Results 71 to 80 of about 112,622 (301)
Regulation of caspase-3 processing by cIAP2 controls the switch between pro-inflammatory activation and cell death in microglia. [PDF]
Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International Licence.
A Castano +30 more
core +3 more sources
CDK11 inhibition stabilises the tumour suppressor p53 and triggers the production of an alternative p21WAF1 splice variant p21L, through the inactivation of the spliceosomal protein SF3B1. Unlike the canonical p21WAF1 protein, p21L is localised in the cytoplasm and has reduced cell cycle‐blocking activity.
Radovan Krejcir +12 more
wiley +1 more source
p21CDKN1A Regulates the Binding of Poly(ADP-Ribose) Polymerase-1 to DNA Repair Intermediates. [PDF]
The cell cycle inhibitor p21CDKN1A was previously found to interact directly with DNA nick-sensor poly(ADP-ribose) polymerase-1 (PARP-1) and to promote base excision repair (BER).
Ilaria Dutto +7 more
doaj +1 more source
Quantitation of intracellular NAD(P)H can monitor an imbalance of DNA single strand break repair in base excision repair deficient cells in real time [PDF]
DNA single strand breaks (SSBs) are one of the most frequent DNA lesions in genomic DNA generated either by oxidative stress or during the base excision repair pathways.
Asakura, Shoji +5 more
core +3 more sources
Clinical trials on PARP inhibitors in urothelial carcinoma (UC) showed limited efficacy and a lack of predictive biomarkers. We propose SLFN5, SLFN11, and OAS1 as UC‐specific response predictors. We suggest Talazoparib as the better PARP inhibitor for UC than Olaparib.
Jutta Schmitz +15 more
wiley +1 more source
Background The efficacy of subsequent therapy after poly-ADP-ribose polymerase (PARP) inhibitor maintenance treatment has raised concerns. Retrospective studies show worse outcomes for platinum-based chemotherapy after progression of PARP inhibitor ...
Nan Zhang +5 more
doaj +1 more source
Exploiting metabolic adaptations to overcome dabrafenib treatment resistance in melanoma cells
We show that dabrafenib‐resistant melanoma cells undergo mitochondrial remodeling, leading to elevated respiration and ROS production balanced by stronger antioxidant defenses. This altered redox state promotes survival despite mitochondrial damage but renders resistant cells highly vulnerable to ROS‐inducing compounds such as PEITC, highlighting redox
Silvia Eller +17 more
wiley +1 more source
Poly(ADP-Ribosyl)ation affects stabilization of CHE-1 protein in response to DNA damage [PDF]
Post-translation modifications play a crucial role in coordinating the cellular response to DNA damage. Double strand DNA breaks (DSBs) trigger the activation of ATM and Chk2 kinases, which represent the primary transducers in the signalling cascade ...
BACALINI, MARIA GIULIA
core
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon +13 more
wiley +1 more source
Advances in the use of PARP inhibitor therapy for breast cancer
Poly-ADP-ribose polymerase 1 (PARP-1) and PARP-2 are DNA damage sensors that are most active during S-phase of the cell cycle and that have wider-reaching roles in DNA repair than originally described.
Kelly E McCann, Sara A Hurvitz
doaj +1 more source

