Protein & Cell >

2018 , Vol. 9 >Issue 12: 1039 - 1044

DOI: https://doi.org/10.1007/s13238-018-0525-8

LETTER

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

  • Liangping Cheng 1,2 ,
  • Peiqiang Li 3,4 ,
  • He Wang 4 ,
  • Xueyan Yang 4 ,
  • Huiming Zhou 1 ,
  • Wufan Tao , 2,5 ,
  • Jie Tian , 1 ,
  • Hongyan Wang , 2,4
Expand
  • 1. Key Laboratory of Pediatrics in Chongqing, Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Department of Cardiovascular Medicine, Children’s Hospital of Chongqing Medical University, Chongqing 400014, China
  • 2. Obstetrics Gynecology Hospital, The Institute of Reproduction and Developmental Biology, Fudan University, Shanghai 200011, China
  • 3. Institute of Genetics, School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China
  • 4. The State Key Laboratory of Genetic Engineering, MOE Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center of Genetics and Development, School of Life Science, Fudan University, Shanghai 200433, China
  • 5. Institute of Developmental Biology and Molecular Medicine, Fudan University, Shanghai 200433, China

Published date: 19 Dec 2018

Copyright

2018 The Author(s) 2018
Fold

Cite this article

Liangping Cheng , Peiqiang Li , He Wang , Xueyan Yang , Huiming Zhou , Wufan Tao , Jie Tian , Hongyan Wang . Decreased activity of RCAN1.4 is a potential risk factor for congenital heart disease in a Han Chinese population[J]. Protein & Cell, 2018 , 9(12) : 1039 -1044 . DOI: 10.1007/s13238-018-0525-8

References

Publishing order | Descend order by publishing year | Descend order by cited within
1
Alghanem AF, Wilkinson EL, Emmett MS, Aljasir MA, Holmes K, Rothermel BA, Simms VA, Heath VL, Cross MJ (2017) RCAN1.4 regulates VEGFR-2 internalisation, cell polarity and migration in human microvascular endothelial cells. Angiogenesis 20:341–358

DOI

2
Cordell HJ, Bentham J, Topf A, Zelenika D, Heath S, Mamasoula C, Cosgrove C, Blue G, Granados-Riveron J, Setchfield K (2013) Genome-wide association study of multiple congenital heart disease phenotypes identifies a susceptibility locus for atrial septal defect at chromosome 4p16. Nat Genet 45:822–824

DOI

3
de la Pompa JL, Timmerman LA, Takimoto H, Yoshida H, Elia AJ, Samper E, Potter J, Wakeham A, Marengere L, Langille BL (1998) Role of the NF-ATc transcription factor in morphogenesis of cardiac valves and septum. Nature 392:182–186

DOI

4
Elmagrpy Z, Rayani A, Shah A, Habas E, Aburawi EH (2011) Down syndrome and congenital heart disease: why the regional difference as observed in the Libyan experience? Cardiovasc J Afr 22:306–309

DOI

5
Fuentes JJ, Pritchard MA, Planas AM, Bosch A, Ferrer I, Estivill X (1995) A new human gene from the down syndrome critical region encodes a proline-rich protein highly expressed in fetal brain and heart. Hum Mol Genet 4:1935–1944

DOI

6
Guo RY, Li XF, Bai S, Guo J, Ding N, Li ZZ (2015) Association between DSCR1 variations and congenital heart disease susceptibility. Med Sci Monit 21:3536–3539

DOI

7
Lange AW, Molkentin JD, Yutzey KE (2004) DSCR1 gene expression is dependent on NFATc1 during cardiac valve formation and colocalizes with anomalous organ development in trisomy 16 mice. Dev Biol 266:346–360

DOI

8
Lange AW, Yutzey KE (2006) NFATc1 expression in the developing heart valves is responsive to the RANKL pathway and is required for endocardial expression of cathepsin K. Dev Biol 292:407–417

DOI

9
Li X, Wang G, An Y, Li H, Li Y, Wu C (2015) Association between sequence variations in RCAN1 promoter and the risk of sporadic congenital heart disease in a Chinese population. Pediatr Cardiol 36:1393–1399

DOI

10
Lyle R, Bena F, Gagos S, Gehrig C, Lopez G, Schinzel A, Lespinasse J, Bottani A, Dahoun S, Taine L (2009) Genotype-phenotype correlations in Down syndrome identified by array CGH in 30 cases of partial trisomy and partial monosomy chromosome 21. Eur J Hum Genet 17:454–466

DOI

11
Qin L, Zhao D, Liu X, Nagy JA, Hoang MV, Brown LF, Dvorak HF, Zeng H (2006) Down syndrome candidate region 1 isoform 1 mediates angiogenesis through the calcineurin-NFAT pathway. Mol Cancer Res 4:811–820

DOI

12
Soemedi R, Topf A, Wilson IJ, Darlay R, Rahman T, Glen E, Hall D, Huang N, Bentham J, Bhattacharya S (2012) Phenotypespecific effect of chromosome 1q21.1 rearrangements and GJA5 duplications in 2436 congenital heart disease patients and 6760 controls. Hum Mol Genet 21:1513–1520

DOI

13
Stoll C, Alembik Y, Dott B, Roth MP (1998) Study of Down syndrome in 238,942 consecutive births. Ann Genet 41:44–51

14
Vis JC, Duffels MG, Winter MM, Weijerman ME, Cobben JM, Huisman SA, Mulder BJ (2009) Down syndrome: a cardiovascular perspective. J Intellect Disabil Res 53:419–425

DOI

15
Yang J, Rothermel B, Vega RB, Frey N, McKinsey TA, Olson EN, Bassel-Duby R, Williams RS (2000) Independent signals control expression of the calcineurin inhibitory proteins MCIP1 and MCIP2 in striated muscles. Circ Res 87:E61–E68

DOI

Options
Outlines

/

〈 〉