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FältnamnIndikatorerMetadata
00004409naa a2200721 4500
001oai:lup.lub.lu.se:0103dfb2-220e-4368-a161-d28266ea8432
003SwePub
008160401s2010 | |||||||||||000 ||eng|
024a https://lup.lub.lu.se/record/15356062 URI
024a https://doi.org/10.1007/s00125-009-1557-72 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
100a Reiling, E.4 aut
2451 0a Genetic association analysis of LARS2 with type 2 diabetes
264 c 2009-10-22
264 1b Springer Science and Business Media LLC,c 2010
520 a LARS2 has been previously identified as a potential type 2 diabetes susceptibility gene through the low-frequency H324Q (rs71645922) variant (minor allele frequency [MAF] 3.0%). However, this association did not achieve genome-wide levels of significance. The aim of this study was to establish the true contribution of this variant and common variants in LARS2 (MAF > 5%) to type 2 diabetes risk. We combined genome-wide association data (n = 10,128) from the DIAGRAM consortium with independent data derived from a tagging single nucleotide polymorphism (SNP) approach in Dutch individuals (n = 999) and took forward two SNPs of interest to replication in up to 11,163 Dutch participants (rs17637703 and rs952621). In addition, because inspection of genome-wide association study data identified a cluster of low-frequency variants with evidence of type 2 diabetes association, we attempted replication of rs9825041 (a proxy for this group) and the previously identified H324Q variant in up to 35,715 participants of European descent. No association between the common SNPs in LARS2 and type 2 diabetes was found. Our replication studies for the two low-frequency variants, rs9825041 and H324Q, failed to confirm an association with type 2 diabetes in Dutch, Scandinavian and UK samples (OR 1.03 [95% CI 0.95-1.12], p = 0.45, n = 31,962 and OR 0.99 [0.90-1.08], p = 0.78, n = 35,715 respectively). In this study, the largest study examining the role of sequence variants in LARS2 in type 2 diabetes susceptibility, we found no evidence to support previous data indicating a role in type 2 diabetes susceptibility.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Endokrinologi och diabetes0 (SwePub)302052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Endocrinology and Diabetes0 (SwePub)302052 hsv//eng
653 a Type 2 diabetes
653 a SNP
653 a Mitochondria
653 a Genetics
653 a LARS2
700a Jafar-Mohammadi, B.4 aut
700a van't Riet, E.4 aut
700a Weedon, M. N.4 aut
700a van Vliet-Ostaptchouk, J. V.4 aut
700a Hansen, T.4 aut
700a Saxena, R.4 aut
700a van Haeften, T. W.4 aut
700a Arp, P. A.4 aut
700a Das, S.4 aut
700a Nijpels, G.4 aut
700a Groenewoud, M. J.4 aut
700a van Hove, E. C.4 aut
700a Uitterlinden, A. G.4 aut
700a Smit, J. W. A.4 aut
700a Morris, A. D.4 aut
700a Doney, A. S. F.4 aut
700a Palmer, C. N. A.4 aut
700a Guiducci, C.4 aut
700a Hattersley, A. T.4 aut
700a Frayling, T. M.4 aut
700a Pedersen, O.4 aut
700a Slagboom, P. E.4 aut
700a Altshuler, D. M.4 aut
700a Groop, Leifu Lund University,Lunds universitet,Genomik, diabetes och endokrinologi,Forskargrupper vid Lunds universitet,Genomics, Diabetes and Endocrinology,Lund University Research Groups4 aut0 (Swepub:lu)endo-lgr
700a Romijn, J. A.4 aut
700a Maassen, J. A.4 aut
700a Hofker, M. H.4 aut
700a Dekker, J. M.4 aut
700a McCarthy, M. I.4 aut
700a 't Hart, L. M.4 aut
710a Genomik, diabetes och endokrinologib Forskargrupper vid Lunds universitet4 org
773t Diabetologiad : Springer Science and Business Media LLCg 53:1, s. 103-110q 53:1<103-110x 1432-0428x 0012-186X
856u http://dx.doi.org/10.1007/s00125-009-1557-7y FULLTEXT
856u https://link.springer.com/content/pdf/10.1007%2Fs00125-009-1557-7.pdf
8564 8u https://lup.lub.lu.se/record/1535606
8564 8u https://doi.org/10.1007/s00125-009-1557-7

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