CA may underlie hepatocellular carcinoma (HCC) [MIM:[https://omim.org/entry/114550 114550].<ref>PMID:15608678</ref> Defects in PIK3CA are a cause of keratosis seborrheic (KERSEB) [MIM:[https://omim.org/entry/182000 182000]. A common benign skin tumor. Seborrheic keratoses usually begin with the appearance of one or more sharply defined, light brown, flat macules. The lesions may be sparse or numerous. As they initially grow, they develop a velvety to finely verrucous surface, followed by an uneven warty surface with multiple plugged follicles and a dull or lackluster appearance.<ref>PMID:17673550</ref> Defects in PIK3CA are the cause of congenital lipomatous overgrowth, vascular malformations, and epidermal nevi (CLOVE) [MIM:[https://omim.org/entry/612918 612918]. CLOVE is a sporadically occurring, non-hereditary disorder characterized by asymmetric somatic hypertrophy and anomalies in multiple organs. It is defined by four main clinical findings: congenital lipomatous overgrowth, vascular malformations, epidermal nevi, and skeletal/spinal abnormalities. The presence of truncal overgrowth and characteristic patterned macrodactyly at birth differentiates CLOVE from other syndromic forms of overgrowth.<ref>PMID:22658544</ref>
	== Function ==		== Function ==
	[~~[http~~://www.uniprot.org/uniprot/PK3CA_HUMAN PK3CA_HUMAN]] Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns (Phosphatidylinositol), PtdIns4P (Phosphatidylinositol 4-phosphate) and PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors. Involved in the activation of AKT1 upon stimulation by receptor tyrosine kinases ligands such as EGF, insulin, IGF1, VEGFA and PDGF. Involved in signaling via insulin-receptor substrate (IRS) proteins. Essential in endothelial cell migration during vascular development through VEGFA signaling, possibly by regulating RhoA activity. Required for lymphatic vasculature development, possibly by binding to RAS and by activation by EGF and FGF2, but not by PDGF. Regulates invadopodia formation in breast cancer cells through the PDPK1-AKT1 pathway. Participates in cardiomyogenesis in embryonic stem cells through a AKT1 pathway. Participates in vasculogenesis in embryonic stem cells through PDK1 and protein kinase C pathway. Has also serine-protein kinase activity: phosphorylates PIK3R1 (p85alpha regulatory subunit), EIF4EBP1 and HRAS.<ref>PMID:21708979</ref> [[http://www.uniprot.org/uniprot/P85A_HUMAN P85A_HUMAN]] Binds to activated (phosphorylated) protein-Tyr kinases, through its SH2 domain, and acts as an adapter, mediating the association of the p110 catalytic unit to the plasma membrane. Necessary for the insulin-stimulated increase in glucose uptake and glycogen synthesis in insulin-sensitive tissues. Plays an important role in signaling in response to FGFR1, FGFR2, FGFR3, FGFR4, KITLG/SCF, KIT, PDGFRA and PDGFRB. Likewise, plays a role in ITGB2 signaling.<ref>PMID:7518429</ref> <ref>PMID:17626883</ref> <ref>PMID:19805105</ref>		[https://www.uniprot.org/uniprot/PK3CA_HUMAN PK3CA_HUMAN] Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns (Phosphatidylinositol), PtdIns4P (Phosphatidylinositol 4-phosphate) and PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors. Involved in the activation of AKT1 upon stimulation by receptor tyrosine kinases ligands such as EGF, insulin, IGF1, VEGFA and PDGF. Involved in signaling via insulin-receptor substrate (IRS) proteins. Essential in endothelial cell migration during vascular development through VEGFA signaling, possibly by regulating RhoA activity. Required for lymphatic vasculature development, possibly by binding to RAS and by activation by EGF and FGF2, but not by PDGF. Regulates invadopodia formation in breast cancer cells through the PDPK1-AKT1 pathway. Participates in cardiomyogenesis in embryonic stem cells through a AKT1 pathway. Participates in vasculogenesis in embryonic stem cells through PDK1 and protein kinase C pathway. Has also serine-protein kinase activity: phosphorylates PIK3R1 (p85alpha regulatory subunit), EIF4EBP1 and HRAS.<ref>PMID:21708979</ref>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
	== Publication Abstract from PubMed ==		== Publication Abstract from PubMed ==
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
	[[Category: ~~Human~~]]		[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
	[[Category: Amzel~~, L M~~]]		[[Category: Amzel LM]]
	[[Category: Gabelli~~, S B~~]]		[[Category: Gabelli SB]]
	[[Category: Miller~~, M S~~]]		[[Category: Miller MS]]
	[[Category: Vogelstein, B]]		[[Category: Vogelstein B]]
	~~[[Category: 3-kinase]]~~
	~~[[Category: Lipid kinase]]~~
	~~[[Category: Phosphoinositide]]~~
	~~[[Category: Signaling]]~~
	~~[[Category: Transferase-transferase inhibitor complex~~]]

