Results 71 to 80 of about 390,973 (308)
Caspase-8 is not activated by caspase-3.
(A) Microscopic images of cells expressing FRET-Bid in the absence or presence of Ac-DEVD-CHO (caspase-3 inhibitor, 20 μM) in Huh-7 and HepG2 cells.
Liping Wu (578606) +6 more
core +1 more source
Conversion of Procaspase-3 to an Autoactivating Caspase by Fusion to the Caspase-2 Prodomain [PDF]
Caspases are cysteine proteases that play an essential role in apoptosis. Initial activation of caspases defines the key step in apoptotic execution. Based on primary structure, caspases can be divided into two groups, those with long amino-terminal prodomains (class I), and those with relatively short prodomains (class II).
Colussi, P. +3 more
openaire +3 more sources
E2A selectively regulates TGF‐β–induced apoptosis in KRAS‐mutant non‐small cell lung cancer
Ability to induce apoptosis by TGF‐β is frequently lost in advanced lung adenocarcinoma despite intact TGF‐β signaling. We identify E2A as a mutant KRAS–dependent mediator of resistance to TGF‐β–induced apoptosis. TGF‐β induces E2A via SMAD3 in mutant KRAS cells, and E2A silencing restores apoptosis and enhances radiation response in cell lines ...
Sergei Chuikov +3 more
wiley +1 more source
RNA profiling of circulating extracellular vesicles (EVs) from blood samples of men undergoing prostate biopsy identifies transcripts associated with clinically significant prostate cancer. Integrative analysis with public tumor datasets links EV‐derived gene signatures to tumor stage and progression‐free survival, highlighting CASP3, XRCC2, and RIT1 ...
Stefan Werner +14 more
wiley +1 more source
The prodomain of caspase-3 regulates its own removal and caspase activation [PDF]
AbstractCaspase-3 is a cysteine–aspartic acid protease that cleaves cellular targets and executes cell death. Our current understanding is caspase-3 is activated by the cleavage of the interdomain linker and then subsequent cleavage of the N-terminal prodomain.
Ponder, Katelyn G., Boise, Lawrence H.
openaire +2 more sources
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Background and Objectives: Various studies have shown that sex steroids affect cancer cells at cellular and molecular level. In this study, the anti-proliferation effects of testosterone, was investigated on gastric cancer cell line (AGS) and activity ...
Neda Amani +4 more
doaj
Cytotoxic chemotherapy, still the most widely adopted anticancer treatment, aims at eliminating cancer cells inducing apoptosis with DNA damaging agents, exploiting the differential replication rate of cancer vs.
Emanuele Bruni +5 more
doaj +1 more source
TNF-α contributes to sarcopenia through caspase-8/caspase-3/GSDME-mediated pyroptosis
Sarcopenia has become a leading cause of disability and mortality in the elderly. It has been reported that programmed cell death (PCD) is associated with the development of sarcopenia that is characterized by reduction of muscle fiber size and number ...
Jingying Wu +9 more
doaj +1 more source
PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines
Talazoparib is the most potent inducer of senescence among different PARP1 inhibitors in human NSCLC cells. In the absence of PARP, no senescence phenotype was observed, demonstrating that PARP1 is necessary for the induction of senescence by this inhibitor.
Camille Huart +7 more
wiley +1 more source

