3f1n - Revision history

OCA at 06:40, 6 September 2023

OCA — Wed, 06 Sep 2023 06:40:27 GMT

←Older revision		Revision as of 06:40, 6 September 2023
Line 3:		Line 3:
	<StructureSection load='3f1n' size='340' side='right'caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>		<StructureSection load='3f1n' size='340' side='right'caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3F1N FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3F1N FirstGlance]. <br>
-	</td></tr><tr id='~~ligand~~'><td class="sblockLbl"><b>[[~~Ligand~~\|~~Ligands~~:]]</b></td><td class="sblockDat" id="~~ligandDat~~">~~<scene name='pdbligand=EDO:~~1~~,2-ETHANEDIOL'>EDO</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]] 1.479Å</td></tr>
-	<tr id='~~related~~'><td class="sblockLbl"><b>[[~~Related_structure~~\|~~Related~~:]]</b></td><td class="sblockDat"><~~div style~~='~~overflow~~: ~~auto; max~~-~~height: 3em;~~'>~~[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]~~</~~div~~>~~</td></tr>~~	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([https://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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [https://pdbe.org/3f1n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [https://www.ebi.ac.uk/pdbsum/3f1n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3f1n 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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [https://pdbe.org/3f1n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [https://www.ebi.ac.uk/pdbsum/3f1n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3f1n ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[https://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>	+	[https://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[https://omim.org/entry/611783 611783]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. [[https://www.uniprot.org/uniprot/ARNT_HUMAN ARNT_HUMAN]] Required for activity of the Ah (dioxin) receptor. This protein is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after ligand binding. The complex then initiates transcription of genes involved in the activation of PAH procarcinogens. The heterodimer with HIF1A or EPAS1/HIF2A functions as a transcriptional regulator of the adaptive response to hypoxia.	+	[https://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD.
	== 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: Bruick~~, R K~~]]	+	[[Category: Bruick RK]]
-	[[Category: Gardner~~, K H~~]]	+	[[Category: Gardner KH]]
-	[[Category: Guo, Y]]	+	[[Category: Guo Y]]
-	[[Category: Machius, M]]	+	[[Category: Machius M]]
-	[[Category: Scheuermann~~, T H~~]]	+	[[Category: Scheuermann TH]]
-	[[Category: Tomchick~~, D R]]~~	+	[[Category: Tomchick DR]]
-	~~[[Category: Activator]]~~	+
-	~~[[Category: Alternative splicing]]~~	+
-	~~[[Category: Angiogenesis]]~~	+
-	~~[[Category: Congenital erythrocytosis]]~~	+
-	~~[[Category: Developmental protein]]~~	+
-	~~[[Category: Differentiation]]~~	+
-	~~[[Category: Disease mutation]]~~	+
-	~~[[Category: Dna-binding]]~~	+
-	~~[[Category: Heterodimer]]~~	+
-	~~[[Category: Hydroxylation]]~~	+
-	~~[[Category: Internal cavity]]~~	+
-	~~[[Category: Nucleus]]~~	+
-	~~[[Category: Pas domain]]~~	+
-	~~[[Category: Phosphoprotein]]~~	+
-	~~[[Category: Polymorphism]]~~	+
-	~~[[Category: Transcription]]~~	+
-	~~[[Category: Transcription regulation]]~~	+
-	~~[[Category: Ubl conjugation~~]]	+

OCA at 19:49, 20 October 2021

OCA — Wed, 20 Oct 2021 19:49:10 GMT

←Older revision		Revision as of 19:49, 20 October 2021
Line 1:		Line 1:

