1eer - Revision history

OCA at 10:01, 20 March 2024

OCA — Wed, 20 Mar 2024 10:01:35 GMT

←Older revision		Revision as of 10:01, 20 March 2024
Line 3:		Line 3:
	<StructureSection load='1eer' size='340' side='right'caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='1eer' size='340' side='right'caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1EER FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1EER 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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [https://pdbe.org/1eer PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [https://www.ebi.ac.uk/pdbsum/1eer PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1eer 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]] 1.9Å</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [https://pdbe.org/1eer PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [https://www.ebi.ac.uk/pdbsum/1eer PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1eer ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[https://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[https://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[https://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref> <ref>PMID:8174675</ref> <ref>PMID:8608241</ref>	+	[https://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[https://omim.org/entry/612623 612623]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis.
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. [[https://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate the LYN tyrosine kinase. Isoform EPOR-T acts as a dominant-negative receptor of EPOR-mediated signaling.	+	[https://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]
Line 20:		Line 21:
	</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=1eer 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=1eer ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
-	<div style="background-color:#fffaf0;">
-	== Publication Abstract from PubMed ==
-	Human erythropoietin is a haematopoietic cytokine required for the differentiation and proliferation of precursor cells into red blood cells. It activates cells by binding and orientating two cell-surface erythropoietin receptors (EPORs) which trigger an intracellular phosphorylation cascade. The half-maximal response in a cellular proliferation assay is evoked at an erythropoietin concentration of 10 pM, 10(-2) of its Kd value for erythropoietin-EPOR binding site 1 (Kd approximately equal to nM), and 10(-5) of the Kd for erythropoietin-EPOR binding site 2 (Kd approximately equal to 1 microM). Overall half-maximal binding (IC50) of cell-surface receptors is produced with approximately 0.18 nM erythropoietin, indicating that only approximately 6% of the receptors would be bound in the presence of 10 pM erythropoietin. Other effective erythropoietin-mimetic ligands that dimerize receptors can evoke the same cellular responses but much less efficiently, requiring concentrations close to their Kd values (approximately 0.1 microM). The crystal structure of erythropoietin complexed to the extracellular ligand-binding domains of the erythropoietin receptor, determined at 1.9 A from two crystal forms, shows that erythropoietin imposes a unique 120 degrees angular relationship and orientation that is responsible for optimal signalling through intracellular kinase pathways.
-
-	Efficiency of signalling through cytokine receptors depends critically on receptor orientation.,Syed RS, Reid SW, Li C, Cheetham JC, Aoki KH, Liu B, Zhan H, Osslund TD, Chirino AJ, Zhang J, Finer-Moore J, Elliott S, Sitney K, Katz BA, Matthews DJ, Wendoloski JJ, Egrie J, Stroud RM Nature. 1998 Oct 1;395(6701):511-6. PMID:9774108<ref>PMID:9774108</ref>
-
-	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	</div>
-	<div class="pdbe-citations 1eer" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
	*[[Erythropoietin\|Erythropoietin]]		*[[Erythropoietin\|Erythropoietin]]
	*[[Erythropoietin receptor\|Erythropoietin receptor]]		*[[Erythropoietin receptor\|Erythropoietin receptor]]
-	== References ==
-	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Li, C]]	+	[[Category: Li C]]
-	[[Category: Syed~~, R S]]~~	+	[[Category: Syed RS]]
-	~~[[Category: Cytokine receptor class 1]]~~	+
-	~~[[Category: Erythropoietin]]~~	+
-	~~[[Category: Erythropoietin receptor]]~~	+
-	~~[[Category: Hematopoietic cytokine]]~~	+
-	~~[[Category: Signal transduction~~]]	+

