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Volumn 90, Issue 6, 2005, Pages 3174-3178

The C42R mutation in the Kir6.2 (KCNJ11) gene as a cause of transient neonatal diabetes, childhood diabetes, or later-onset, apparently type 2 diabetes mellitus

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; AUTOANTIBODY; INWARDLY RECTIFYING POTASSIUM CHANNEL SUBUNIT KIR6.2; DNA; INWARDLY RECTIFYING POTASSIUM CHANNEL; PRIMER DNA;

EID: 21244487124     PISSN: 0021972X     EISSN: None     Source Type: Journal    
DOI: 10.1210/jc.2005-0096     Document Type: Article
Times cited : (107)

References (16)
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    • UK Prospective Diabetes Study (UKPDS 53). Association studies of variants in promoter and coding regions of β-cell ATP-sensitive K-channel genes SUR1 and Kir6.2 with type 2 diabetes mellitus (UKPDS 53)
    • Gloyn AL, Hashim Y, Ashcroft SJ, Ashfield R, Wiltshire S, Turner RC 2001 UK Prospective Diabetes Study (UKPDS 53). Association studies of variants in promoter and coding regions of β-cell ATP-sensitive K-channel genes SUR1 and Kir6.2 with type 2 diabetes mellitus (UKPDS 53). Diabet Med 18:206-212
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    • Hani EH, Boutin P, Durand E, Inoue H, Permutt MA, Velho G, Froguel P 1998 Missense mutations in the pancreatic islet β cell inwardly rectifying K+ channel gene (KIR6.2/BIR): a meta-analysis suggests a role in the polygenic basis of type II diabetes mellitus in Caucasians. Diabetologia 41:1511-1515
    • (1998) Diabetologia , vol.41 , pp. 1511-1515
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  • 13
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* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.