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In JoVE (1)
Other Publications (1)
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Articles by Daniel Hidalgo in JoVE
זיהוי וניתוח של אבות עכבר Erythroid באמצעות CD71/TER119 Flow-cytometric Assay
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
שיטה זרימה cytometric לזיהוי וניתוח מולקולרית של התמיינות בשלב ספציפי אבות Murine erythroid ומבשרי, ישירות במח שאך שנקטפו עכבר העצם, בטחול או בכבד העובר. Assay מסתמך על פני קרום התא הסמנים CD71, Ter119, וגודל התא.
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.