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| Content Provider | IEEE Xplore Digital Library |
|---|---|
| Author | Jiao Chuan-zhen Tian Zhi-huan Wei Zhen-lin Wana Zai-zhao |
| Copyright Year | 2008 |
| Description | Author affiliation: Biol. Sci. Dept., DeZhou Univ., Dezhou (Jiao Chuan-zhen; Tian Zhi-huan; Wei Zhen-lin; Wana Zai-zhao) |
| Abstract | The SNP rs7903146 in human TCF7L2 gene has associated with type 2 diabetes (T2D) in multiple cohorts. TCF7L2 expression in human islets was increased in T2D, particularly in carriers of the TT genotype of SNP rs7903146. Over expression of TCF7L2 in human islets reduced glucose-stimulated insulin secretion. The question of why the TCF7L2 genetic variants effect it's self s expression remained unanswered. We analyzed the sequence of about 20 kb range in vicinity of rs7903146 SNP in combination with multiple bioinformatics programs in this study. We predicted 3 real pre-microRNAs on forward strand and 3 on reverse strand of 20 kb vicinity sequence of rs7903146 respectively. Five potential promoters on forward strand and seven on reverse strand were also predicted. The TFSEARCH web server predicted the type 2 diabetes risk "T" allele of rs7903146 SNP has an E4BP4 binding site and two CDX1 binding sites which the common "C" allele has not. We hypothesized that E4BP4, CDX1 and some microRNAs in intron3 transcribed with host gene or independently in intron3 of TCF7L2 are involved in predisposing T2D by TCF7L2 gene variants. |
| Starting Page | 50 |
| Ending Page | 53 |
| File Size | 269928 |
| Page Count | 4 |
| File Format | |
| ISBN | 9781424417476 |
| DOI | 10.1109/ICBBE.2008.19 |
| Language | English |
| Publisher | Institute of Electrical and Electronics Engineers, Inc. (IEEE) |
| Publisher Date | 2008-05-16 |
| Publisher Place | China |
| Access Restriction | Subscribed |
| Rights Holder | Institute of Electrical and Electronics Engineers, Inc. (IEEE) |
| Subject Keyword | Couplings Sequences RNA Humans Fluids and secretions Biology Diabetes Insulin Bioinformatics Biological cells |
| Content Type | Text |
| Resource Type | Article |
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