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Xinli Hu 阅读次数:

Xinli Hu, Ph.D.

Associate Investigator

Co-Principal Investigator, Transgenic and knockout Mouse Core

Ying-Jie Conference Center,

Peking University, Beijing, China100871

Email: huxxx025@pku.edu.cn

Dr. Hu received her PhD degree in Cell Biology from Peking University in July, 1996. From 1996 to 2005, she worked first as a postdoctoral associate, subsequently a research associate at the Department of Pharmacology, University of Minnesota. During this time, her studies focused on gene regulation, with special emphasis on the functions of nuclear receptors and their co-regulators on chromatin structure and transcriptional regulation. In 2005, Dr. Hu joined the Department of Medicine, Cardiovascular Division, Lillehei Heart Institute where she applied her expertise in molecular biology to the field of cardiovascular research. She used transgenic mouse models and molecular biology approaches to study energy metabolism related gene regulation by cardiac KATP channel and AMP activated protein kinase (AMPK) during the development of ventricular hypertrophy and heart failure. Meanwhile, Dr. Hu developed a conditional DDAH1 gene deficient mouse strain, which provides a unique tool for understanding the function of NOS signaling pathway in different tissue types and at different development stages. She joined IMM in the middle of 2011 and is now in charge of the Transgenic and Knockout Mouse Core.

Dr. Hu has published over 40 papers in peer-reviewed scientific journals, such as Circulation, Circulation Research, and Journal of Biological Chemistry. Her presentation based on the studies of endothelial specific DDAH1 deficient mice won the Young Investigators Travel Award at 2008 AHA Scientific Session. Her abstract about global DDAH1 deficient mice was selected for AHA Best of Specialty Conferences Poster Session at Scientific Sessions 2010.

 

Selected Publications:

12. Liu F, Song R, Feng Y, Guo J, Chen Y, Zhang Y, Chen T, Wang Y, Huang Y, Li CY, Cao C, Zhang Y, Hu X*, Xiao RP*. Upregulation of MG53 induces diabetic cardiomyopathy through transcriptional activation of peroxisome proliferation-activated receptor α. Circulation, 131(9):795-804, 2015.

11. Wang H, Xu X, Fassett J, Kwak D, Liu X, Hu X, Falls TJ, Bell JC, Li H, Bitterman P, Bache RJ, Chen Y. Double-stranded RNA–dependent protein kinase deficiency protects the heart from systolic overload-induced congestive heart failure. Circulation, 129(13): 1397-1406, 2014.

10. Hu X*, Chang N, Wang X, Zhou F, Zhou X, Zhu X, Xiong JW*. Heritable gene-targeting with gRNA/Cas9 in rats. Cell Research. 23(11):1322-5, 2013.

9. Hu XL, Zhang P, Xu X, Lu Z, Zhu G, Fassett J, Viollet B, Zhuo M, Tao Y, Chen Y.AMPK?2 regulates expression of ERR?, a metabolic transcription factor related to heart failure development. Hypertension, 58(4): 696-703. 2011

8. Hu XL, Atzler D, Xu X, Zhang P, Guo H, Lu Z, Fassett J, Schwedhelm E, B?ger RH, Bache RJ, Chen Y. Global Dimethylarginine Dimethylaminohydrolase-1 (DDAH1) Gene-Deficient Mice Reveal That DDAH1 Is the Critical Enzyme for Degrading the Cardiovascular Risk Factor Asymmetrical Dimethylarginine. Arteriosclerosis, Thrombosis, and Vascular Biology, 31(7): 1540-1546. 2011

7. Hu XL, Xu X, Zhu G, Atzler D, Kimoto M; Chen J; Schwedhelm E, Lüneburg N; B?ger RH, Zhang P, Chen Y. Vascular endothelial specific DDAH1 gene deficient mice reveal vascular endothelium as the primary site to remove toxic methylarginines. Circulation, 120: 2222 – 2229. 2009

6. Xu X*, Hu X*, Lu Z, Zhang P, Zhao L, Wessale JL, Bache RJ, Chen Y. Xanthine oxidase inhibition with Febuxostat attenuates systolic overload-induced left ventricular hypertrophy and dysfunction in mice. Journal of Cardiac Failure. 2008; 14(9):746-753.

5. Hu X, Xu X, Huang Y, Fassett J, Flagg TP, Zhang Y, Nichols CG, Bache RJ, Chen Y. Disruption of Sarcolemmal ATP-Sensitive Potassium Channel Activity Impairs the Cardiac Response to Systolic Overload. Circulation Research. 103(9):1009-17. 2008

4. Hu XL, Chen YX, Farooqui M, Chiang CM, Wu SH, Wei LN, Ligand-dependent, negative modulation of retinoic acid-induced transcriptional activation by antagonism of receptor interacting protein 140 (RIP 140) toward p300/CBP-associated factor P/CAF. Journal of Biological Chemistry, Vol. 279(1): 51-60, 2004

3. Hu XL, Bi J, Loh H, Wei LN, Regulation of Mouse Opioid Receptor Gene Expression by Different 3'-Untranslated Regions and the Effect of Retinoic Acid. Molecular Pharmacology, Vol. 62: 881 – 887, 2002

2. Hu XL, Bi J, Loh H, Wei LN, An intronic Ikaros-binding element mediates retinoic acid suppression of Kappa opioid receptor gene, accompanied by recruiting histone deacetylases. Journal of Biological Chemistry, Vol. 276(7): 4597-4603, 2001

1. Hu XL, Cao S, Loh H, and Wei, LN, Promoter activity of mouse k opioid receptor gene in transgenic mouse. Molecular Brain Research, 69(1): 35-43, 1999