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Long-term memory requires polyADP-ribosylation.
Science
June 2004
Neufeld Cardiac Research Institute, Sheba Medical Center, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv 69978, Israel.
PolyADP-ribose-polymerase 1 is activated in neurons that mediate several forms of long-term memory in Aplysia. Because polyADP-ribosylation of nuclear proteins is a response to DNA damage in virtually all eukaryotic cells, it is surprising that activation of the polymerase occurs during learning and is required for long-term memory. We suggest that fast and transient decondensation of chromatin structure by polyADP-ribosylation enables the transcription needed to form long-term memory without strand breaks in DNA.
View Article and Find Full Text PDFPoly(ADP-ribose) polymerase: early involvement in glutamate-induced neurotoxicity in cultured cerebellar granule cells.
J Neurosci Res
September 1994
Fidia Research Laboratories, Abano Terme, Italy.
Glutamate neurotoxicity is correlated with an increase of cytosolic free Ca2+. In some cell systems, activation of Ca2+ dependent endonucleases or formation of free radicals can damage DNA and activate the chromatin bound enzyme poly(ADP-ribose) polymerase (pADPRP). We have investigated whether pADPRP may be involved in glutamate neurotoxicity in vitro.
View Article and Find Full Text PDFPhenotypic correction of a human cell line (46BR) with aberrant DNA ligase I activity.
Mutat Res
June 1993
Institute of Cell and Molecular Biology, University of Edinburgh, Scotland, UK.
Ligation of DNA after replication and repair is a prerequisite for the preservation of DNA and chromosome structure and function. Biochemical studies with Bloom's syndrome cells have revealed an abnormal DNA ligase I activity. However, genetic analysis has not revealed any differences in transcript levels or in the cDNA sequences of DNA ligase I between Bloom's syndrome and normal cells.
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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