1yvl - Revision history

OCA at 08:06, 15 May 2024

OCA — Wed, 15 May 2024 08:06:38 GMT

←Older revision		Revision as of 08:06, 15 May 2024
Line 3:		Line 3:
	<StructureSection load='1yvl' size='340' side='right'caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>		<StructureSection load='1yvl' size='340' side='right'caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://proteopedia.org/fgij/fg.htm?mol=1YVL FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1yvl]] 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1YVL FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=AU:GOLD+ION'>AU</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]] 3Å</td></tr>
-	<tr id='~~NonStdRes~~'><td class="sblockLbl"><b>[[~~Non-Standard_Residue~~\|~~NonStd Res~~:]]</b></td><td class="sblockDat"><scene name='pdbligand=~~PTR~~:~~O-PHOSPHOTYROSINE~~'>~~PTR~~</scene><~~/td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene>, <scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>
-	~~<tr id~~='~~gene'><td class~~=~~"sblockLbl"><b>[[Gene\|Gene~~:~~]]</b~~></td>~~<td class="sblockDat">STAT1 ([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'>[https://proteopedia.org/fgij/fg.htm?mol=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [https://pdbe.org/1yvl PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [https://www.ebi.ac.uk/pdbsum/1yvl PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1yvl ProSAT]</span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://proteopedia.org/fgij/fg.htm?mol=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [~~http~~://pdbe.org/1yvl PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1yvl PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1yvl ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Defects in STAT1 are the cause of STAT1 deficiency complete (STAT1D) [MIM:[~~http~~://omim.org/entry/613796 613796]]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial and viral infections. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref> <ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[~~http~~://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref> <ref>PMID:16934001</ref> <ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[~~http~~://omim.org/entry/614162 614162]]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans. Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type 17 helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa (PubMed:21714643).<ref>PMID:21727188</ref> <ref>PMID:21714643</ref>	+	[https://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN] Defects in STAT1 are the cause of STAT1 deficiency complete (STAT1D) [MIM:[https://omim.org/entry/613796 613796]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial and viral infections. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref> <ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[https://omim.org/entry/209950 209950]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref> <ref>PMID:16934001</ref> <ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[https://omim.org/entry/614162 614162]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans. Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type 17 helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa (PubMed:21714643).<ref>PMID:21727188</ref> <ref>PMID:21714643</ref>
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4.<ref>PMID:9724754</ref> <ref>PMID:12855578</ref> <ref>PMID:12764129</ref> <ref>PMID:15322115</ref> <ref>PMID:19088846</ref>	+	[https://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN] Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4.<ref>PMID:9724754</ref> <ref>PMID:12855578</ref> <ref>PMID:12764129</ref> <ref>PMID:15322115</ref> <ref>PMID:19088846</ref>
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
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	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Chen, X]]	+	[[Category: Chen X]]
-	[[Category: Darnell~~, J E~~]]	+	[[Category: Darnell Jr JE]]
-	[[Category: Demeler, B]]	+	[[Category: Demeler B]]
-	[[Category: Mao, X]]	+	[[Category: Mao X]]
-	[[Category: McMurray~~, J S~~]]	+	[[Category: McMurray JS]]
-	[[Category: Parker~~, G N~~]]	+	[[Category: Parker GN]]
-	[[Category: Pastorello~~, M A~~]]	+	[[Category: Pastorello MA]]
-	[[Category: Ren, Z]]	+	[[Category: Ren Z]]
-	[[Category: Sondermann, H]]	+	[[Category: Sondermann H]]
-	[[Category: Wang, W]]	+	[[Category: Wang W]]
-	~~[[Category: Signaling protein~~]]	+

OCA at 08:53, 20 January 2021

OCA — Wed, 20 Jan 2021 08:53:41 GMT

←Older revision		Revision as of 08:53, 20 January 2021
Line 1:		Line 1:

