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Decreased activity of RCAN1.4 is a potential risk factor for congenital heart disease in a Han Chinese population

Protein & Cell 2018年第12期9卷 1039-1044页

作者： Liangping Cheng Peiqiang Li He Wang Xueyan Yang Huiming Zhou Wufan Tao Jie Tian Hongyan Wang Key Laboratory of Pediatrics in Chongqing Chongqing Interna-tional Science and Technology Cooperation Center for Child Development and DisordersDepartment of Cardiovascular MedicineChildren's Hospital of Chongqing Medical UniversityChongqing 400014China Obstetrics Gynecology Hospital The Institute of Reproduction and Developmental BiologyFudan UniversityShanghai 200011China Institute of Genetics School of Basic Medical SciencesLanzhou UniversityLanzhou 730000China The State Key Laboratory of Genetic Engineering MOE Key Laboratory of Contemporary AnthropologyCollaborative Innova-tion Center of Genetics and DevelopmentSchool of Life ScienceFudan UniversityShanghai 200433China Institute of Developmental Biology and Molecular Medicine Fudan UniversityShanghai 200433China

Congenital heart disease (CHD) is a major birth defect worldwide. However, the aetiology of CHD remains unclear and the detailed molecular mechanisms underlying CHD pathogenesis have not been fully understood. The human regulator of calcineurin (RCAN1) gene is highly expressed in human hearts and brains (Fuentes et al., 1995) and composed of seven exons that are alternatively spliced and/or transcribed by differential promoters to produce different isoforms (Fig. 1A) (Yang et al., 2000). RCAN1.1 (NM_004414) and RCAN1.4 (NM_203418) are the two major isoforms differentially expressed in many tissues and cells. RCAN1.1 is constitutively expressed while the expression of RCAN1.4 is induced by diverse stimuli (Yang et al., 2000; Lange et al., 2004). RCAN1.4 negatively regulates NFAT-mediated transcription (Lange and Yutzey, 2006; Qin et al., 2006), which is an important regulator for early heart development (de la Pompa et al., 1998). Although SNPs rs149048873, rs193289374 and rs143081213 in the RCAN1.1 promoter were not associated with sporadic CHD (Guo et al., 2015; Li et al., 2015), the function of RCAN1.4 in CHD remains elusive.

关键词： down-syndrome ASSOCIATION EXPRESSION NFATC1 VALVES GENE

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