Transcriptional reprogramming and resistance to colonic mucosal injury in PARP1-deficient mice

ABSTRACT: Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate, and participate to the control of gene transcription and DNA repair. PARP1, the most abundant isoform, regulates the expression of proinflammatory mediator - cytokines, chemokines and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmune diseases in several experimental models, including colitis. However, the mechanism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which Parp1 deletion has the most significant impact are unknown. The objective of the current study was to

ORGANISM(S): Mus musculus

SUBMITTER: Pawel Kiela 

PROVIDER: E-GEOD-76658 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress