PARP1: Difference between revisions

PARP1 is required for [[NF-κB]] [[Transcription (biology)|transcription]] of [[Inflammation|proinflammatory]] mediators such as [[tumor necrosis factor]], [[interleukin 6]], and inducible [[nitric oxide synthase]].<ref name="pmid23050038" /><ref name="pmid28974953">{{cite journal | vauthors=Sethi GS, Dharwal V, Naura AS | title=Poly(ADP-Ribose)Polymerase-1 in Lung Inflammatory Disorders: A Review | journal=[[Frontiers in Immunology]] | volume=8 | pages=1172 | year=2017 | doi = 10.3389/fimmu.2017.01172 | pmc=5610677 | pmid=28974953}}</ref> PARP1 activity contributes to the proinflammatory [[macrophage]]s that increase with age in many tissues.<ref name="pmid32774895">{{cite journal | vauthors=Yarbro JR, Emmons RS, Pence BD | title=Macrophage Immunometabolism and Inflammaging: Roles of Mitochondrial Dysfunction, Cellular Senescence, CD38, and NAD | journal=[[Immunometabolism (journal)|Immunometabolism]] | volume=2 | issue=3 | pages=e200026 | year=2020 | doi = 10.20900/immunometab20200026 | pmc=7409778 | pmid=32774895}}</ref> ADP-riboyslation of the [[HMGB1]] [[high-mobility group]] protein by PARP1 inhibits removal of [[apoptosis|apoptotic]] cells, thereby sustaining inflammation.<ref name="pmid31877876">{{cite journal | vauthors=Pazzaglia S, Pioli C | title=Multifaceted Role of PARP-1 in DNA Repair and Inflammation: Pathological and Therapeutic Implications in Cancer and Non-Cancer Diseases | journal=[[Cells]] | volume=9 | issue=1 | pages=41 | year=2019 | doi = 10.3390/cells9010041 | pmc=7017201 | pmid=31877876}}</ref>