TY - JOUR
T1 - Signaling mechanism of poly(ADP-ribose) polymerase-1 (PARP-1) in inflammatory diseases
AU - Ba, Xueqing
AU - Garg, Nisha Jain
N1 - Funding Information:
Supported by grants from the NIH ( AI053098 and HL094802 to N.J.G.) for work performed in the laboratory related to mitochondrial dysfunction and chronic inflammation.
PY - 2011/3
Y1 - 2011/3
N2 - Poly(ADP-ribosyl)ation, attaching the ADP-ribose polymer chain to the receptor protein, is a unique posttranslational modification. Poly(ADP-ribose) polymerase-1 (PARP-1) is a well-characterized member of the PARP family. In this review, we provide a general update on molecular structure and structure-based activity of this enzyme. However, we mainly focus on the roles of PARP-1 in inflammatory diseases. Specifically, we discuss the signaling pathway context that PARP-1 is involved in to regulate the pathogenesis of inflammation. PARP-1 facilitates diverse inflammatory responses by promoting inflammation-relevant gene expression, such as cytokines, oxidation-reduction - related enzymes, and adhesion molecules. Excessive activation of PARP-1 induces mitochondria- associated cell death in injured tissues and constitutes another mechanism for exacerbating inflammation.
AB - Poly(ADP-ribosyl)ation, attaching the ADP-ribose polymer chain to the receptor protein, is a unique posttranslational modification. Poly(ADP-ribose) polymerase-1 (PARP-1) is a well-characterized member of the PARP family. In this review, we provide a general update on molecular structure and structure-based activity of this enzyme. However, we mainly focus on the roles of PARP-1 in inflammatory diseases. Specifically, we discuss the signaling pathway context that PARP-1 is involved in to regulate the pathogenesis of inflammation. PARP-1 facilitates diverse inflammatory responses by promoting inflammation-relevant gene expression, such as cytokines, oxidation-reduction - related enzymes, and adhesion molecules. Excessive activation of PARP-1 induces mitochondria- associated cell death in injured tissues and constitutes another mechanism for exacerbating inflammation.
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U2 - 10.1016/j.ajpath.2010.12.004
DO - 10.1016/j.ajpath.2010.12.004
M3 - Review article
C2 - 21356345
AN - SCOPUS:79952768723
SN - 0002-9440
VL - 178
SP - 946
EP - 955
JO - American Journal of Pathology
JF - American Journal of Pathology
IS - 3
ER -