Functional Role of ADP-Ribosyl-Acceptor Hydrolase 3 in poly(ADP-Ribose) Polymerase-1 Response to Oxidative Stress.
Functional Role of ADP-Ribosyl-Acceptor Hydrolase 3 in poly(ADP-Ribose) Polymerase-1 Response to Oxidative Stress.
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DOI：
10.2174/1389203717666160419144603
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发表时间：
2016
影响因子：
2.8
通讯作者：
Moss J
中科院分区：
文献类型：
--
作者：
Mashimo M;Moss J
聚ADP核糖基化被认为是一种可逆的蛋白质修饰，参与多种细胞功能，包括DNA修复、染色质重塑、遗传稳定性、有丝分裂和细胞死亡。聚ADP核糖基化是通过NAD+的ADP核糖部分首先转移到靶蛋白中谷氨酸和天冬氨酸残基的羧基以及赖氨酸残基的氨基上，然后通过α-O-糖苷（C-1″-C-2′）核糖-核糖键延长聚ADP核糖（PAR）链而引发的。PAR由ADP-核糖聚合物（最多200个单元）组成，通过α-O-糖苷（C-1-C-2″）核糖-核糖键支化。此外，每个ADP-核糖的焦磷酸基团具有两个负电荷。因此，在经PAR修饰的蛋白质中，具有负电荷的复杂结构可能导致功能的动态变化。PAR的形成由聚（ADP-核糖）聚合酶（PARP）催化，并由几种具有PAR降解活性的酶终止;聚（ADP-核糖）糖水解酶（PARG）、ADP-核糖基受体水解酶（ARH）3、ARH 1和含大结构域的蛋白质。PARG被认为是PAR降解的主要原因。2006年，ARH 3被克隆并鉴定为另一种PAR降解蛋白。尽管ARH 3的PAR降解活性低于PARG，但PAR识别的不同机制和ARH 3的细胞定位似乎是ARH 3参与PAR的独特细胞作用的原因。在本综述中，我们集中在我们的研究结果，ARH 3的结构，生物学特性和细胞功能。此外，我们描述了目前的知识，聚ADP核糖基化和细胞死亡途径调节PARP 1，PARG，ARH 3。
Poly-ADP-ribosylation has been proposed to be a reversible protein modification, participating in diverse cellular functions including DNA repair, chromatin remodeling, genetic stability, mitosis, and cell death. Poly-ADP-ribosylation is initiated by the transfer of the ADP-ribose moiety of NAD+ primarily to the carboxyl groups of glutamate and aspartate and amino group of lysine residues in target proteins, followed by elongation of poly(ADP-ribose) (PAR) chains via α-O-glycosidic (C-1″-C-2′) ribose-ribose bonds. PAR consists of polymers of ADP-ribose (up to 200 units) with branching via α-O-glycosidic (C-1‴-C-2″) ribose-ribose bonds. Further, the pyrophosphate group of each ADP-ribose has two negative charges. Therefore, in proteins modified by PAR, a complex structure with negative charges may lead to dynamic changes of functions. PAR formation is catalyzed by poly(ADP-ribose) polymerases (PARPs) and terminated by several types of enzymes with PAR-degrading activities; poly(ADP-ribose) glycohydrolase (PARG), ADP-ribosyl-acceptor hydrolase (ARH) 3, ARH1, and macrodomain-containing proteins. PARG has been thought to be primarily responsible for PAR degradation. In 2006, ARH3 was cloned and identified as another type of PAR-degrading protein. Although PAR-degrading activity of ARH3 is less than that of PARG, different mechanisms of PAR recognition and the cellular localization of ARH3 appear to be responsible for unique cellular roles of ARH3 involving PAR. In the present review, we focused on our findings regarding structure, biological properties, and cellular functions of ARH3. In addition, we describe the current knowledge of poly-ADP-ribosylation and cell death pathways regulated PARP1, PARG, and ARH3.
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影响因子：
4.3
作者：
Helleday, T;Bryant, HE;Schultz, N
通讯作者：
Schultz, N
影响因子：
14.9
作者：
Gagne, Jean-Philippe;Isabelle, Maxim;Lo, Ken Sin;Bourassa, Sylvie;Hendzel, Michael J.;Dawson, Valina L.;Dawson, Ted M.;Poirier, Guy G.
通讯作者：
Poirier, Guy G.
DOI：
10.1073/pnas.0606526103
发表时间：
2006-11-28
影响因子：
11.1
作者：
Andrabi, Shaida A.;Kim, No Soo;Dawson, Ted M.
通讯作者：
Dawson, Ted M.
DOI：
10.1073/pnas.2237114100
发表时间：
2004-01-06
影响因子：
11.1
作者：
Hanai, S;Kanai, M;Miwa, M
通讯作者：
Miwa, M
影响因子：
8.8
作者：
Fouquerel E;Goellner EM;Yu Z;Gagné JP;Barbi de Moura M;Feinstein T;Wheeler D;Redpath P;Li J;Romero G;Migaud M;Van Houten B;Poirier GG;Sobol RW
通讯作者：
Sobol RW