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Posttranscriptional Regulation of mRNA by HuR Facilitates DNA Repair and Resistance to PARP Inhibitors.
Cancer Res
September 2017
Department of Surgery, The Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania.
The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9-mediated silencing of the HuR locus increases the relative sensitivity of PDAC cells to PARP inhibitors (PARPi). PDAC cells treated with PARPi stimulated translocation of HuR from the nucleus to the cytoplasm, specifically promoting stabilization of a new target, poly (ADP-ribose) glycohydrolase () mRNA, by binding a unique sequence embedded in its 3' untranslated region.
View Article and Find Full Text PDFPolyADP-ribose polymerase activities were measured in bovine lens. Activities similar to those in brain were found in the epithelial cells; none activity was detected in the fiber cells. During aging ADP-ribosyl transferase activity of epithelial cells raised, the number of polyADP-ribose chains increased while the average chain length decreased.
View Article and Find Full Text PDFIn vivo treatment of rats with triiodothyronine (0.3 micrograms per g body wt for four consecutive days) increases both poly (ADP-ribose) polymerase activity and DNA synthesis in myocardial nuclei obtained from 18-21-days-old rats. The same T3-treatment in 30-33-days-old rats inhibits poly(ADP-ribose) polymerase activity and simultaneously increases RNA syntheses in myocardial nuclei.
View Article and Find Full Text PDFInvolvement of polyADP-ribose polymerase in the initiation of phytohemagglutinin induced human lymphocyte proliferation.
Biochem Biophys Res Commun
October 1983
Nicotinamide (10 mM) or 3-aminobenzamide (5 mM) added at the onset of phytohemagglutinin (PHA) treated human lymphocyte cultures provoke a marked inhibition of the PHA induced DNA synthesis and cell proliferation as well as of poly(ADPR) polymerase activity. When the inhibitors of poly(ADPR) polymerase are added at a later stage of culture (48 h) no inhibition of the stimulation of DNA synthesis and cell proliferation by PHA in human lymphocyte cultures is observed. The intervention of ADP ribosylation at the initiation of DNA synthesis is suggested.
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