Disrupted cholecystokinin type-A receptor (CCKAR) gene in OLETF rats
1997; Elsevier BV; Volume: 197; Issue: 1-2 Linguagem: Inglês
10.1016/s0378-1119(97)00259-x
ISSN1879-0038
AutoresSoichi Takiguchi, Yutaka Takata, Akihiro Funakoshi, Kyoko Miyasaka, Kazuhiro Kataoka, Yoshiteru Fujimura, Toshihiro Goto, Akira Kono,
Tópico(s)Cardiovascular, Neuropeptides, and Oxidative Stress Research
ResumoOLETF rats develop hyperglycemia, hyperinsulinemia and mild obesity, which is characteristic of human non-insulin-dependent diabetes mellitus (NIDDM). We cloned and sequenced the cholecystokinin type-A receptor (CCKAR) gene in the rats. Comparing the DNA sequences of the OLETF CCKAR gene and LETO CCKAR gene, normal gene, we found a deletion in the OLETF gene, 6847 bases in length, which was flanked by two 3-base-pair direct repeats (5′-TGT-3′) at positions −2407/−2405 and 4441/4443, numbered according to the LETO gene sequence, one of which was lost. The promoter region, the first and second exons were missing in the mutant. The region upstream and downstream of the deletion, including exons 3, 4 and 5, was conserved between the two strains, and did not contain any base changes. We found that the gene mapped to chromosome 14 in rats. OLETF rats are the naturally occurring knockout animals with the homozygously disrupted CCKAR gene.
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