	==Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.==		==Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.==
-	<StructureSection load='3f1n' size='340' side='right' caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>	+	<StructureSection load='3f1n' size='340' side='right'caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=3F1N FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3F1N FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>
-	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</td></tr>	+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</div></td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([~~http~~://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([~~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">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([https://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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [~~http~~://pdbe.org/3f1n PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/3f1n PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=3f1n 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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [https://pdbe.org/3f1n PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [https://www.ebi.ac.uk/pdbsum/3f1n PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3f1n ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[~~http~~://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>	+	[[https://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[https://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. [[~~http~~://www.uniprot.org/uniprot/ARNT_HUMAN ARNT_HUMAN]] Required for activity of the Ah (dioxin) receptor. This protein is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after ligand binding. The complex then initiates transcription of genes involved in the activation of PAH procarcinogens. The heterodimer with HIF1A or EPAS1/HIF2A functions as a transcriptional regulator of the adaptive response to hypoxia.	+	[[https://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. [[https://www.uniprot.org/uniprot/ARNT_HUMAN ARNT_HUMAN]] Required for activity of the Ah (dioxin) receptor. This protein is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after ligand binding. The complex then initiates transcription of genes involved in the activation of PAH procarcinogens. The heterodimer with HIF1A or EPAS1/HIF2A functions as a transcriptional regulator of the adaptive response to hypoxia.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/f1/3f1n_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/f1/3f1n_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>
Line 32:		Line 32:
	</div>		</div>
	<div class="pdbe-citations 3f1n" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3f1n" style="background-color:#fffaf0;"></div>
		+
		+	==See Also==
		+	*[[Factor inhibiting HIF\|Factor inhibiting HIF]]
		+	*[[3D structures of hypoxia-inducible factor\|3D structures of hypoxia-inducible factor]]
	== References ==		== References ==
	<references/>		<references/>
Line 37:		Line 41:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Bruick, R K]]		[[Category: Bruick, R K]]
	[[Category: Gardner, K H]]		[[Category: Gardner, K H]]

OCA at 09:24, 25 October 2017

OCA — Wed, 25 Oct 2017 09:24:55 GMT

←Older revision		Revision as of 09:24, 25 October 2017
Line 1:		Line 1:
		+
	==Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.==		==Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.==
	<StructureSection load='3f1n' size='340' side='right' caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>		<StructureSection load='3f1n' size='340' side='right' caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>
Line 6:		Line 7:
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</td></tr>
	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([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">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [http://pdbe.org/3f1n PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [http://www.ebi.ac.uk/pdbsum/3f1n 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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [http://pdbe.org/3f1n PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [http://www.ebi.ac.uk/pdbsum/3f1n PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3f1n ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 31:		Line 32:
	</div>		</div>
	<div class="pdbe-citations 3f1n" style="background-color:#fffaf0;"></div>		<div class="pdbe-citations 3f1n" style="background-color:#fffaf0;"></div>
-
-	==See Also==
-	*[[Factor inhibiting HIF\|Factor inhibiting HIF]]
	== References ==		== References ==
	<references/>		<references/>
Line 46:		Line 44:
	[[Category: Tomchick, D R]]		[[Category: Tomchick, D R]]
	[[Category: Activator]]		[[Category: Activator]]
		+	[[Category: Alternative splicing]]
	[[Category: Angiogenesis]]		[[Category: Angiogenesis]]
	[[Category: Congenital erythrocytosis]]		[[Category: Congenital erythrocytosis]]
Line 58:		Line 57:
	[[Category: Pas domain]]		[[Category: Pas domain]]
	[[Category: Phosphoprotein]]		[[Category: Phosphoprotein]]
		+	[[Category: Polymorphism]]
	[[Category: Transcription]]		[[Category: Transcription]]
	[[Category: Transcription regulation]]		[[Category: Transcription regulation]]
		+	[[Category: Ubl conjugation]]

