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http://dx.doi.org/10.1074/jbc.A115.698357 | DOI Listing |
Cells
May 2022
The Sackler School of Medicine, Deptartment of Physiology and Pharmacology, Sagol School of Neuroscience, Tel-Aviv University, Tel-Aviv 69978, Israel.
This overview presents recent evidence for a long-lasting PARP1 activation by a variety of signal transduction mechanisms, mediating signal-induced gene expression and chromatin remodeling. This mode of PARP1 activation has been reported in a variety of cell types, under physiological conditions. In this mechanism, PARP1 is not transiently activated by binding to DNA breaks.
View Article and Find Full Text PDFCurr Protein Pept Sci
February 2017
Drug Development Service Segment LSI Medience Corporation, 13-4, Uchikanda 1-chome, Chiyodaku, Tokyo 101-8517, Japan.
Accumulating evidence suggests that cloned mice production by the injection of a somatic cell nucleus into an enucleated oocyte is inefficient. DNA damage and chromatin remodeling failures that occur during embryogenesis following nuclear transfer (NT) might explain the poor development of cloned embryos. To avoid these problems, it is important to elucidate somatic chromatin remodeling after NT.
View Article and Find Full Text PDFCancer Sci
February 2012
Faculty of Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama, Japan.
Centrosome amplification (also known as centrosome overduplication) is common in cancer cells and can be induced by DNA damaging agents. However, the mechanism and significance of centrosome amplification during carcinogenesis or after DNA damage are not clear. Previously, we showed that centrosome amplification could be induced by 3-aminobenzamide (3-AB), an inhibitor of poly(ADP-ribose) polymerases (PARPs) in mouse embryonic fibroblasts.
View Article and Find Full Text PDFMol Cancer Res
October 2008
Cancer Research, GPRD, Abbott Laboratories, Abbott Park, IL, USA.
Poly(ADP-ribose) polymerase (PARP) senses DNA breaks and facilitates DNA repair via the polyADP-ribosylation of various DNA binding and repair proteins. We explored the mechanism of potentiation of temozolomide cytotoxicity by the PARP inhibitor ABT-888. We showed that cells treated with temozolomide need to be exposed to ABT-888 for at least 17 to 24 hours to achieve maximal cytotoxicity.
View Article and Find Full Text PDFMed Hypotheses
May 1993
Canadian Institute of Theoretical Biology, Nova Scotia.
A specific mechanism was given for ethionine-induced alpha-fetoprotein gene activity and is as follows: 1. Ethionine acts on competent cell types (e.g.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!