OCA at 09:36, 21 July 2021

OCA — Wed, 21 Jul 2021 09:36:20 GMT

←Older revision		Revision as of 09:36, 21 July 2021
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	<StructureSection load='1eer' size='340' side='right'caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='1eer' size='340' side='right'caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=1EER FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=1EER FirstGlance]. <br>
-	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [~~http~~://pdbe.org/1eer PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/1eer PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=1eer 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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [https://pdbe.org/1eer PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [https://www.ebi.ac.uk/pdbsum/1eer PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=1eer ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[~~http~~://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[~~http~~://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[~~http~~://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[~~http~~://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref> <ref>PMID:8174675</ref> <ref>PMID:8608241</ref>	+	[[https://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[https://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[https://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[https://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref> <ref>PMID:8174675</ref> <ref>PMID:8608241</ref>
	== Function ==		== Function ==
-	[[~~http~~://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. [[~~http~~://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate the LYN tyrosine kinase. Isoform EPOR-T acts as a dominant-negative receptor of EPOR-mediated signaling.	+	[[https://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. [[https://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate the LYN tyrosine kinase. Isoform EPOR-T acts as a dominant-negative receptor of EPOR-mediated signaling.
	== Evolutionary Conservation ==		== Evolutionary Conservation ==
	[[Image:Consurf_key_small.gif\|200px\|right]]		[[Image:Consurf_key_small.gif\|200px\|right]]

OCA at 14:21, 16 October 2019

OCA — Wed, 16 Oct 2019 14:21:49 GMT

←Older revision		Revision as of 14:21, 16 October 2019
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	==CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS==		==CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS==
-	<StructureSection load='1eer' size='340' side='right' caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>	+	<StructureSection load='1eer' size='340' side='right'caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>		<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>
Line 32:		Line 32:
	==See Also==		==See Also==
	*[[Erythropoietin\|Erythropoietin]]		*[[Erythropoietin\|Erythropoietin]]
		+	*[[Erythropoietin receptor\|Erythropoietin receptor]]
	== References ==		== References ==
	<references/>		<references/>
Line 37:		Line 38:
	</StructureSection>		</StructureSection>
	[[Category: Human]]		[[Category: Human]]
		+	[[Category: Large Structures]]
	[[Category: Li, C]]		[[Category: Li, C]]
	[[Category: Syed, R S]]		[[Category: Syed, R S]]

OCA at 07:17, 20 December 2017

OCA — Wed, 20 Dec 2017 07:17:17 GMT

←Older revision		Revision as of 07:17, 20 December 2017
Line 1:		Line 1:
		+
	==CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS==		==CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS==
	<StructureSection load='1eer' size='340' side='right' caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='1eer' size='340' side='right' caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>		<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>
-	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://pdbe.org/1eer PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum]</span></td></tr>	+	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://pdbe.org/1eer PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=1eer ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 13:		Line 14:
	Check<jmol>		Check<jmol>
	<jmolCheckbox>		<jmolCheckbox>
-	<scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ee/1eer_consurf.spt"</scriptWhenChecked>	+	<scriptWhenChecked>; select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/ee/1eer_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 31:		Line 32:
	==See Also==		==See Also==
	*[[Erythropoietin\|Erythropoietin]]		*[[Erythropoietin\|Erythropoietin]]
-	*[[Erythropoietin receptor\|Erythropoietin receptor]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 06:46, 8 February 2016

OCA — Mon, 08 Feb 2016 06:46:00 GMT

←Older revision		Revision as of 06:46, 8 February 2016
Line 17:		Line 17:
	<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=1eer ConSurf].
	<div style="clear:both"></div>		<div style="clear:both"></div>
	<div style="background-color:#fffaf0;">		<div style="background-color:#fffaf0;">

OCA at 08:56, 10 September 2015

OCA — Thu, 10 Sep 2015 08:56:16 GMT

←Older revision		Revision as of 08:56, 10 September 2015
Line 2:		Line 2:
	<StructureSection load='1eer' size='340' side='right' caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>		<StructureSection load='1eer' size='340' side='right' caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>
-	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum]</span></td></tr>	+	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://pdbe.org/1eer PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
Line 27:		Line 27:
	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 1eer" style="background-color:#fffaf0;"></div>