OCA at 03:12, 10 February 2016

OCA — Wed, 10 Feb 2016 03:12:18 GMT

←Older revision		Revision as of 03:12, 10 February 2016
Line 2:		Line 2:
	<StructureSection load='3f1n' size='340' side='right' caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>		<StructureSection load='3f1n' size='340' side='right' caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3F1N FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3F1N FirstGlance]. <br>
	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>		</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>
	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</td></tr>		<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 ~~Homo sapiens~~]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([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">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [http://www.ebi.ac.uk/pdbsum/3f1n 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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [http://pdbe.org/3f1n PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [http://www.ebi.ac.uk/pdbsum/3f1n PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
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=3f1n ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">
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 3f1n" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
Line 37:		Line 38:
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Bruick, R K]]		[[Category: Bruick, R K]]
	[[Category: Gardner, K H]]		[[Category: Gardner, K H]]

OCA at 13:52, 18 December 2014

OCA — Thu, 18 Dec 2014 13:52:53 GMT

←Older revision		Revision as of 13:52, 18 December 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_3f1n\| PDB=3f1n \| SCENE= }}~~	+	==Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.==
-	===Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.===	+	<StructureSection load='3f1n' size='340' side='right' caption='[[3f1n]], [[Resolution\|resolution]] 1.48Å' scene=''>
-	~~{{ABSTRACT_PUBMED_19129502}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[3f1n]] 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=3F1N OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3F1N FirstGlance]. <br>
-	==Disease==	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene></td></tr>
		+	<tr id='related'><td class="sblockLbl"><b>[[Related_structure\|Related:]]</b></td><td class="sblockDat">[[1x0o\|1x0o]], [[1p97\|1p97]], [[2b02\|2b02]], [[2a24\|2a24]], [[3f1o\|3f1o]], [[3f1p\|3f1p]]</td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">EPAS1, HIF2A, Hypoxia-Inducible Factor 2 alpha, MOP2 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens]), ARNT, Aryl Hydrocarbon Receptor Nuclear Translocator ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</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=3f1n FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3f1n OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3f1n RCSB], [http://www.ebi.ac.uk/pdbsum/3f1n PDBsum]</span></td></tr>
		+	</table>
		+	== Disease ==
	[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[http://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>		[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[http://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>
-		+	== Function ==
-	==Function==	+
	[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. [[http://www.uniprot.org/uniprot/ARNT_HUMAN ARNT_HUMAN]] Required for activity of the Ah (dioxin) receptor. This protein is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after ligand binding. The complex then initiates transcription of genes involved in the activation of PAH procarcinogens. The heterodimer with HIF1A or EPAS1/HIF2A functions as a transcriptional regulator of the adaptive response to hypoxia.		[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. [[http://www.uniprot.org/uniprot/ARNT_HUMAN ARNT_HUMAN]] Required for activity of the Ah (dioxin) receptor. This protein is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after ligand binding. The complex then initiates transcription of genes involved in the activation of PAH procarcinogens. The heterodimer with HIF1A or EPAS1/HIF2A functions as a transcriptional regulator of the adaptive response to hypoxia.
		+	== 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/f1/3f1n_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 hypoxia-inducible factor (HIF) basic helix-loop-helix Per-aryl hydrocarbon receptor nuclear translocator (ARNT)-Sim (bHLH-PAS) transcription factors are master regulators of the conserved molecular mechanism by which metazoans sense and respond to reductions in local oxygen concentrations. In humans, HIF is critically important for the sustained growth and metastasis of solid tumors. Here, we describe crystal structures of the heterodimer formed by the C-terminal PAS domains from the HIF2alpha and ARNT subunits of the HIF2 transcription factor, both in the absence and presence of an artificial ligand. Unexpectedly, the HIF2alpha PAS-B domain contains a large internal cavity that accommodates ligands identified from a small-molecule screen. Binding one of these ligands to HIF2alpha PAS-B modulates the affinity of the HIF2alpha:ARNT PAS-B heterodimer in vitro. Given the essential role of PAS domains in forming active HIF heterodimers, these results suggest a presently uncharacterized ligand-mediated mechanism for regulating HIF2 activity in endogenous and clinical settings.

