Signaling Mechanism of Poly(ADP-Ribose) Polymerase-1 (PARP-1) in Inflammatory Diseases

被引：198

作者：

Ba, Xueqing ^{[1
]}

Garg, Nisha Jain ^{[1
,2
,3
,4
]}

机构：

[1] Univ Texas Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA

[2] Univ Texas Med Branch, Dept Pathol, Galveston, TX 77555 USA

[3] Univ Texas Med Branch, Inst Human Infect & Immun, Galveston, TX 77555 USA

[4] Univ Texas Med Branch, Sealy Ctr Vaccine Dev, Galveston, TX 77555 USA

来源：

AMERICAN JOURNAL OF PATHOLOGY | 2011年 / 178卷 / 03期

关键词：

NF-KAPPA-B; POLY(ADENOSINE DIPHOSPHATE-RIBOSE) POLYMERASE; APOPTOSIS-INDUCING FACTOR; ADP-RIBOSE POLYMERASE-1; NITRIC-OXIDE SYNTHASE; NECROTIC CELL-DEATH; SPINAL-CORD-INJURY; DNA-BINDING; PHARMACOLOGICAL INHIBITION; ACTIVATOR PROTEIN-1;

D O I：

10.1016/j.ajpath.2010.12.004

中图分类号：

R36 [病理学];

学科分类号：

100103 [病原生物学];

摘要：

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. (Am J Pathol 2011, 178:946-955; DOI: 10.1016/j.ajpath.2010.12.004)

引用

页码：946 / 955

页数：10

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