	==See Also==		==See Also==
	*[[Erythropoietin\|Erythropoietin]]		*[[Erythropoietin\|Erythropoietin]]
		+	*[[Erythropoietin receptor\|Erythropoietin receptor]]
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Homo sapiens~~]]	+	[[Category: Human]]
	[[Category: Li, C]]		[[Category: Li, C]]
	[[Category: Syed, R S]]		[[Category: Syed, R S]]

OCA at 06:17, 16 February 2015

OCA — Mon, 16 Feb 2015 06:17:41 GMT

←Older revision		Revision as of 06:17, 16 February 2015
Line 27:		Line 27:
	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>
		+
		+	==See Also==
		+	*[[Erythropoietin\|Erythropoietin]]
	== References ==		== References ==
	<references/>		<references/>

OCA at 23:58, 22 December 2014

OCA — Mon, 22 Dec 2014 23:58:28 GMT

←Older revision		Revision as of 23:58, 22 December 2014
Line 3:		Line 3:
	== Structural highlights ==		== Structural highlights ==
	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>		<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>
-	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum]</span></td></tr>	+	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum]</span></td></tr>
-	<table>	+	</table>
	== Disease ==		== Disease ==
	[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[http://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[http://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref> <ref>PMID:8174675</ref> <ref>PMID:8608241</ref>		[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[http://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[http://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref> <ref>PMID:8174675</ref> <ref>PMID:8608241</ref>
Line 32:		Line 32:
	</StructureSection>		</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
-	[[Category: Li, C.]]	+	[[Category: Li, C]]
-	[[Category: Syed, R S.]]	+	[[Category: Syed, R S]]
	[[Category: Cytokine receptor class 1]]		[[Category: Cytokine receptor class 1]]
	[[Category: Erythropoietin]]		[[Category: Erythropoietin]]

OCA at 17:09, 29 September 2014

OCA — Mon, 29 Sep 2014 17:09:30 GMT

←Older revision		Revision as of 17:09, 29 September 2014
Line 1:		Line 1:
-	~~{{STRUCTURE_1eer\| PDB=1eer \| SCENE= }}~~	+	==CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS==
-	===CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS===	+	<StructureSection load='1eer' size='340' side='right' caption='[[1eer]], [[Resolution\|resolution]] 1.90Å' scene=''>
-	~~{{ABSTRACT_PUBMED_9774108}}~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>[[1eer]] is a 3 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=1EER OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=1EER FirstGlance]. <br>
-	==Disease==	+	</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=1eer FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=1eer OCA], [http://www.rcsb.org/pdb/explore.do?structureId=1eer RCSB], [http://www.ebi.ac.uk/pdbsum/1eer PDBsum]</span></td></tr>
-	[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[http://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[http://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref><ref>PMID:8174675</ref><ref>PMID:8608241</ref>	+	<table>
-		+	== Disease ==
-	==Function==	+	[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[http://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[http://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref> <ref>PMID:8174675</ref> <ref>PMID:8608241</ref>
		+	== Function ==
	[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate the LYN tyrosine kinase. Isoform EPOR-T acts as a dominant-negative receptor of EPOR-mediated signaling.		[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate the LYN tyrosine kinase. Isoform EPOR-T acts as a dominant-negative receptor of EPOR-mediated signaling.
		+	== 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/ee/1eer_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 ==
		+	Human erythropoietin is a haematopoietic cytokine required for the differentiation and proliferation of precursor cells into red blood cells. It activates cells by binding and orientating two cell-surface erythropoietin receptors (EPORs) which trigger an intracellular phosphorylation cascade. The half-maximal response in a cellular proliferation assay is evoked at an erythropoietin concentration of 10 pM, 10(-2) of its Kd value for erythropoietin-EPOR binding site 1 (Kd approximately equal to nM), and 10(-5) of the Kd for erythropoietin-EPOR binding site 2 (Kd approximately equal to 1 microM). Overall half-maximal binding (IC50) of cell-surface receptors is produced with approximately 0.18 nM erythropoietin, indicating that only approximately 6% of the receptors would be bound in the presence of 10 pM erythropoietin. Other effective erythropoietin-mimetic ligands that dimerize receptors can evoke the same cellular responses but much less efficiently, requiring concentrations close to their Kd values (approximately 0.1 microM). The crystal structure of erythropoietin complexed to the extracellular ligand-binding domains of the erythropoietin receptor, determined at 1.9 A from two crystal forms, shows that erythropoietin imposes a unique 120 degrees angular relationship and orientation that is responsible for optimal signalling through intracellular kinase pathways.

