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Publication : Requirement for p38alpha in erythropoietin expression: a role for stress kinases in erythropoiesis.

First Author  Tamura K Year  2000
Journal  Cell Volume  102
Issue  2 Pages  221-31
PubMed ID  10943842 Mgi Jnum  J:63425
Mgi Id  MGI:1860996 Doi  10.1016/s0092-8674(00)00027-1
Citation  Tamura K, et al. (2000) Requirement for p38alpha in erythropoietin expression: a role for stress kinases in erythropoiesis. Cell 102(2):221-31
abstractText  Activity of the p38alpha MAP kinase is stimulated by various stresses and hematopoietic growth factors. A role for p38alpha in mouse development and physiology was investigated by targeted disruption of the p38alpha locus. Whereas some p38alpha(-/-) embryos die between embryonic days 11.5 and 12.5, those that develop past this stage have normal morphology but are anemic owing to failed definitive erythropoiesis, caused by diminished erythropoietin (Epo) gene expression. As p38alpha-deficient hematopoietic stem cells reconstitute lethally irradiated hosts, p38alpha function is not required downstream of Epo receptor. Inhibition of p38 activity also interferes with stabilization of Epo mRNA in human hepatoma cells undergoing hypoxic stress. The p38alpha MAP kinase plays a critical role linking developmental and stress-induced erythropoiesis through regulation of Epo expression.
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