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10.1016/j.cell.2014.07.048 http://scihub22266oqcxt.onion/10.1016/j.cell.2014.07.048 C4197056!4197056!25215489     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2014 ; 158 (6): 1309-23 Nephropedia Template TP {{tp|p=25215489|t=2014. Cell state-specific metabolic dependency in hematopoiesis and leukemogenesis |pdf=|usr=}}{{25215489}} gab.com Text Cell state-specific metabolic dependency in hematopoiesis and leukemogenesis JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=25215489 #FOAvip The balance between oxidative and non-oxidative glucose metabolism is essential for a number of pathophysiological processes. By deleting enzymes that affect aerobic glycolysis with different potencies, we examine how modulating glucose metabolism specifically affects hematopoietic and leukemic cell populations. We find that deficiency in the M2 pyruvate kinase isoform (PKM2) reduces levels of metabolic intermediates important for biosynthesis and impairs progenitor function without perturbing hematopoietic stem cells (HSC), whereas lactate dehydrogenase-A (LDHA) deletion significantly inhibits the function of both HSC and progenitors during hematopoiesis. In contrast, leukemia initiation by transforming alleles putatively affecting either HSC or progenitors is inhibited in the absence of either PKM2 or LDHA, indicating that the cell state-specific responses to metabolic manipulation in hematopoiesis do not apply to the setting of leukemia. This finding suggests that fine-tuning the level of glycolysis may be therapeutically explored for treating leukemia while preserving HSC function. Twit Text FOAVip Cell state-specific metabolic dependency in hematopoiesis and leukemogenesis ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=25215489 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25215489 #FOAvip English Wikipedia <ref>{{Cite pmid|25215489}}</ref> Cell state-specific metabolic dependency in hematopoiesis and leukemogenesis #MMPMID25215489 Wang YH; Israelsen WJ; Lee D; Yu VW; Jeanson NT; Clish CB; Cantley LC; Heiden MGV; Scadden DT Cell 2014[Sep]; 158 (6): 1309-23 PMID25215489show ga The balance between oxidative and non-oxidative glucose metabolism is essential for a number of pathophysiological processes. By deleting enzymes that affect aerobic glycolysis with different potencies, we examine how modulating glucose metabolism specifically affects hematopoietic and leukemic cell populations. We find that deficiency in the M2 pyruvate kinase isoform (PKM2) reduces levels of metabolic intermediates important for biosynthesis and impairs progenitor function without perturbing hematopoietic stem cells (HSC), whereas lactate dehydrogenase-A (LDHA) deletion significantly inhibits the function of both HSC and progenitors during hematopoiesis. In contrast, leukemia initiation by transforming alleles putatively affecting either HSC or progenitors is inhibited in the absence of either PKM2 or LDHA, indicating that the cell state-specific responses to metabolic manipulation in hematopoiesis do not apply to the setting of leukemia. This finding suggests that fine-tuning the level of glycolysis may be therapeutically explored for treating leukemia while preserving HSC function. äCell state-specific metabolic dependency in hematopoiesis and leukemog(epmc).pdf DeepDyve Pubget Overpricing