PubMed:10618679 JSONTXT

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    PubTator4TogoVar

    {"project":"PubTator4TogoVar","denotations":[{"id":"10618679_0","span":{"begin":25,"end":30},"obj":"ProteinMutation"},{"id":"10618679_1","span":{"begin":163,"end":167},"obj":"ProteinMutation"},{"id":"10618679_2","span":{"begin":327,"end":331},"obj":"ProteinMutation"},{"id":"10618679_3","span":{"begin":442,"end":447},"obj":"ProteinMutation"},{"id":"10618679_4","span":{"begin":711,"end":716},"obj":"ProteinMutation"},{"id":"10618679_5","span":{"begin":1400,"end":1405},"obj":"ProteinMutation"},{"id":"10618679_6","span":{"begin":1571,"end":1575},"obj":"ProteinMutation"},{"id":"10618679_7","span":{"begin":1631,"end":1635},"obj":"ProteinMutation"}],"attributes":[{"id":"10618679_0_ProteinMutation","pred":"proteinmutation","subj":"10618679_0","obj":"rs699"},{"id":"10618679_1_ProteinMutation","pred":"proteinmutation","subj":"10618679_1","obj":"rs699"},{"id":"10618679_2_ProteinMutation","pred":"proteinmutation","subj":"10618679_2","obj":"rs699"},{"id":"10618679_3_ProteinMutation","pred":"proteinmutation","subj":"10618679_3","obj":"rs699"},{"id":"10618679_4_ProteinMutation","pred":"proteinmutation","subj":"10618679_4","obj":"rs699"},{"id":"10618679_5_ProteinMutation","pred":"proteinmutation","subj":"10618679_5","obj":"rs699"},{"id":"10618679_6_ProteinMutation","pred":"proteinmutation","subj":"10618679_6","obj":"rs699"},{"id":"10618679_7_ProteinMutation","pred":"proteinmutation","subj":"10618679_7","obj":"rs699"}],"text":"Relationship between the M235T and G(-6)A polymorphisms of the angiotensinogen gene.\nAIMS: Previous studies have reported tight linkage disequilibrium between the T235 and the A(-6) molecular variants of the angiotensinogen gene. This study was designed primarily to ascertain whether a similar relationship exists between the M235 and the G(-6) variants of the gene. We have investigated the degree of agreement between the genotypes of the M235T and the G(-6)A polymorphisms in two ethnic groups.\nMETHODS: Subjects were an heterogeneous group of normotensive and hypertensive subjects of Caucasian (n = 77) and Afro-Caribbean (n = 51) origin. DNA was extracted from whole blood and was genotyped for both the M235T and G(-6)A polymorphisms using PCR-based methods.\nRESULTS: The distribution frequencies of the MM, MT, and TT genotypes were 0.39, 0.42, and 0.20 in white subjects, and 0.09, 0.17, and 0.74 in black subjects, respectively (chi-square, P \u003c 0.0001). The distribution of AA, GA, and GG genotypes also differed between the two groups as follows: 0.22, 0.48, and 0.30 in white subjects, and 0.82 and 0.18 and 0 in black subjects respectively (chi-square, P \u003c 0.0001). The agreement for TT-AA, MT-GA, and MM-GG was 93%, 91%, and 76% respectively in white and 100%, 67% and 0% respectively in black subjects.\nCONCLUSIONS: The results indicate ethnic differences in the distribution of both M235T and G(-6)A genotypes. The trend towards a decrease in the degree of agreement in the order of TT-AA \u003e MT-GA \u003e MM-GG suggests that linkage disequilibrium between the M235 and G-6 variant does not mirror that observed with the T235 and A-6 variants. These observations may have significant implications regarding the associations between the G(-6)A polymorphism and hypertension. However, this needs to be further investigated."}