-	~~==About this Structure==~~	+	Artificial ligand binding within the HIF2alpha PAS-B domain of the HIF2 transcription factor.,Scheuermann TH, Tomchick DR, Machius M, Guo Y, Bruick RK, Gardner KH Proc Natl Acad Sci U S A. 2009 Jan 13;106(2):450-5. Epub 2009 Jan 7. PMID:19129502<ref>PMID:19129502</ref>
-	~~[[3f1n]] 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=3F1N OCA].~~	+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>

	==See Also==		==See Also==
	*[[Factor inhibiting HIF\|Factor inhibiting HIF]]		*[[Factor inhibiting HIF\|Factor inhibiting HIF]]
-		+	== References ==
-	==~~Reference~~==	+	<references/>
-	~~<ref group="xtra">PMID:019129502</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Bruick, R K.]]	+	[[Category: Bruick, R K]]
-	[[Category: Gardner, K H.]]	+	[[Category: Gardner, K H]]
-	[[Category: Guo, Y.]]	+	[[Category: Guo, Y]]
-	[[Category: Machius, M.]]	+	[[Category: Machius, M]]
-	[[Category: Scheuermann, T H.]]	+	[[Category: Scheuermann, T H]]
-	[[Category: Tomchick, D R.]]	+	[[Category: Tomchick, D R]]
	[[Category: Activator]]		[[Category: Activator]]
	[[Category: Angiogenesis]]		[[Category: Angiogenesis]]

OCA at 11:03, 24 July 2013

OCA — Wed, 24 Jul 2013 11:03:22 GMT

←Older revision		Revision as of 11:03, 24 July 2013
Line 4:		Line 4:

	==Disease==		==Disease==
-	[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[http://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref><ref>PMID:18378852</ref><ref>PMID:18184961</ref><ref>PMID:22367913</ref>	+	[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[http://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref> <ref>PMID:18378852</ref> <ref>PMID:18184961</ref> <ref>PMID:22367913</ref>

	==Function==		==Function==

OCA at 23:15, 24 March 2013

OCA — Sun, 24 Mar 2013 23:15:09 GMT

←Older revision		Revision as of 23:15, 24 March 2013
Line 1:		Line 1:
-	[[Image:3f1n.png\|left\|200px]]
-
	{{STRUCTURE_3f1n\| PDB=3f1n \| SCENE= }}		{{STRUCTURE_3f1n\| PDB=3f1n \| SCENE= }}
-
	===Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.===		===Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.===
		+	{{ABSTRACT_PUBMED_19129502}}

-	~~{{ABSTRACT_PUBMED_19129502}}~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Defects in EPAS1 are the cause of familial erythrocytosis type 4 (ECYT4) [MIM:[http://omim.org/entry/611783 611783]]. ECYT4 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin concentration and hematocrit, and normal platelet and leukocyte counts.<ref>PMID:19208626</ref><ref>PMID:18378852</ref><ref>PMID:18184961</ref><ref>PMID:22367913</ref>
		+
		+	==Function==
		+	[[http://www.uniprot.org/uniprot/EPAS1_HUMAN EPAS1_HUMAN]] Transcription factor involved in the induction of oxygen regulated genes. Binds to core DNA sequence 5'-[AG]CGTG-3' within the hypoxia response element (HRE) of target gene promoters. Regulates the vascular endothelial growth factor (VEGF) expression and seems to be implicated in the development of blood vessels and the tubular system of lung. May also play a role in the formation of the endothelium that gives rise to the blood brain barrier. Potent activator of the Tie-2 tyrosine kinase expression. Activation seems to require recruitment of transcriptional coactivators such as CREBPB and probably EP300. Interaction with redox regulatory protein APEX seems to activate CTAD. [[http://www.uniprot.org/uniprot/ARNT_HUMAN ARNT_HUMAN]] Required for activity of the Ah (dioxin) receptor. This protein is required for the ligand-binding subunit to translocate from the cytosol to the nucleus after ligand binding. The complex then initiates transcription of genes involved in the activation of PAH procarcinogens. The heterodimer with HIF1A or EPAS1/HIF2A functions as a transcriptional regulator of the adaptive response to hypoxia.

