JAK2V617F drives Mcl-1 expression and sensitizes hematologic cell lines to dual inhibition of JAK2 and Bcl-xL.

Assim sugere-se que a linhagem celular Granta-519 utilizou outro mecanismo de morte celular (Necrose) e que essa sinalização pode ter ocorrido pela inibição da

Expressão dos genes anti-apoptóticos a1, bcl-2, bcl-x L , bcl-w, c-flip, ciap- 1, ciap-2 e mcl-1 nos grupos de pacientes com LMC em remissão citogenética e refratários após

Antiapoptotic members of the Bcl-2 family (B cell CLL/lymphoma 2), that belong to the intrinsic route of the activation of caspases, such as Bcl-xL (extra-large B-cell lymphoma)

Furthermore, treatment with MT-3 caused a dose-de- pendent increase in Bcl-2 levels and the levels of Bcl-2 in SAMP8 mice treated with high doses of MT-3 were signiicantly higher

Here, we found that inhibition of EGFR by erlotinib results in phosphorylation of STAT3 at Tyr705 leading to its activation and to increased levels of Bcl2/Bcl-XL at both mRNA

Furthermore, either suppres- sion of Mcl-1 or induction of NOXA sensitizes cells to ABT-737 in a variety of tumor models, suggesting that a treatment regime combining ABT-737 with

The expression of Bcl-2 and Bcl-x and the presence of cleaved caspase 3 were compared to clinicopathological features of malignant peripheral nerve sheath tumors and their impact

Studies in B16-F10 melanoma and MCF-7 breast cancer cell lines indicated that PHOS-S can induce tumor cell apoptosis regardless of blocking of the Bcl-2 protein.. Loss of