BCL-XL expression promotes survival of immature B cells expression of BCL-2 is important for survival of mature B cells and long-lived plasma cells (PC) and expression of MCL-1 is important for survival throughout B-cell development.
analysis of the role of BCL-XL or MCL-1 in the development and sustained growth of thymic lymphoma elicited by loss of p53 reveals that only MCL-1 is critical
A double-mutant knockin of the CD28 YMNM and PYAP motifs reveals a critical role for the YMNM motif in regulation of T cell proliferation and Bcl-xL expression.
Data indicate that Mcl-1 deficient embryonic fibroblasts (MEFs) reliant only on Bcl-XL for survival and Bax/Bak deficient MEFs support a mechanism-based induction of apoptosis.
Bcl-xL has crucial anti-apoptotic roles at multistages in the megakaryocytic lineage making possible prevention of lethal or severe spontaneous hemorrhage.
Bcl-2 Bcl-x(L) and Bcl-w have only minor roles in thymic lymphoma development elicited by defects in p53 and this may indicate that Mcl-1 and/or A1 may feature more prominently in this process.
Fas-mediated death of mitogen-activated T cells was caspase dependent and could be blocked by FLIP(L) overexpression only with the minor involvement of Bcl-x(L) or RIPDeltakin inhibitable pathways.
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