-
Differential roles for FL_BID and t-BID in Burkitt's lymphoma during apoptosis. There is a functional cooperation between BAK and BAX during VT-1-induced apoptosis and, unexpectedly, that activation of caspase-8 and production of t-BID were not mandatory for initiation of the cell death process.
-
These results identify a role for Bid in homeostatic mitochondrial cristae reorganization, that we link to human cardiac disease.
-
results suggest that histone modifications in the promoter region of miR-500a may be responsible for the increased expression of miR-500a in Hepatocellular carcinoma (HCC), which promotes cancer progression by targeting BID, indicating that miR-500a may be a potential prognostic predictor and therapeutic target for HCC patients.
-
The caspase-8/Bid/cytochrome c axis links signals from death receptors to mitochondrial reactive oxygen species production.
-
administration of SMAC or BH3 mimetics following short-term paclitaxel treatment could be an effective therapeutic strategy for TNBC, while only BH3-mimetics could effectively overcome long-term paclitaxel resistance
-
caspase-10 was dispensable for enhancement of cisplatin/LA-12 and TRAIL combination-induced cell death and stimulation of Bid cleavage
-
an oligomeric arrangement of Bid, Bax, and possibly other members of the Bcl-2 family of proteins that form a self-propagating network that permeabilizes the outer-mitochondrial membrane.
-
Combined therapy with Seliciclib((R)) and Belinostat((R)) results in eradication of non-small cell lung cancer via apoptosis induction and BID activation.
-
Results from genome-wide DNA methylation, functional network analysis and pyrosequencing, show selective CpG sites (NOS1AP, BID, and GABRB1) differentially methylated in smokers and chronic obstructive pulmonary disease patients compared to nonsmokers.
-
The adenovirus-mediated truncated Bid overexpression induced by the Cre/LoxP system can effectively eliminate CD133+ ovarian cancer stem cells, representing a novel therapeutic strategy for the treatment of ovarian cancer.
-
MiR-20a-directed regulation of BID in colorectal cancer.
-
the results establish that cleavage by caspase 8 and the subsequent association with the outer mitochondrial membrane are two critical events that activate Bid during death receptor-mediated apoptosis.
-
The results indicate that BID-independent pathways are responsible for FAS-dependent human islet cell death in Type 1 diabetes.
-
The BID-MTCH2 axis regulates the differentiation/apoptosis of stem cells and mitochondrial metabolism. (Review)
-
Data suggest, in models of spatial propagation of mitochondrial permeabilization during apoptosis, there appears to be requirement for cooperative signaling involving truncated-BID and ROS (reactive oxygen species) for efficient/ robust propagation.
-
this study emphasizes that the coordinated action of hGzmB-activated p53 and GzmB-cleaved Bid is important for GzmB-induced cell death and for cytotoxic lymphocyte/Natural Killer Cell-mediated killing of target cells.
-
Motifs of VDAC2 required for mitochondrial Bak import and tBid-induced apoptosis.
-
Tax confers apoptosis resistance to HTLV-1-infected T cells by suppressing the expression of Bim and Bid.
-
EG also activated the death receptor-dependent pathway of apoptosis by enhancing the expression of caspases-8, -9, and -3 and the Bcl-2 interacting domain (Bid).
-
Inhibition of NANOGP8 or NANOG enhances the cytotoxicity of BH3 mimetics.
