Resistance to HSP90 inhibition involving loss of MCL1 addiction.
Lexington, United States. In Oncogene, 22 Jul 2015
We show for the first time that, to induce apoptosis, HSP90 inhibition requires the cooperation of multi BH3-only proteins (BID, BIK, PUMA) and the reciprocal suppression of the pro-survival BCL-2 family member MCL1, which occurs via inhibition of STAT5A.
MicroRNAs in B cell lymphomas: How a complex biology gets more complex.
Brno, Czech Republic. In Leukemia, Jan 2015
We focus on miR-contribution to the regulation of important signalling pathways (like NF-κB, PI3K/AKT, TGF-β), BCR signalling and its modulators (like PTEN, SHIP-1, ZAP-70, GAB1, BTK), anti- and pro-apoptotic proteins (like BCL2, MCL1, TCL1, BIM, p53, SIRT1), and transcription factors (like MYC, MYB, PU.1, FOXP1, BCL6).
Anti-apoptotic BCL-2 family proteins in acute neural injury.
Dublin, Ireland. In Front Cell Neurosci, 2013
We discuss overlapping and differential effects of the individual family members BCL-2, BCL-extra long (BCL-XL), myeloid cell leukemia 1 (MCL-1), and BCL2-like 2 (BCL-W) in the control of survival during development and pathophysiological processes such as trophic factor withdrawal, ischemic injury, excitotoxicity, oxidative stress and energy stress.
Reprogramming cell death: BCL2 family inhibition in hematological malignancies.
Milano, Italy. In Immunol Lett, 2013
The BCL2 family members play a central role in regulating programmed cell death (apoptosis) and arbitrating the cellular fate through an accurate balance between pro-apoptotic (BAX, BAK, and BH3-only proteins) and pro-survival (BCL2 and its closest homologues, BCLXL, BCLW and MCL-1) factors.
BH3 mimetics: status of the field and new developments.
More papers using
Paris, France. In Mol Cancer Ther, 2013
The prototype BH3 mimetic ABT-737 selectively targets the three prosurvival proteins BCL-XL, BCL-2, and BCL-W (but not MCL-1 or A1) and its oral derivative ABT-263 has proved promising in clinical trials.