OCA at 09:19, 4 December 2019

2019-12-04T09:19:13Z

← Older revision		Revision as of 09:19, 4 December 2019
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	==Crystal Structure of PI3Kalpha in complex with fragments 17 and 27==		==Crystal Structure of PI3Kalpha in complex with fragments 17 and 27==
	<StructureSection load='5swt' size='340' side='right' caption='[[5swt]], [[Resolution\|resolution]] 3.49Å' scene=''>		<StructureSection load='5swt' size='340' side='right'caption='[[5swt]], [[Resolution\|resolution]] 3.49Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[5swt]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5SWT OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5SWT FirstGlance]. <br>		<table><tr><td colspan='2'>[[5swt]] 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=5SWT OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5SWT FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=71A:PYRIDIN-3-OL'>71A</scene>, <scene name='pdbligand=71B:3-FLUORO-4-METHOXYANILINE'>71B</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=71A:PYRIDIN-3-OL'>71A</scene>, <scene name='pdbligand=71B:3-FLUORO-4-METHOXYANILINE'>71B</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=SEP:PHOSPHOSERINE'>SEP</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5sw8\|5sw8]], [[5swg\|5swg]], [[5swo\|5swo]], [[5swp\|5swp]], [[5swr\|5swr]], [[5sx8\|5sx8]], [[5sx9\|5sx9]], [[5sxa\|5sxa]], [[5sxb\|5sxb]], [[5sxc\|5sxc]], [[5sxd\|5sxd]], [[5sxe\|5sxe]], [[5sxf\|5sxf]], [[5sxi\|5sxi]], [[5sxj\|5sxj]], [[5sxk\|5sxk]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[5sw8\|5sw8]], [[5swg\|5swg]], [[5swo\|5swo]], [[5swp\|5swp]], [[5swr\|5swr]], [[5sx8\|5sx8]], [[5sx9\|5sx9]], [[5sxa\|5sxa]], [[5sxb\|5sxb]], [[5sxc\|5sxc]], [[5sxd\|5sxd]], [[5sxe\|5sxe]], [[5sxf\|5sxf]], [[5sxi\|5sxi]], [[5sxj\|5sxj]], [[5sxk\|5sxk]]</td></tr>
			<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PIK3CA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), PIK3R1, GRB1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</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=5swt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5swt OCA], [http://pdbe.org/5swt PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5swt RCSB], [http://www.ebi.ac.uk/pdbsum/5swt PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5swt ProSAT]</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=5swt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5swt OCA], [http://pdbe.org/5swt PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5swt RCSB], [http://www.ebi.ac.uk/pdbsum/5swt PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5swt ProSAT]</span></td></tr>
	</table>		</table>
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	</div>		</div>
	<div class="pdbe-citations 5swt" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5swt" style="background-color:#fffaf0;"></div>

			==See Also==
			*[[Phosphoinositide 3-kinase 3D structures\|Phosphoinositide 3-kinase 3D structures]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
			[[Category: Human]]
			[[Category: Large Structures]]
	[[Category: Amzel, L M]]		[[Category: Amzel, L M]]
	[[Category: Gabelli, S B]]		[[Category: Gabelli, S B]]

OCA at 18:52, 15 November 2017

2017-11-15T18:52:19Z

← Older revision		Revision as of 18:52, 15 November 2017
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	</div>		</div>
	<div class="pdbe-citations 5swt" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5swt" style="background-color:#fffaf0;"></div>

	~~==See Also==~~
	*[[Phosphoinositide 3-Kinases\|Phosphoinositide 3-Kinases]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 04:47, 21 September 2017

2017-09-21T04:47:28Z

← Older revision		Revision as of 04:47, 21 September 2017
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	</div>		</div>
	<div class="pdbe-citations 5swt" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 5swt" style="background-color:#fffaf0;"></div>

			==See Also==
			*[[Phosphoinositide 3-Kinases\|Phosphoinositide 3-Kinases]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 17:44, 10 March 2017

2017-03-10T17:44:04Z

@@ Line 1: / Line 1: @@
-The entry 5swt is ON HOLD  until Paper Publication
+==Crystal Structure of PI3Kalpha in complex with fragments 17 and 27==
-Authors:
+Identification of allosteric binding sites for PI3Kalpha oncogenic mutant specific inhibitor design.,Miller MS, Maheshwari S, McRobb FM, Kinzler KW, Amzel LM, Vogelstein B, Gabelli SB Bioorg Med Chem. 2017 Feb 15;25(4):1481-1486. doi: 10.1016/j.bmc.2017.01.012., Epub 2017 Jan 16. PMID:28129991<ref>PMID:28129991</ref>
-Description:
+From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
-[[Category: Unreleased Structures]]
+</div>

OCA: Protected "5swt" [edit=sysop:move=sysop]

2016-09-09T15:22:11Z

Protected "5swt" [edit=sysop:move=sysop]

← Older revision	Revision as of 15:22, 9 September 2016
(No difference)

OCA: New page: '''Unreleased structure''' The entry 5swt is ON HOLD until Paper Publication Authors: Description: Category: Unreleased Structures

2016-09-09T15:22:10Z

New page: '''Unreleased structure''' The entry 5swt is ON HOLD until Paper Publication Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 5swt is ON HOLD until Paper Publication

Authors:

Description:
[[Category: Unreleased Structures]]