	==Structure of Unphosphorylated STAT1==		==Structure of Unphosphorylated STAT1==
-	<StructureSection load='1yvl' size='340' side='right' caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>	+	<StructureSection load='1yvl' size='340' side='right'caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1YVL FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://proteopedia.org/fgij/fg.htm?mol=1YVL FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">STAT1 ([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">STAT1 ([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=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://pdbe.org/1yvl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1yvl ProSAT]</span></td></tr>	+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://proteopedia.org/fgij/fg.htm?mol=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://pdbe.org/1yvl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1yvl ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 37:		Line 37:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Chen, X]]		[[Category: Chen, X]]
	[[Category: Darnell, J E]]		[[Category: Darnell, J E]]

OCA at 06:21, 25 April 2018

OCA — Wed, 25 Apr 2018 06:21:54 GMT

←Older revision		Revision as of 06:21, 25 April 2018
Line 1:		Line 1:
		+
	==Structure of Unphosphorylated STAT1==		==Structure of Unphosphorylated STAT1==
	<StructureSection load='1yvl' size='340' side='right' caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>		<StructureSection load='1yvl' size='340' side='right' caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>
Line 6:		Line 7:
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">STAT1 ([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">STAT1 ([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=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://pdbe.org/1yvl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl 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=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://pdbe.org/1yvl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1yvl ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 16:		Line 17:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/yv/1yvl_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/yv/1yvl_consurf.spt"</scriptWhenChecked>
	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>		<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>

OCA at 05:27, 9 February 2016

OCA — Tue, 09 Feb 2016 05:27:41 GMT

←Older revision		Revision as of 05:27, 9 February 2016
Line 20:		Line 20:
	<text>to colour the structure by Evolutionary Conservation</text>		<text>to colour the structure by Evolutionary Conservation</text>
	</jmolCheckbox>		</jmolCheckbox>
-	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/~~chain_selection~~.php?pdb_ID=~~2ata~~ ConSurf].	+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/main_output.php?pdb_ID=1yvl ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 19:04, 10 September 2015

OCA — Thu, 10 Sep 2015 19:04:47 GMT

←Older revision		Revision as of 19:04, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='1yvl' size='340' side='right' caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>		<StructureSection load='1yvl' size='340' side='right' caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1YVL FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1YVL FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene></td></tr>
	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>		<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">STAT1 ([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">STAT1 ([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=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl 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=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://pdbe.org/1yvl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 30:		Line 30:
	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 1yvl" style="background-color:#fffaf0;"></div>
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Chen, X]]		[[Category: Chen, X]]
	[[Category: Darnell, J E]]		[[Category: Darnell, J E]]

OCA at 08:49, 8 January 2015

OCA — Thu, 08 Jan 2015 08:49:42 GMT

←Older revision		Revision as of 08:49, 8 January 2015
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1YVL FirstGlance]. <br>		<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1YVL FirstGlance]. <br>
-	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene><br>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>	+	<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>
-	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">STAT1 ([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">STAT1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
-	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl 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=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Defects in STAT1 are the cause of STAT1 deficiency complete (STAT1D) [MIM:[http://omim.org/entry/613796 613796]]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial and viral infections. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref> <ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[http://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref> <ref>PMID:16934001</ref> <ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[http://omim.org/entry/614162 614162]]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans. Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type 17 helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa (PubMed:21714643).<ref>PMID:21727188</ref> <ref>PMID:21714643</ref>		[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Defects in STAT1 are the cause of STAT1 deficiency complete (STAT1D) [MIM:[http://omim.org/entry/613796 613796]]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial and viral infections. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref> <ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[http://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref> <ref>PMID:16934001</ref> <ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[http://omim.org/entry/614162 614162]]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans. Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type 17 helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa (PubMed:21714643).<ref>PMID:21727188</ref> <ref>PMID:21714643</ref>
Line 35:		Line 35:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Chen, X.]]	+	[[Category: Chen, X]]
-	[[Category: Darnell, J E.]]	+	[[Category: Darnell, J E]]
-	[[Category: Demeler, B.]]	+	[[Category: Demeler, B]]
-	[[Category: Mao, X.]]	+	[[Category: Mao, X]]
-	[[Category: McMurray, J S.]]	+	[[Category: McMurray, J S]]
-	[[Category: Parker, G N.]]	+	[[Category: Parker, G N]]
-	[[Category: Pastorello, M A.]]	+	[[Category: Pastorello, M A]]
-	[[Category: Ren, Z.]]	+	[[Category: Ren, Z]]
-	[[Category: Sondermann, H.]]	+	[[Category: Sondermann, H]]
-	[[Category: Wang, W.]]	+	[[Category: Wang, W]]
	[[Category: Signaling protein]]		[[Category: Signaling protein]]

