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      Genetic polymorphism of vascular endothelial growth factor (VEGF C936T) in the Korean population

      1 , 2 , 2 , 2 , 3 , 4
      Korean Journal of Biological Sciences
      Informa UK Limited

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          A common polymorphism in the 5'-untranslated region of the VEGF gene is associated with diabetic retinopathy in type 2 diabetes.

          Vascular endothelial growth factor (VEGF), a major mediator of vascular permeability and angiogenesis, may play a pivotal role in mediating the development and progression of diabetic retinopathy. In the present study, we examined the genetic variations of the VEGF gene to assess its possible relation to diabetic retinopathy in type 2 diabetic patients. Among seven common polymorphisms in the promoter region, 5'-untranslated region (UTR) and 3'UTR of the VEGF gene, genotype distribution of the C(-634)G polymorphism differed significantly (P = 0.011) between patients with (n = 150) and without (n = 118) retinopathy, and the C allele was significantly increased in patients with retinopathy compared with those without retinopathy (P = 0.0037). The odds ratio (OR) for the CC genotype of C(-634)G to the GG genotype was 3.20 (95% CI 1.45-7.05, P = 0.0046). The -634C allele was significantly increased in patients with nonproliferative diabetic retinopathy (non-PDR) (P = 0.0026) and was insignificantly increased in patients with proliferative diabetic retinopathy (PDR) (P = 0.081) compared with patients without retinopathy, although frequencies of the allele did not differ significantly between the non-PDR and PDR groups. Logistic regression analysis revealed that the C(-634)G polymorphism was strongly associated with an increased risk of retinopathy (P = 0.0018). Furthermore, VEGF serum levels were significantly higher in healthy subjects with the CC genotype of the C(-634)G polymorphism than in those with the other genotypes. These data suggest that the C(-634)G polymorphism in the 5'UTR of the VEGF gene is a novel genetic risk factor for diabetic retinopathy.
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            A Common 936 C/T Mutation in the Gene for Vascular Endothelial Growth Factor Is Associated with Vascular Endothelial Growth Factor Plasma Levels

            Background: Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis. Strong interindividual variations of VEGF plasma levels have been reported previously. Aim of the present study was to search for mutations in the 3′ untranslated region (3′-UTR) of the VEGF gene and to analyze their relation to VEGF plasma levels. Methods: The complete 3′-UTR (nucleotide 700–2622) of the VEGF gene was screened for sequence variations by single-strand conformation polymorphism (SSCP) analysis. Frequencies of mutated alleles were determined in 119 healthy subjects; VEGF plasma levels were analyzed in a subgroup of 23 healthy men aged 18–36 years. Results: Three novel mutations (702 C/T, 936 C/T, 1612 G/A) were found, allele frequencies of 702T, 936T and 1612A were of 0.017, 0.160 and 0.471, respectively. VEGF plasma levels were significantly lower in carriers of the 936T allele (9.1 ± 2.7 pg/ml, mean ± SEM) than in noncarriers (28.0 ± 5.5 pg/ml, p = 0.033), whereas the 702 C/T and the 1612 G/A mutations showed no association with VEGF plasma levels. The 936 C/T exchange led to the loss of a potential binding site for transcription factor AP-4, although the functionality of this binding site remains unclear. Conclusion: We have found three common mutations in the VEGF gene; one of them, a 936 C/T exchange, may be an important determinant of VEGF plasma levels.
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              Enhancer binding factors AP-4 and AP-1 act in concert to activate SV40 late transcription in vitro.

              The simian virus 40 (SV40) transcriptional enhancer is composed of multiple cis-acting DNA sequence motifs, each individually having a two- to fourfold effect on the efficiency of transcription. When various distinct cis-elements act in combination, however, a dramatic enhancement of transcription initiation often results. SV40-enhancer A-domain sequences were previously shown to be important for early and late transcription in vivo. Here we report the isolation of the enhancer binding factor AP-4, which recognizes a motif in this domain. Purified AP-4 activates SV40 late transcription in vitro, and this stimulation is augmented by the addition of transcription factor AP-1 which binds to adjacent sequences in the A-domain, suggesting coordinate action of the two factors for transcriptional enhancement. AP-1 also represses late transcription from a major in vitro start site which is poorly used in vivo, indicating that AP-1 can act as both a positive and negative regulator of SV40 late transcription. Thus by manipulating the levels of different trans-acting factors in vitro, we can recreate the pattern of SV40 late initiation observed during the viral lytic cycle in vivo.
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                Author and article information

                Journal
                Korean Journal of Biological Sciences
                Korean Journal of Biological Sciences
                Informa UK Limited
                1226-5071
                November 22 2010
                January 2003
                November 22 2010
                January 2003
                : 7
                : 3
                : 261-264
                Affiliations
                [1 ] a Graduate School of Life Science and Biotechnology , Pochon CHA University , Sungnam , 463–712 , Korea
                [2 ] b Institute for Clinical Research , Pochon CHA University , Sungnam , 463–712 , Korea
                [3 ] c Department of Neurosurgery, College of Medicine , Pochon CHA University , Sungnam , 463–712 , Korea
                [4 ] d Institute for Clinical Research , Pochon CHA University , Sungnam , 463–712 , Korea Phone: Fax: E-mail:
                Article
                10.1080/12265071.2003.9647713
                63322da0-6100-4f7b-8361-6643ed39120a
                © 2003
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