Sökning: WFRF:(Naluai AT) > Variation in the CT...
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000 | 03549naa a2200517 4500 | |
001 | oai:lup.lub.lu.se:8cf1e0ff-71cd-4555-af26-80e82b2eb83f | |
003 | SwePub | |
008 | 160401s2002 | |||||||||||000 ||eng| | |
024 | 7 | a https://lup.lub.lu.se/record/3318302 URI |
024 | 7 | a https://doi.org/10.1046/j.1469-1809.2002.00102.x2 DOI |
040 | a (SwePub)lu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a art2 swepub-publicationtype |
072 | 7 | a ref2 swepub-contenttype |
100 | 1 | a Popat, S4 aut |
245 | 1 0 | a Variation in the CTLA4/CD28 gene region confers an increased risk of coeliac disease |
264 | 1 | b Wiley,c 2002 |
520 | a Susceptibility to coeliae disease involves HLA and non-HLA-linked genes. The CTLA4/CD28 gene region encodes immune regulatory T-cell surface molecules and is a strong candidate as a susceptibility locus. We evaluated CTLA4/CD28 in coeliac disease by genetic linkage and association and combined Our findings with published studies through a meta-analysis. 116 multiplex families were genotyped across CTLA4/CD28 using eight markers. The contribution of CTLA4/CD28 to coeliac disease was assessed by non-parametric linkage and association analyses. Seven studies were identified that had evaluated the relationship between CTLA4/CD28 and coeliac disease and a pooled analysis of data undertaken. In our study there was evidence for a relationship between variation in the CTLA4/CD28 region and coeliae disease by linkage and association analyses. However. the findings did not attain formal statistical significance (p=0.004 and 0.039. respectively). Pooling findings with published results showed significant evidence for linkage (504 families) and association (910 families) : p values. 0.0001 and 0.0014 at D2S2214. respectively. and 0.0008 and 0.0006 at D2S116, respectively. These findings suggest that variation in the CD28/CTLA4 gene region is a determinant of coeliac disease susceptibility. Dissecting the sequence variation underlying this relationship will depend on further analyses utilising denser sets of markers. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng |
700 | 1 | a Hearle, N4 aut |
700 | 1 | a Hogberg, L4 aut |
700 | 1 | a Braegger, CP4 aut |
700 | 1 | a O'Donoghue, D4 aut |
700 | 1 | a Falth-Magnusson, K4 aut |
700 | 1 | a Holmes, GKT4 aut |
700 | 1 | a Howdle, PD4 aut |
700 | 1 | a Jenkins, H4 aut |
700 | 1 | a Johnston, S4 aut |
700 | 1 | a Kennedy, NP4 aut |
700 | 1 | a Kumar, PJ4 aut |
700 | 1 | a Logan, RFA4 aut |
700 | 1 | a Marsh, MN4 aut |
700 | 1 | a Mulder, CJ4 aut |
700 | 1 | a Naluai, AT4 aut |
700 | 1 | a Sjöberg, Klasu Lund University,Lunds universitet,Gastroenterologi,Forskargrupper vid Lunds universitet,Enheten för kroniska inflammatoriska och degenerativa sjukdomar,Gastroenterology,Lund University Research Groups,Chronic Inflammatory and Degenerative Diseases Research Unit4 aut0 (Swepub:lu)medf-ksj |
700 | 1 | a Stenhammar, L4 aut |
700 | 1 | a Walters, JRF4 aut |
700 | 1 | a Jewell, DP4 aut |
700 | 1 | a Houlston, RS4 aut |
710 | 2 | a Gastroenterologib Forskargrupper vid Lunds universitet4 org |
773 | 0 | t Annals of Human Geneticsd : Wileyg 66:2, s. 125-137q 66:2<125-137x 1469-1809x 0003-4800 |
856 | 4 | u http://dx.doi.org/10.1046/j.1469-1809.2002.00102.xy FULLTEXT |
856 | 4 8 | u https://lup.lub.lu.se/record/331830 |
856 | 4 8 | u https://doi.org/10.1046/j.1469-1809.2002.00102.x |
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