-	~~==About this Structure==~~	+	Efficiency of signalling through cytokine receptors depends critically on receptor orientation.,Syed RS, Reid SW, Li C, Cheetham JC, Aoki KH, Liu B, Zhan H, Osslund TD, Chirino AJ, Zhang J, Finer-Moore J, Elliott S, Sitney K, Katz BA, Matthews DJ, Wendoloski JJ, Egrie J, Stroud RM Nature. 1998 Oct 1;395(6701):511-6. PMID:9774108<ref>PMID:9774108</ref>
-	~~[[1eer]] is a 3 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=1EER OCA].~~	+

-	~~==Reference==~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	<~~ref group="xtra"~~>~~PMID:009774108~~</~~ref~~>~~<ref group~~=~~"xtra">PMID:012215425</ref>~~<references ~~group="xtra"~~/><~~references~~/>	+	</div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Li, C.]]		[[Category: Li, C.]]

OCA at 06:13, 25 March 2013

OCA — Mon, 25 Mar 2013 06:13:07 GMT

←Older revision		Revision as of 06:13, 25 March 2013
Line 1:		Line 1:
-	[[Image:1eer.png\|left\|200px]]
-
	{{STRUCTURE_1eer\| PDB=1eer \| SCENE= }}		{{STRUCTURE_1eer\| PDB=1eer \| SCENE= }}
		+	===CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT 1.9 ANGSTROMS===
		+	{{ABSTRACT_PUBMED_9774108}}

-	===~~CRYSTAL STRUCTURE OF HUMAN ERYTHROPOIETIN COMPLEXED TO ITS RECEPTOR AT~~ 1.~~9 ANGSTROMS===~~	+	==Disease==
		+	[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Genetic variation in EPO is associated with susceptbility to microvascular complications of diabetes type 2 (MVCD2) [MIM:[http://omim.org/entry/612623 612623]]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM:[http://omim.org/entry/133100 133100]]. ECYT1 is an autosomal dominant disorder characterized by increased serum red blood cell mass, elevated hemoglobin and hematocrit, hypersensitivity of erythroid progenitors to erythropoietin, erythropoietin low serum levels, and no increase in platelets nor leukocytes. It has a relatively benign course and does not progress to leukemia.<ref>PMID:8506290</ref><ref>PMID:8174675</ref><ref>PMID:8608241</ref>

		+	==Function==
		+	[[http://www.uniprot.org/uniprot/EPO_HUMAN EPO_HUMAN]] Erythropoietin is the principal hormone involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. [[http://www.uniprot.org/uniprot/EPOR_HUMAN EPOR_HUMAN]] Receptor for erythropoietin. Mediates erythropoietin-induced erythroblast proliferation and differentiation. Upon EPO stimulation, EPOR dimerizes triggering the JAK2/STAT5 signaling cascade. In some cell types, can also activate STAT1 and STAT3. May also activate the LYN tyrosine kinase. Isoform EPOR-T acts as a dominant-negative receptor of EPOR-mediated signaling.

	==About this Structure==		==About this Structure==
Line 10:		Line 13:

	==Reference==		==Reference==
-	<ref group="xtra">PMID:009774108</ref><ref group="xtra">PMID:012215425</ref><references group="xtra"/>	+	<ref group="xtra">PMID:009774108</ref><ref group="xtra">PMID:012215425</ref><references group="xtra"/><references/>
	[[Category: Homo sapiens]]		[[Category: Homo sapiens]]
	[[Category: Li, C.]]		[[Category: Li, C.]]