Lack of association of ACP1 gene with inflammatory bowel disease: a case-control study

被引:2
作者
Teruel, M. [1 ]
Martin, J. E. [1 ]
Gomez-Garcia, M. [2 ]
Cardena, C. [3 ]
Rodrigo, L. [4 ]
Nieto, A. [5 ]
Alcain, G. [6 ]
Cueto, I. [6 ]
Lopez-Nevot, M. A. [7 ]
Martin, J. [1 ]
机构
[1] CSIC, IPBLN, Armilla, Granada, Spain
[2] Hosp Virgen de las Nieves, Dept Gastroenterol, Granada, Spain
[3] Hosp Clin San Cecilio, Dept Gastroenterol, Granada, Spain
[4] Univ Oviedo, Hosp Cent Asturias, Dept Gastroenterol, E-33080 Oviedo, Spain
[5] Hosp Puerta del Mar, Dept Immunol, Cadiz, Spain
[6] Hosp Virgen de la Victoria, Dept Gastroenterol, Malaga, Spain
[7] Hosp Virgen de las Nieves, Dept Immunol, Granada, Spain
来源
TISSUE ANTIGENS | 2012年 / 80卷 / 01期
关键词
Crohn's disease; polymorphisms; single-nucleotide polymorphism; susceptibility; PROTEIN-TYROSINE-PHOSPHATASE; CROHNS-DISEASE; POLYMORPHISM; RECEPTOR; GENDER; KINASE; PDGF;
D O I
10.1111/j.1399-0039.2012.01861.x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The red cell acid phosphatease (ACP1) gene, which encodes a low molecular weight phosphotyrosine phosphatase (LMW-PTP), has been suggested as a common genetic factor of autoimmunity. In the present study, we aimed to investigate the possible influence of ACP1 polymorphisms in the susceptibility of inflammatory bowel disease (IBD). A total of 1271 IBD Spanish patients [720 Crohn's disease (CD) and 551 ulcerative colitis (UC)] and 1877 healthy subjects were included. Four single-nucleotide polymorphisms (SNPs), rs10167992, rs11553742, rs7576247 and rs3828329, were genotyped using TaqMan SNP genotyping assays. Common ACP1 alleles (i.e. ACP1*A, ACP1*B and ACP1*C) were determined by two of these SNPs. After the analysis, no evidence of association of the ACP1 genetic variants was found with CD or UC. Therefore, our results suggest that the ACP1 gene may not play a relevant role in the development of IBD.
引用
收藏
页码:61 / 64
页数:4
相关论文
共 31 条
[1]   Investigation of Crohn's Disease Risk Loci in Ulcerative Colitis Further Defines Their Molecular Relationship [J].
Anderson, Carl A. ;
Massey, Dunecan C. O. ;
Barrett, Jeffrey C. ;
Prescott, Natalie J. ;
Tremelling, Mark ;
Fisher, Sheila A. ;
Gwilliam, Rhian ;
Jacob, Jemima ;
Nimmo, Elaine R. ;
Drummond, Hazel ;
Lees, Charlie W. ;
Onnie, Clive M. ;
Hanson, Catherine ;
Blaszczyk, Katarzyna ;
Ravindrarajah, Radhi ;
Hunt, Sarah ;
Varma, Dhiraj ;
Hammond, Naomi ;
Lewis, Gregory ;
Attlesey, Heather ;
Watkins, Nick ;
Ouwehand, Willem ;
Strachan, David ;
McArdle, Wendy ;
Lewis, Cathryn M. ;
Lobo, Alan ;
Sanderson, Jeremy ;
Jewell, Derek P. ;
Deloukas, Panos ;
Mansfield, John C. ;
Mathew, Christopher G. ;
Satsangi, Jack ;
Parkes, Miles .
GASTROENTEROLOGY, 2009, 136 (02) :523-529
[2]   ACP1 genotype, glutathione reductase activity, and riboflavin uptake affect cardiovascular risk in the obese [J].
Apelt, Nadja ;
da Silva, Alda Pereira ;
Ferreira, Joana ;
Alho, Irina ;
Monteiro, Cristina ;
Marinho, Claudia ;
Teixeira, Pedro ;
Sardinha, Luis ;
Laires, Ma Jose ;
Mascarenhas, Mario Rui ;
Bicho, Manuel Pires .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2009, 58 (10) :1415-1423
[3]   ACP1 Genetic Polymorphism and Coronary Artery Disease: An Association Study [J].
Banci, M. ;
Saccucci, P. ;
D'Annibale, F. ;
Dofcaci, A. ;
Trionfera, G. ;
Magrini, A. ;
Bottini, N. ;
Bottini, E. ;
Gloria-Bottini, F. .
CARDIOLOGY, 2009, 113 (04) :236-242
[4]   Haploview: analysis and visualization of LD and haplotype maps [J].
Barrett, JC ;
Fry, B ;
Maller, J ;
Daly, MJ .
BIOINFORMATICS, 2005, 21 (02) :263-265
[5]   ACP1 AND HUMAN ADAPTABILITY .1. ASSOCIATION WITH COMMON DISEASES - A CASE-CONTROL STUDY [J].
BOTTINI, E ;
GLORIABOTTINI, F ;
BORGIANI, P .
HUMAN GENETICS, 1995, 96 (06) :629-637
[6]   Allergy and ACP1 genetic polymorphism [J].
Bottini, Egidio ;
Bergarnaschi, Antonio ;
Magrini, Andrea ;
Spina, Claudio ;
Ammendola, Leonardo ;
Grassi, Saverio ;
Bottini, Nonzio ;
Gloria-Bottini, Fulvia .
ALLERGY AND ASTHMA PROCEEDINGS, 2007, 28 (01) :87-92
[7]  
Bottini N, 2002, ARCH IMMUNOL THER EX, V50, P95
[8]   Genetic control of serum IgE levels: a study of low molecular weight protein tyrosine phosphatase [J].
Bottini, N ;
Otsu, A ;
Borgiani, P ;
Saccucci, P ;
Stefanini, L ;
Greco, E ;
Fontana, L ;
Hopkins, JM ;
Mao, XQ ;
Shirakawa, T .
CLINICAL GENETICS, 2003, 63 (03) :228-231
[9]   Activation of ZAP-70 through specific dephosphorylation at the inhibitory Tyr-292 by the low molecular weight phosphotyrosine phosphatase (LMPTP) [J].
Bottini, N ;
Stefanini, L ;
Williams, S ;
Alonso, A ;
Jascur, T ;
Abraham, RT ;
Couture, C ;
Mustelin, T .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (27) :24220-24224
[10]   Inflammatory bowel disease: Are there gender differences in the genetics of signal transduction? A preliminary study of cytosolic low molecular weight protein tyrosine phosphatase [J].
Bottini, N ;
Gloria-Bottini, F ;
Lucarini, N ;
Ronchetti, PG ;
Fontana, L .
DISEASE MARKERS, 2000, 16 (3-4) :163-166