Poly(ADP-ribosyl)ation by PARP-1: 'PAR-laying' NAD+ into a nuclear signal.
By M. Y. Kim, Tong Zhang, W. Kraus. Genes & Development, 2005
887 citations recorded by the source corpus.
Poly(ADP-ribose) (PAR) and the PAR polymerases (PARPs) that catalyze its synthesis from donor nicotinamide adenine dinucleotide (NAD+) molecules have received considerable attention in the recent literature. Poly(ADP-ribosyl)ation (PARylation) plays diverse roles in many molecular and cellular processes, including DNA damage detection and repair, chromatin modification, transcription, cell death pathways, insulator function, and mitotic apparatus function. These processes are critical for many physiological and pathophysiological outcomes, including genome maintenance, carcinogenesis, aging, inflammation, and neuronal function. This review highlights recent work on the biochemistry, molecular biology, physiology, and pathophysiology of PARylation, focusing on the activity of PARP-1, the most abundantly expressed member of a family of PARP proteins. In addition, connections between nuclear NAD+ metabolism and nuclear signaling through PARP-1 are discussed.
Subfields: Electrical and Electronic Engineering, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/3f7ccbe1a9f9321bb5c9090f554195b84166e5e5
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Citations in the corpus
- PARPs and ADP-ribosylation: recent advances linking molecular functions to biological outcomes (2017, background): “Furthermore, nicotinamide, a product of the reactions catalyzed by both PARP-1 and Sirt1, can inhibit both of their enzymatic activities (Rongvaux et al. 2003; Kim et al. 2005).”
- Necrotic death as a cell fate. (2006, background): “In response to DNA damage, PARP is activated by binding to DNA strand breaks, and catalyzes poly(ADP)-ribosylation of a variety of proteins by converting NAD into NAM and ADP-ribose (D’Amours et al. 1999; Kim et al. 2005).”
- The General Transcription Machinery and General Cofactors (2006, background): “%) of yeast and human genes whose promoters are predominantly TATA-less (Huisinga and Pugh, 2004; Kim et al., 2005a) and primarily for housekeeping, such as the ribosomal proteinencoding gene promoters (Mencia et al., 2002).”
- Age Related Changes in NAD+ Metabolism Oxidative Stress and Sirt1 Activity in Wistar Rats (2011, background): “The DNA damage associated with oxidative stress is known to activate the NAD-dependent DNA repair enzyme, PARP, which assists in combination with the enzymes of the baseexcision-and-repair complex of the cell in energy-consuming repair processes [12,52,53].”
- The epithelial–mesenchymal transition: new insights in signaling, development, and disease (2006, neutral): “PARP-1 regulates transcription by modifying chromatin structure and through interaction with other transcription factors ( Kim et al., 2005 ).”
- On PAR with PARP: cellular stress signaling through poly(ADP-ribose) and PARP-1. (2012, background): “…stresses leads to transcription and DNA repair responses that help to maintain genome stability, promote transient innate immune and proinflammatory responses, clear and remove oxidized or damaged proteins, and re-establish homeostasis (Kim et al. 2005; Gagne et al. 2006; Hassa and Hottiger 2008).”
- Simultaneous phenotyping of leaf growth and chlorophyll fluorescence via GROWSCREEN FLUORO allows detection of stress tolerance in Arabidopsis thaliana and other rosette plants. (2009, background): “ROSinduced DNA damage activates poly(ADP-ribose) polymerase (PARP) (Berglund 1994; Kim et al. 2005 ).”