OCA at 20:17, 29 September 2014

OCA — Mon, 29 Sep 2014 20:17:05 GMT

←Older revision		Revision as of 20:17, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1yvl~~\| ~~PDB~~=1yvl \| ~~SCENE~~= }}	+	==Structure of Unphosphorylated STAT1==
-	===~~Structure~~ of ~~Unphosphorylated~~ STAT1===	+	<StructureSection load='1yvl' size='340' side='right' caption='[[1yvl]], [[Resolution\|resolution]] 3.00Å' scene=''>
-	~~{{ABSTRACT_PUBMED_15780933}}~~	+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[1yvl]] is a 4 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=1YVL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1YVL FirstGlance]. <br>
		+	</td></tr><tr><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AU:GOLD+ION'>AU</scene><br>
		+	<tr><td class="sblockLbl"><b>[[Non-Standard_Residue\|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></td></tr>
		+	<tr><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">STAT1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr>
		+	<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1yvl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1yvl OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1yvl RCSB], [http://www.ebi.ac.uk/pdbsum/1yvl PDBsum]</span></td></tr>
		+	<table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Defects in STAT1 are the cause of STAT1 deficiency complete (STAT1D) [MIM:[http://omim.org/entry/613796 613796]]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial and viral infections. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref> <ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[http://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref> <ref>PMID:16934001</ref> <ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[http://omim.org/entry/614162 614162]]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans. Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type 17 helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa (PubMed:21714643).<ref>PMID:21727188</ref> <ref>PMID:21714643</ref>
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4.<ref>PMID:9724754</ref> <ref>PMID:12855578</ref> <ref>PMID:12764129</ref> <ref>PMID:15322115</ref> <ref>PMID:19088846</ref>
		+	== Evolutionary Conservation ==
		+	[[Image:Consurf_key_small.gif\|200px\|right]]
		+	Check<jmol>
		+	<jmolCheckbox>
		+	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/yv/1yvl_consurf.spt"</scriptWhenChecked>
		+	<scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked>
		+	<text>to colour the structure by Evolutionary Conservation</text>
		+	</jmolCheckbox>
		+	</jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary\|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf].
		+	<div style="clear:both"></div>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	The crystal structure has been determined at 3.0 A resolution for an unphosphorylated STAT1 (1-683) complexed with a phosphopeptide derived from the alpha chain of interferon gamma (IFNgamma) receptor. Two dimer interfaces are seen, one between the N domains (NDs) (amino acid residues 1-123) and the other between the core fragments (CFs) (residues 132-683). Analyses of the wild-type (wt) and mutant STAT1 proteins by static light scattering, analytical ultracentrifugation, and coimmunoprecipitation suggest that STAT1 is predominantly dimeric prior to activation, and the dimer is mediated by the ND interactions. The connecting region between the ND and the CF is flexible and allows two interconvertable orientations of the CFs, termed "antiparallel" or "parallel," as determined by SH2 domain orientations. Functional implications of these dimer conformations are discussed. Also revealed in this structure is the detailed interaction between STAT1 SH2 domain and its docking site on IFNgamma receptor.

-	~~==Disease==~~	+	Structural bases of unphosphorylated STAT1 association and receptor binding.,Mao X, Ren Z, Parker GN, Sondermann H, Pastorello MA, Wang W, McMurray JS, Demeler B, Darnell JE Jr, Chen X Mol Cell. 2005 Mar 18;17(6):761-71. PMID:15780933<ref>PMID:15780933</ref>
-	~~[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Defects in STAT1 are the cause~~ of STAT1 ~~deficiency complete (STAT1D) [MIM:[http://omim.org/entry/613796 613796]]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial~~ and ~~viral infections~~. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref><ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[http://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, ~~such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria~~, ~~and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections~~, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, ~~whereas others develop~~, ~~later in life~~, ~~disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive~~, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref><ref>PMID:16934001</ref><ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[http://omim.org/entry/614162 614162]]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, ~~selective against Candida. It is characterized by persistent and/or recurrent infections of the skin~~, ~~nails and mucous membranes caused by organisms of the genus Candida~~, ~~mainly Candida albicans~~. ~~Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type~~ 17 ~~helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa~~ (~~PubMed~~:~~21714643)~~.~~<ref>~~PMID:~~21727188</ref>~~<ref>PMID:~~21714643~~</ref>	+

