Results 121 to 130 of about 1,287,961 (310)

CDK11 inhibition induces cytoplasmic p21WAF1 splice variant by p53 stabilisation and SF3B1 inactivation

open access: yesMolecular Oncology, EarlyView.
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

Attenuated DNA damage responses and increased apoptosis characterize human hematopoietic stem cells exposed to irradiation [PDF]

open access: gold, 2018
Shahar Biechonski   +14 more
openalex   +1 more source

Supplementary Figures 1-6 from Pierce1, a Novel p53 Target Gene Contributing to the Ultraviolet-Induced DNA Damage Response

open access: gold, 2023
Young Hoon Sung   +7 more
openalex   +1 more source

Improving PARP inhibitor efficacy in bladder cancer without genetic BRCAness by combination with PLX51107

open access: yesMolecular Oncology, EarlyView.
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

Variation in DNA-Damage Responses to an Inhalational Carcinogen (1,3-Butadiene) in Relation to Strain-Specific Differences in Chromatin Accessibility and Gene Transcription Profiles in C57BL/6J and CAST/EiJ Mice [PDF]

open access: diamond, 2017
Grace A. Chappell   +11 more
openalex   +1 more source

Supplementary Material and Methods from DNA Damage Response Inhibitor Combinations Exert Synergistic Antitumor Activity in Aggressive B-Cell Lymphomas

open access: gold, 2023
Valentina Restelli   +9 more
openalex   +1 more source

The DNA damage response: making it safe to play with knives.

open access: yesMolecules and Cells, 2010
Alberto Ciccia, S. Elledge
semanticscholar   +1 more source

Class IIa HDACs forced degradation allows resensitization of oxaliplatin‐resistant FBXW7‐mutated colorectal cancer

open access: yesMolecular Oncology, EarlyView.
HDAC4 is degraded by the E3 ligase FBXW7. In colorectal cancer, FBXW7 mutations prevent HDAC4 degradation, leading to oxaliplatin resistance. Forced degradation of HDAC4 using a PROTAC compound restores drug sensitivity by resetting the super‐enhancer landscape, reprogramming the epigenetic state of FBXW7‐mutated cells to resemble oxaliplatin ...
Vanessa Tolotto   +13 more
wiley   +1 more source

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