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10.1172/JCI78440 http://scihub22266oqcxt.onion/10.1172/JCI78440 C4362230!4362230!25664853     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Clin+Invest 2015 ; 125 (3): 1286-98 Nephropedia Template TP {{tp|p=25664853|t=2015. Musashi2 sustains the mixed-lineage leukemia?driven stem cell regulatory program |pdf=|usr=}}{{25664853}} gab.com Text Musashi2 sustains the mixed-lineage leukemia driven stem cell regulatory program JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25664853 #FOAvip Leukemia stem cells (LSCs) are found in most aggressive myeloid diseases and contribute to therapeutic resistance. Leukemia cells exhibit a dysregulated developmental program as the result of genetic and epigenetic alterations. Overexpression of the RNA-binding protein Musashi2 (MSI2) has been previously shown to predict poor survival in leukemia. Here, we demonstrated that conditional deletion of Msi2 in the hematopoietic compartment results in delayed leukemogenesis, reduced disease burden, and a loss of LSC function in a murine leukemia model. Gene expression profiling of these Msi2-deficient animals revealed a loss of the hematopoietic/leukemic stem cell self-renewal program and an increase in the differentiation program. In acute myeloid leukemia patients, the presence of a gene signature that was similar to that observed in Msi2-deficent murine LSCs correlated with improved survival. We determined that MSI2 directly maintains the mixed-lineage leukemia (MLL) self-renewal program by interacting with and retaining efficient translation of Hoxa9, Myc, and Ikzf2 mRNAs. Moreover, depletion of MLL target Ikzf2 in LSCs reduced colony formation, decreased proliferation, and increased apoptosis. Our data provide evidence that MSI2 controls efficient translation of the oncogenic LSC self-renewal program and suggest MSI2 as a potential therapeutic target for myeloid leukemia. Twit Text FOAVip Musashi2 sustains the mixed-lineage leukemia driven stem cell regulatory program ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=25664853 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25664853 #FOAvip English Wikipedia <ref>{{Cite pmid|25664853}}</ref> Musashi2 sustains the mixed-lineage leukemia?driven stem cell regulatory program #MMPMID25664853 Park SM; Gönen M; Vu L; Minuesa G; Tivnan P; Barlowe TS; Taggart J; Lu Y; Deering RP; Hacohen N; Figueroa ME; Paietta E; Fernandez HF; Tallman MS; Melnick A; Levine R; Leslie C; Lengner CJ; Kharas MG J Clin Invest 2015[Mar]; 125 (3): 1286-98 PMID25664853show ga Leukemia stem cells (LSCs) are found in most aggressive myeloid diseases and contribute to therapeutic resistance. Leukemia cells exhibit a dysregulated developmental program as the result of genetic and epigenetic alterations. Overexpression of the RNA-binding protein Musashi2 (MSI2) has been previously shown to predict poor survival in leukemia. Here, we demonstrated that conditional deletion of Msi2 in the hematopoietic compartment results in delayed leukemogenesis, reduced disease burden, and a loss of LSC function in a murine leukemia model. Gene expression profiling of these Msi2-deficient animals revealed a loss of the hematopoietic/leukemic stem cell self-renewal program and an increase in the differentiation program. In acute myeloid leukemia patients, the presence of a gene signature that was similar to that observed in Msi2-deficent murine LSCs correlated with improved survival. We determined that MSI2 directly maintains the mixed-lineage leukemia (MLL) self-renewal program by interacting with and retaining efficient translation of Hoxa9, Myc, and Ikzf2 mRNAs. Moreover, depletion of MLL target Ikzf2 in LSCs reduced colony formation, decreased proliferation, and increased apoptosis. Our data provide evidence that MSI2 controls efficient translation of the oncogenic LSC self-renewal program and suggest MSI2 as a potential therapeutic target for myeloid leukemia. äMusashi2 sustains the mixed-lineage leukemia?driven stem cell regulato(epmc).pdf DeepDyve Pubget Overpricing