-	~~==Function==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	~~[[http:~~/~~/www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs)~~, cytokine KITLG/SCF and other cytokines and growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a ~~complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription~~ of ~~interferon stimulated genes, which drive~~ the ~~cell in an antiviral state~~. ~~In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated~~. ~~It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression~~ of ~~the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4~~.<~~ref~~>~~PMID:9724754~~</~~ref~~>~~<ref>PMID:12855578</ref><ref>PMID:12764129</ref><ref>PMID:15322115</ref><ref>PMID:19088846</ref>~~	+	</div>
-		+	== References ==
-	==~~About this Structure==~~	+	<references/>
-	[[1yvl]] is a 4 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=1YVL OCA].	+	__TOC__
-		+	</StructureSection>
-	~~==Reference~~==	+
-	~~<ref group="xtra">PMID:015780933</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Chen, X.]]		[[Category: Chen, X.]]

OCA at 03:08, 25 March 2013

OCA — Mon, 25 Mar 2013 03:08:49 GMT

←Older revision		Revision as of 03:08, 25 March 2013
Line 1:		Line 1:
-	[[Image:1yvl.png\|left\|200px]]
-
	{{STRUCTURE_1yvl\| PDB=1yvl \| SCENE= }}		{{STRUCTURE_1yvl\| PDB=1yvl \| SCENE= }}
-
	===Structure of Unphosphorylated STAT1===		===Structure of Unphosphorylated STAT1===
		+	{{ABSTRACT_PUBMED_15780933}}

-	~~{{ABSTRACT_PUBMED_15780933}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Defects in STAT1 are the cause of STAT1 deficiency complete (STAT1D) [MIM:[http://omim.org/entry/613796 613796]]. STAT1D is a disorder characterized by susceptibility to severe mycobacterial and viral infections. Affected individuals can develop disseminated infections and die of viral illness.<ref>PMID:12590259</ref><ref>PMID:20841510</ref> Defects in STAT1 are a cause of Mendelian susceptibility to mycobacterial disease (MSMD) [MIM:[http://omim.org/entry/209950 209950]]; also known as familial disseminated atypical mycobacterial infection. This rare condition confers predisposition to illness caused by moderately virulent mycobacterial species, such as Bacillus Calmette-Guerin (BCG) vaccine and environmental non-tuberculous mycobacteria, and by the more virulent Mycobacterium tuberculosis. Other microorganisms rarely cause severe clinical disease in individuals with susceptibility to mycobacterial infections, with the exception of Salmonella which infects less than 50% of these individuals. The pathogenic mechanism underlying MSMD is the impairment of interferon-gamma mediated immunity whose severity determines the clinical outcome. Some patients die of overwhelming mycobacterial disease with lepromatous-like lesions in early childhood, whereas others develop, later in life, disseminated but curable infections with tuberculoid granulomas. MSMD is a genetically heterogeneous disease with autosomal recessive, autosomal dominant or X-linked inheritance.<ref>PMID:11452125</ref><ref>PMID:16934001</ref><ref>PMID:22573496</ref> Defects in STAT1 are the cause of familial candidiasis type 7 (CANDF7) [MIM:[http://omim.org/entry/614162 614162]]. A primary immunodeficiency disorder with altered immune responses and impaired clearance of fungal infections, selective against Candida. It is characterized by persistent and/or recurrent infections of the skin, nails and mucous membranes caused by organisms of the genus Candida, mainly Candida albicans. Note=STAT1 mutations in patients with autosomal dominant candidiasis lead to defective responses of type 1 and type 17 helper T-cells, characterized by reduced production of interferon-alpha, interleukin-17, and interleukin-22. These cytokines are crucial for the antifungal defense of skin and mucosa (PubMed:21714643).<ref>PMID:21727188</ref><ref>PMID:21714643</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/STAT1_HUMAN STAT1_HUMAN]] Signal transducer and transcription activator that mediates cellular responses to interferons (IFNs), cytokine KITLG/SCF and other cytokines and growth factors. Following type I IFN (IFN-alpha and IFN-beta) binding to cell surface receptors, signaling via protein kinases leads to activation of Jak kinases (TYK2 and JAK1) and to tyrosine phosphorylation of STAT1 and STAT2. The phosphorylated STATs dimerize, associate with ISGF3G/IRF-9 to form a complex termed ISGF3 transcription factor, that enters the nucleus. ISGF3 binds to the IFN stimulated response element (ISRE) to activate the transcription of interferon stimulated genes, which drive the cell in an antiviral state. In response to type II IFN (IFN-gamma), STAT1 is tyrosine- and serine-phosphorylated. It then forms a homodimer termed IFN-gamma-activated factor (GAF), migrates into the nucleus and binds to the IFN gamma activated sequence (GAS) to drive the expression of the target genes, inducing a cellular antiviral state. Becomes activated in response to KITLG/SCF and KIT signaling. May mediate cellular responses to activated FGFR1, FGFR2, FGFR3 and FGFR4.<ref>PMID:9724754</ref><ref>PMID:12855578</ref><ref>PMID:12764129</ref><ref>PMID:15322115</ref><ref>PMID:19088846</ref>

