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In JoVE (1)
Other Publications (1)
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Articles by Daniel Hidalgo in JoVE
पहचान और माउस Erythroid progenitors के विश्लेषण CD71/TER119 परख फ्लो - cytometric का उपयोग
Miroslav Koulnis*, Ramona Pop*, Ermelinda Porpiglia*, Jeffrey R. Shearstone*, Daniel Hidalgo, Merav Socolovsky
Department of Pediatrics and Department of Cancer Biology, University of Massachusetts Medical School
प्रवाह cytometric पहचान और भेदभाव मंच विशिष्ट murine erythroid progenitors और हौसले से काटा माउस अस्थि मज्जा, प्लीहा या भ्रूण जिगर में सीधे व्यापारियों, आणविक विश्लेषण के लिए एक तरीका है. परख सेल सतह CD71 मार्करों, Ter119, और सेल के आकार पर निर्भर करता है.
Other articles by Daniel Hidalgo on PubMed
Blood. Feb, 2012 | Pubmed ID: 22086418
Survival signaling by the erythropoietin (Epo) receptor (EpoR) is essential for erythropoiesis and for its acceleration in hypoxic stress. Several apparently redundant EpoR survival pathways were identified in vitro, raising the possibility of their functional specialization in vivo. Here we used mouse models of acute and chronic stress, including a hypoxic environment and β-thalassemia, to identify two markedly different response dynamics for two erythroblast survival pathways in vivo. Induction of the antiapoptotic protein Bcl-x(L) is rapid but transient, while suppression of the proapoptotic protein Bim is slower but persistent. Similar to sensory adaptation, however, the Bcl-x(L) pathway "resets," allowing it to respond afresh to acute stress superimposed on a chronic stress stimulus. Using "knock-in" mouse models expressing mutant EpoRs, we found that adaptation in the Bcl-x(L) response occurs because of adaptation of its upstream regulator Stat5, both requiring the EpoR distal cytoplasmic domain. We conclude that survival pathways show previously unsuspected functional specialization for the acute and chronic phases of the stress response. Bcl-x(L) induction provides a "stop-gap" in acute stress, until slower but permanent pathways are activated. Furthermore, pathologic elevation of Bcl-x(L) may be the result of impaired adaptation, with implications for myeloproliferative disease mechanisms.