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Hongyan Wang

职称Professor
电话

021-31246611

地址A609. School of Life Sciences Building
摘要Birth defects could be induced by folate deficiency and gene mutations. Our lab has been focusing on identifying genetic contributors and the underlying molecular mechanism of how supplemented folate preventing birth defects. With a particular emphasis on genetics analysis strategies fitting to complex disease such as neural tube defects (NTDs), we demonstrated that the genomewide threshold of singleton lose-of-function perfectly distinguishes NTDs from controls. We are also using the latest androgenetic haploid embryonic stem cells technologies as a reverse genetic screening to identify the causative mutation for congenital heart disease or NTDs. More recently, the PB mice system makes us to explore new genes or intergenic regions involved in occurrence of NTD. So the research scope of our lab has been expanded to explore how the disrupted noncoding regions led to birth defects or other malformations.
Principal Investigator of the current grants: (1) National Key Basic Research Program (S973 project, 2012CB945400, 2012-2017); (2) National Key Research and Development Program (2016YFC1000502, 2016-2021); (3) National Natural Science Foundation for Innovation Group (31521003, 2015-2019); (4) National Natural Science Foundation for Key Program (81430005, 2014-2018); (5) Basic Research Project of “Innovation Action Plan” from Shanghai Science and Technology Commission (17jc1400902, 2017-2020).
工作经历

1.  Ph.D. in Mol. Genet. at Shanghai Brain Research Institute, Chinese
2.  Academy of Science(1996-1999)
3.  Post-doctoral fellow at Monell Chemical Senses Center, Philadelphia(1999-2002)
4.  Res. Associate at Center for Research on Reproduction & Women’s Health, University of Pennsylvania(2002-2007)
5.  Professor/Deputy-Dean, School of Life Sciences, Fudan University(2007/08-2015)
6.  Professor in Obstetrics & Gynecology Hospital and Director at Institute of Reproduction & Development Fudan University(Since 2015)

研究方向

Birth defects could be induced by folate deficiency and gene mutations. Our lab has been focusing on identifying genetic contributors and the underlying molecular mechanism of how supplemented folate preventing birth defects. With a particular emphasis on genetics analysis strategies fitting to complex disease such as neural tube defects (NTDs), we demonstrated that the genomewide threshold of singleton lose-of-function perfectly distinguishes NTDs from controls. We are also using the latest androgenetic haploid embryonic stem cells technologies as a reverse genetic screening to identify the causative mutation for congenital heart disease or NTDs. More recently, the PB mice system makes us to explore new genes or intergenic regions involved in occurrence of NTD. So the research scope of our lab has been expanded to explore how the disrupted noncoding regions led to birth defects or other malformations.
Principal Investigator of the current grants: (1) National Key Basic Research Program (S973 project, 2012CB945400, 2012-2017); (2) National Key Research and Development Program (2016YFC1000502, 2016-2021); (3) National Natural Science Foundation for Innovation Group (31521003, 2015-2019); (4) National Natural Science Foundation for Key Program (81430005, 2014-2018); (5) Basic Research Project of “Innovation Action Plan” from Shanghai Science and Technology Commission (17jc1400902, 2017-2020).

代表论文

1. Wang D#, Wang F#, Shi KH#, Tao H, Li Y, Zhao R, Lu H, Duan WY, Qiao, B, Zhao SM*, Wang HY*,Zhao JY* (2017). The Circulating Folate Decrease Induced by a Fidgetin Intronic Variant Is Associated with Reduced Congenital Heart Disease Susceptibility. Circulation (accepted)
2. Zhao JY#, Qiao B#, Duan WY#, Gong XH, Jiang SS, Ye ZZ, Wang J, Gu ZY, Shen HB, Shi KH, Sun SN, Huang GY*, Jin L*, Wang HY*(2013). Genetic variants reducing MTR gene expression increase risk of congenital heart disease in a Chinese population. European Heart Journal  DOI: 10.1093 /eurheartj/eht221
3. Zhao JY#, Yang XY#, Shi KH#, Sun SN, Hou J, Ye ZZ, Wang J, Duan WY, Qiao Bin, Chen YJ, Shen HB, Huang GY, Jin L, Wang HY* (2013). A Functional Variant in the Cystathionine b-Synthase Gene Promoter Significantly Reduces Congenital Heart Disease Susceptibility in Han Chinese Population. Cell Research 23:242-253
4. Zhao JY, Yang XY, Gong XH, Gu ZY, Duan WY, Wang J, Ye ZZ, Shen HB, Shi KH, Hou J, Huang GY, Jin L, Qiao B*, and Wang HY* (2012). A functional variant in MTRR intron-1 significantly increases risk of congenital heart disease in Han Chinese population. Circulation 125:482-490
5. Lei YP, Zhang T, Li H, Wu BL, Jin L, Wang HY* (2010). VANGL2 Mutations Identified in Human Cranial Neural-Tube Defects. N Engl J of Med 362 (23):2232-2235
6. Wang H, Parry S, Macones G, Sammel MD, Kuivaniemi H, Tromp G, Halder I, Shriver MD, Romero R, Strauss JF (2006) A Functional SNP in the Promoter of the SERPINH1 Gene Encoding Hsp47 Increases Risk of Preterm Premature Rupture of Membranes and Preterm Birth in African-Americans. PNAS103(36):13463-13467
7. Wang H, Parry S, Macones G, Sammel MD, Ferrand PE, Kuivaniemi H, Tromp G, Halder I, Shriver MD, Romero R, Strauss JF (2004) Functionally significant SNP MMP8 promoter haplotypes and preterm premature rupture of membranes (PPROM). Hum Mol Genet 13(21):2659-2669
8. Wang HY, Zhang FC, Gao JJ, Fan JB, Liu P, Zheng ZJ, Xi H, Sun Y, Gao XC, Huang TZ, Ke ZJ, Guo GR, Feng GY, Breen G, St Clair D, He L (2000) Apolipoprotein E is a genetic risk factor for fetal iodine deficiency disorder in China. Molecular Psychiatry 5(4): 363-368

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