	==About this Structure==		==About this Structure==
Line 11:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:015780933</ref><references group="xtra"/>	+	<ref group="xtra">PMID:015780933</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Chen, X.]]		[[Category: Chen, X.]]

OCA: Protected "1yvl" [edit=sysop:move=sysop]

OCA — Sat, 05 Jan 2013 16:58:10 GMT

Protected "1yvl" [edit=sysop:move=sysop]

←Older revision

Revision as of 16:58, 5 January 2013

OCA at 16:58, 5 January 2013

OCA — Sat, 05 Jan 2013 16:58:08 GMT

←Older revision		Revision as of 16:58, 5 January 2013
Line 1:		Line 1:
-	{{Seed}}
	[[Image:1yvl.png\|left\|200px]]		[[Image:1yvl.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_1yvl", creates the "Structure Box" on the page.
-	You may change the PDB parameter (which sets the PDB file loaded into the applet)
-	or the SCENE parameter (which sets the initial scene displayed when the page is loaded),
-	or leave the SCENE parameter empty for the default display.
-	-->
	{{STRUCTURE_1yvl\| PDB=1yvl \| SCENE= }}		{{STRUCTURE_1yvl\| PDB=1yvl \| SCENE= }}

	===Structure of Unphosphorylated STAT1===		===Structure of Unphosphorylated STAT1===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_15780933}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 15780933 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_15780933}}		{{ABSTRACT_PUBMED_15780933}}
-
-	==Disease==
-	Known disease associated with this structure: Mycobacterial infection, atypical, familial disseminated OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600555 600555]], STAT1 deficiency, complete OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=600555 600555]]

	==About this Structure==		==About this Structure==
-	~~1YVL~~ is a 4 ~~chains~~ structure ~~of sequences~~ 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=1YVL OCA].	+	[[1yvl]] is a 4 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=1YVL OCA].

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~15780933~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:015780933</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Chen, X.]]		[[Category: Chen, X.]]
		+	[[Category: Darnell, J E.]]
	[[Category: Demeler, B.]]		[[Category: Demeler, B.]]
-	[[Category: Jr., J E.Darnell.]]
	[[Category: Mao, X.]]		[[Category: Mao, X.]]
	[[Category: McMurray, J S.]]		[[Category: McMurray, J S.]]
Line 39:		Line 24:
	[[Category: Wang, W.]]		[[Category: Wang, W.]]
	[[Category: Signaling protein]]		[[Category: Signaling protein]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Tue Feb 17 06:50:17 2009''