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The FHA domain of aprataxin interacts with the C-terminal region of XRCC1

被引：42
作者：
Date, H
Igarashi, S [1 ]
Sano, Y
Takahashi, T
Takahashi, T
Takano, H
Tsuji, S
Nishizawa, M
Onodera, O
机构：
[1] Niigata Univ, Brain Res Inst, Dept Neurol, Niigata, Japan
[2] Niigata Univ, Brain Res Inst, Ctr Bioresource Based Res, Resource Branch Brain Dis Res,Dept Mol Neurosci, Niigata, Japan
[3] Yamaguchi Univ, Dept Neurol, Yamaguchi 753, Japan
[4] Univ Tokyo, Grad Sch Med, Dept Neurol, Tokyo, Japan
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2004年 / 325卷 / 04期
基金：
日本学术振兴会;
关键词：
aprataxin; SSBR; XRCC1; DNA repair; single strand break repair; PNKP; ligase; PARP; neuronal death; neuronal loss; AOA; EAOH; spinocerebellar ataxia; ataxia; FHA; FHA domain; BRCT; oxidative stress;
D O I：
10.1016/j.bbrc.2004.10.162
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Aprataxin (APTX) is the causative gene product for early-onset ataxia with ocular motor apraxia and hypoalbuminemia (EAOH/AOA1). In our previous study, we found that APTX interacts with X-ray repair cross-complementing group 1 (XRCC1), a scaffold protein with an essential role in single-strand DNA break repair (SSBR). To further characterize the functions of APTX, we determined the domains of APTX and XRCC1 required for the interaction. We demonstrated that the 20 N-terminal amino acids of the FHA domain of APTX are important for its interaction with the C-terminal region (residues 492-574) of XRCC1. Moreover, we found that poly (ADP-ribose) polymerase-1 (PARP-1) is also co-immunoprecipitated with APTX. These findings suggest that APTX, together with XRCC1 and PARP-1, plays an essential role in SSBR. (C) 2004 Elsevier Inc. All rights reserved.
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页码：1279 / 1285
页数：7
相关论文
共 22 条
[1]   ATAXIA-OCULAR MOTOR APRAXIA - A SYNDROME MIMICKING ATAXIA-TELANGIECTASIA [J].
AICARDI, J ;
BARBOSA, C ;
ANDERMANN, E ;
ANDERMANN, F ;
MORCOS, R ;
GHANEM, Q ;
FUKUYAMA, Y ;
AWAYA, Y ;
MOE, P .
ANNALS OF NEUROLOGY, 1988, 24 (04) :497-502
[2]   DNA repair in neural cells: basic science and clinical implications [J].
Brooks, PJ .
MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS, 2002, 509 (1-2) :93-108
[3]   XRCC1 polypeptide interacts with DNA polymerase beta and possibly poly(ADP-ribose) polymerase, and DNA ligase III is a novel molecular 'nick-sensor' in vitro [J].
Caldecott, KW ;
Aoufouchi, S ;
Johnson, P ;
Shall, S .
NUCLEIC ACIDS RESEARCH, 1996, 24 (22) :4387-4394
[4]   DNA single-strand break repair and spinocerebellar ataxia [J].
Caldecott, KW .
CELL, 2003, 112 (01) :7-10
[5]   XRCC1 and DNA strand break repair [J].
Caldecott, KW .
DNA REPAIR, 2003, 2 (09) :955-969
[6]   Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene [J].
Date, H ;
Onodera, O ;
Tanaka, H ;
Iwabuchi, K ;
Uekawa, K ;
Igarashi, S ;
Koike, R ;
Hiroi, T ;
Yuasa, T ;
Awaya, Y ;
Sakai, T ;
Takahashi, T ;
Nagatomo, H ;
Sekijima, Y ;
Kawachi, I ;
Takiyama, Y ;
Nishizawa, M ;
Fukuhara, N ;
Saito, K ;
Sugano, S ;
Tsuji, S .
NATURE GENETICS, 2001, 29 (02) :184-188
[7]   The FHA domain [J].
Durocher, D ;
Jackson, SP .
FEBS LETTERS, 2002, 513 (01) :58-66
[8]   The molecular basis of FHA Domain:Phosphopeptide binding specificity and implications for phospho-dependent signaling mechanisms [J].
Durocher, D ;
Taylor, IA ;
Sarbassova, D ;
Haire, LF ;
Westcott, SL ;
Jackson, SP ;
Smerdon, SJ ;
Yaffe, MB .
MOLECULAR CELL, 2000, 6 (05) :1169-1182
[9]   HEREDITARY MOTOR ADD SENSORY NEUROPATHY ASSOCIATED WITH CEREBELLAR ATROPHY (HMSNCA) - A NEW DISEASE [J].
FUKUHARA, N ;
NAKAJIMA, T ;
SAKAJIRI, K ;
MATSUBARA, N ;
FUJITA, M .
JOURNAL OF THE NEUROLOGICAL SCIENCES, 1995, 133 (1-2) :140-151
[10]   Molecular cloning of the human gene, PNKP, encoding a polynucleotide kinase 3′-phosphatase and evidence for its role in repair of DNA strand breaks caused by oxidative damage [J].
Jilani, A ;
Ramotar, D ;
Slack, C ;
Ong, C ;
Yang, XM ;
Scherer, SW ;
Lasko, DD .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (34) :24176-24186
123