	==About this Structure==		==About this Structure==
Line 14:		Line 16:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:019129502</ref><references group="xtra"/>	+	<ref group="xtra">PMID:019129502</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Bruick, R K.]]		[[Category: Bruick, R K.]]

OCA at 16:07, 20 October 2012

OCA — Sat, 20 Oct 2012 16:07:54 GMT

←Older revision		Revision as of 16:07, 20 October 2012
Line 8:		Line 8:

	==About this Structure==		==About this Structure==
-	[[3f1n]] is a 2 chain structure ~~of [[Factor inhibiting HIF]]~~ 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=3F1N OCA].	+	[[3f1n]] 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=3F1N OCA].

	==See Also==		==See Also==

OCA: Protected "3f1n" [edit=sysop:move=sysop]

OCA — Thu, 26 Jul 2012 20:42:00 GMT

Protected "3f1n" [edit=sysop:move=sysop]

←Older revision

Revision as of 20:42, 26 July 2012

OCA at 20:41, 26 July 2012

OCA — Thu, 26 Jul 2012 20:41:58 GMT

←Older revision		Revision as of 20:41, 26 July 2012
Line 1:		Line 1:
-	{{Seed}}
	[[Image:3f1n.png\|left\|200px]]		[[Image:3f1n.png\|left\|200px]]

-	<!--
-	The line below this paragraph, containing "STRUCTURE_3f1n", 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_3f1n\| PDB=3f1n \| SCENE= }}		{{STRUCTURE_3f1n\| PDB=3f1n \| SCENE= }}

	===Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.===		===Crystal structure of a high affinity heterodimer of HIF2 alpha and ARNT C-terminal PAS domains, with internally bound ethylene glycol.===

-
-	<!--
-	The line below this paragraph, {{ABSTRACT_PUBMED_19129502}}, adds the Publication Abstract to the page
-	(as it appears on PubMed at http://www.pubmed.gov), where 19129502 is the PubMed ID number.
-	-->
	{{ABSTRACT_PUBMED_19129502}}		{{ABSTRACT_PUBMED_19129502}}

	==About this Structure==		==About this Structure==
-	~~3F1N~~ is a 2 ~~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=3F1N OCA].	+	[[3f1n]] is a 2 chain structure of [[Factor inhibiting HIF]] 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=3F1N OCA].
		+
		+	==See Also==
		+	*[[Factor inhibiting HIF\|Factor inhibiting HIF]]

	==Reference==		==Reference==
-	<ref group="xtra">PMID:~~19129502~~</ref><references group="xtra"/>	+	<ref group="xtra">PMID:019129502</ref><references group="xtra"/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Bruick, R K.]]		[[Category: Bruick, R K.]]
Line 32:		Line 23:
	[[Category: Tomchick, D R.]]		[[Category: Tomchick, D R.]]
	[[Category: Activator]]		[[Category: Activator]]
-	[[Category: Alternative splicing]]
	[[Category: Angiogenesis]]		[[Category: Angiogenesis]]
	[[Category: Congenital erythrocytosis]]		[[Category: Congenital erythrocytosis]]
Line 45:		Line 35:
	[[Category: Pas domain]]		[[Category: Pas domain]]
	[[Category: Phosphoprotein]]		[[Category: Phosphoprotein]]
-	[[Category: Polymorphism]]
	[[Category: Transcription]]		[[Category: Transcription]]
	[[Category: Transcription regulation]]		[[Category: Transcription regulation]]
-	[[Category: Ubl conjugation]]
-
-	''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Sun Mar 22 10:31:58 2009''