8d3f - Revision history

OCA at 10:06, 25 October 2023

OCA — Wed, 25 Oct 2023 10:06:18 GMT

←Older revision		Revision as of 10:06, 25 October 2023
Line 4:		Line 4:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[8d3f]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Toxoplasma_gondii_GT1 Toxoplasma gondii GT1]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8D3F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8D3F FirstGlance]. <br>		<table><tr><td colspan='2'>[[8d3f]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Toxoplasma_gondii_GT1 Toxoplasma gondii GT1]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8D3F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8D3F FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8d3f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8d3f OCA], [https://pdbe.org/8d3f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8d3f RCSB], [https://www.ebi.ac.uk/pdbsum/8d3f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8d3f ProSAT]</span></td></tr>	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.97Å</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=8d3f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8d3f OCA], [https://pdbe.org/8d3f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8d3f RCSB], [https://www.ebi.ac.uk/pdbsum/8d3f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8d3f ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==

OCA at 07:46, 18 January 2023

OCA — Wed, 18 Jan 2023 07:46:35 GMT

←Older revision		Revision as of 07:46, 18 January 2023
Line 7:		Line 7:
	</table>		</table>
	== Disease ==		== Disease ==
-	[[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>	+	[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 ==
-	[[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> [[https://www.uniprot.org/uniprot/A0A7J6KA90_TOXGO A0A7J6KA90_TOXGO]]	+	[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> [https://www.uniprot.org/uniprot/A0A7J6KA90_TOXGO A0A7J6KA90_TOXGO]
	== References ==		== References ==
	<references/>		<references/>

OCA at 06:50, 8 September 2022

OCA — Thu, 08 Sep 2022 06:50:58 GMT

←Older revision		Revision as of 06:50, 8 September 2022
Line 1:		Line 1:

	==Crystal structure of human STAT1 in complex with the repeat region from Toxoplasma protein TgIST==		==Crystal structure of human STAT1 in complex with the repeat region from Toxoplasma protein TgIST==
-	<StructureSection load='8d3f' size='340' side='right'caption='[[8d3f]]' scene=''>	+	<StructureSection load='8d3f' size='340' side='right'caption='[[8d3f]], [[Resolution\|resolution]] 2.97Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8D3F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8D3F FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[8d3f]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [https://en.wikipedia.org/wiki/Toxoplasma_gondii_GT1 Toxoplasma gondii GT1]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8D3F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8D3F FirstGlance]. <br>
	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=8d3f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8d3f OCA], [https://pdbe.org/8d3f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8d3f RCSB], [https://www.ebi.ac.uk/pdbsum/8d3f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8d3f ProSAT]</span></td></tr>		</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=8d3f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8d3f OCA], [https://pdbe.org/8d3f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8d3f RCSB], [https://www.ebi.ac.uk/pdbsum/8d3f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8d3f ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[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 ==
		+	[[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> [[https://www.uniprot.org/uniprot/A0A7J6KA90_TOXGO A0A7J6KA90_TOXGO]]
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
		+	[[Category: Toxoplasma gondii GT1]]
	[[Category: Amarasinghe GK]]		[[Category: Amarasinghe GK]]
	[[Category: Huang Z]]		[[Category: Huang Z]]

OCA at 16:16, 6 July 2022

OCA — Wed, 06 Jul 2022 16:16:42 GMT

←Older revision		Revision as of 16:16, 6 July 2022
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry~~ 8d3f is ~~ON HOLD until Paper Publication~~	+	==Crystal structure of human STAT1 in complex with the repeat region from Toxoplasma protein TgIST==
-		+	<StructureSection load='8d3f' size='340' side='right'caption='[[8d3f]]' scene=''>
-	~~Authors~~:	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8D3F OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8D3F FirstGlance]. <br>
-	~~Description~~:	+	</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=8d3f FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8d3f OCA], [https://pdbe.org/8d3f PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8d3f RCSB], [https://www.ebi.ac.uk/pdbsum/8d3f PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8d3f ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased Structures~~]]	+	</table>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Amarasinghe GK]]
		+	[[Category: Huang Z]]
		+	[[Category: Liu H]]
		+	[[Category: Nix JC]]
		+	[[Category: Sibley LD]]

OCA at 07:25, 22 June 2022

OCA — Wed, 22 Jun 2022 07:25:27 GMT

←Older revision		Revision as of 07:25, 22 June 2022
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 8d3f is ON HOLD	+	The entry 8d3f is ON HOLD until Paper Publication

	Authors:		Authors:

OCA: Protected "8d3f" [edit=sysop:move=sysop]

OCA — Wed, 08 Jun 2022 04:35:19 GMT

Protected "8d3f" [edit=sysop:move=sysop]

←Older revision

Revision as of 04:35, 8 June 2022

OCA: New page: '''Unreleased structure''' The entry 8d3f is ON HOLD Authors: Description: Category: Unreleased Structures

OCA — Wed, 08 Jun 2022 04:35:18 GMT

New page: '''Unreleased structure''' The entry 8d3f is ON HOLD Authors: Description: Category: Unreleased Structures

New page

'''Unreleased structure'''

The entry 8d3f is ON HOLD

Authors:

Description:
[[Category: Unreleased Structures]]