期刊
NEUROCHEMICAL RESEARCH
卷 33, 期 12, 页码 2583-2592出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-008-9835-1
关键词
PARP; LPS/ IFNgamma; Inflammatory stress; Cell death
资金
- Ricerca Ateneo
- University of Catania [FIRB RBNE03PX83, 2005054147]
The enzyme poly(ADP-ribose) polymerase ( PARP) has a leader role in the DNA damage survey mechanisms by its nick-sensor function, but it is also involved in the early events of the programmed cell death, particularly during inflammatory injury, as a coactivator of NF-kB. In the present study, we evaluated the PARP involvement in the mechanisms of protection and/or cell death in rat astroglial cell cultures during the early phase of proinflammatory commitment after lipopolysaccharide and interferon gamma treatment. According with the recent findings that PARP-1 phosphorylation by MAPK/ERK-2 pathway seems to modulate PARP activation, in time course experiments we demonstrated that a very early PARP activation and expression is able to trigger a cell death pathway, DNA damage independent, during strong proinflammatory insults, maintaining its role of guardian of the genome stability only during the normal cell cycling.
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