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Gain-of-function mutations in NOTCH1 are among the most frequent genetic alterations in T cell acute lymphoblastic leukemia (T-ALL), making the Notch signaling pathway a promising therapeutic target for personalized medicine. Yet, a major limitation for long-term success of targeted therapy is relap...
ORGANISM(S): Homo sapiens (Human) 
2024-01-26 | PXD038908 | Pride
Primary mouse cells (CD4-CD8- (DN) and CD4+CD8+ (DP) thymus and T-ALL (early-stage - ES and late-stage - LS) and mouse T-ALL cell line M295 were assessed for microRNA expression For DN, DP, ES_T-ALL and LS_T-ALL cells, n=3 biological replicates were used. M295 is one 1 replicate
ORGANISM(S): Mus musculus 
T-ALL cell line CUTLL1 was assessed for microRNA expression. Cells were treated with DMSO (ctr) or DAPT (10uM) to inhibit Notch1 cleavage for 3d and then harvested. 3 biological replicates were used per group (DMSO, n=3; DAPT, n=3).
ORGANISM(S): Homo sapiens 
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