1ebp

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[[Image:1ebp.png|left|200px]]
 
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{{STRUCTURE_1ebp| PDB=1ebp | SCENE= }}
{{STRUCTURE_1ebp| PDB=1ebp | SCENE= }}
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===COMPLEX BETWEEN THE EXTRACELLULAR DOMAIN OF ERYTHROPOIETIN (EPO) RECEPTOR [EBP] AND AN AGONIST PEPTIDE [EMP1]===
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{{ABSTRACT_PUBMED_8662530}}
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===COMPLEX BETWEEN THE EXTRACELLULAR DOMAIN OF ERYTHROPOIETIN (EPO) RECEPTOR [EBP] AND AN AGONIST PEPTIDE [EMP1]===
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==Disease==
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[[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>
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==Function==
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[[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==
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==Reference==
==Reference==
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<ref group="xtra">PMID:008662530</ref><ref group="xtra">PMID:009774108</ref><references group="xtra"/>
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<ref group="xtra">PMID:008662530</ref><ref group="xtra">PMID:009774108</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Livnah, O.]]
[[Category: Livnah, O.]]

Revision as of 01:25, 25 March 2013

Template:STRUCTURE 1ebp

Contents

COMPLEX BETWEEN THE EXTRACELLULAR DOMAIN OF ERYTHROPOIETIN (EPO) RECEPTOR [EBP] AND AN AGONIST PEPTIDE [EMP1]

Template:ABSTRACT PUBMED 8662530

Disease

[EPOR_HUMAN] Defects in EPOR are the cause of familial erythrocytosis type 1 (ECYT1) [MIM: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.[1][2][3]

Function

[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

1ebp is a 4 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

Reference

  • Livnah O, Stura EA, Johnson DL, Middleton SA, Mulcahy LS, Wrighton NC, Dower WJ, Jolliffe LK, Wilson IA. Functional mimicry of a protein hormone by a peptide agonist: the EPO receptor complex at 2.8 A. Science. 1996 Jul 26;273(5274):464-71. PMID:8662530
  • 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. Efficiency of signalling through cytokine receptors depends critically on receptor orientation. Nature. 1998 Oct 1;395(6701):511-6. PMID:9774108 doi:http://dx.doi.org/10.1038/26773
  1. ↑ de la Chapelle A, Traskelin AL, Juvonen E. Truncated erythropoietin receptor causes dominantly inherited benign human erythrocytosis. Proc Natl Acad Sci U S A. 1993 May 15;90(10):4495-9. PMID:8506290
  2. ↑ Sokol L, Prchal JF, D'Andrea A, Rado TA, Prchal JT. Mutation in the negative regulatory element of the erythropoietin receptor gene in a case of sporadic primary polycythemia. Exp Hematol. 1994 May;22(5):447-53. PMID:8174675
  3. ↑ Le Couedic JP, Mitjavila MT, Villeval JL, Feger F, Gobert S, Mayeux P, Casadevall N, Vainchenker W. Missense mutation of the erythropoietin receptor is a rare event in human erythroid malignancies. Blood. 1996 Feb 15;87(4):1502-11. PMID:8608241

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