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PMID:15591122

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Citation

Lenox, LE, Perry, JM and Paulson, RF (2005) BMP4 and Madh5 regulate the erythroid response to acute anemia. Blood 105:2741-8

Abstract

Acute anemia initiates a systemic response that results in the rapid mobilization and differentiation of erythroid progenitors in the adult spleen. The flexed-tail (f) mutant mice exhibit normal steady-state erythropoiesis but are unable to rapidly respond to acute erythropoietic stress. Here, we show that f/f mutant mice have a mutation in Madh5. Our analysis shows that BMP4/Madh5-dependent signaling, regulated by hypoxia, initiates the differentiation and expansion of erythroid progenitors in the spleen. These findings suggest a new model where stress erythroid progenitors, resident in the spleen, are poised to respond to changes in the microenvironment induced by acute anemia.

Links

PubMed Online version:10.1182/blood-2004-02-0703

Keywords

Acute Disease; Alleles; Anemia/pathology; Anemia/physiopathology; Animals; Bone Morphogenetic Protein 4; Bone Morphogenetic Proteins/genetics; Bone Morphogenetic Proteins/metabolism; Cell Differentiation/physiology; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; Erythroid Cells/cytology; Erythroid Cells/metabolism; Erythropoiesis/physiology; Hematopoietic Stem Cells/cytology; Hematopoietic Stem Cells/metabolism; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Phosphoproteins/genetics; Phosphoproteins/metabolism; Signal Transduction/physiology; Smad5 Protein; Spleen/cytology; Trans-Activators/genetics; Trans-Activators/metabolism

Significance

Annotations

Gene product Qualifier GO ID GO term name Evidence Code with/from Aspect Notes Status


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References

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