||Qiurong Ding Ph.D., Professor
|Laboratory of Human Genetics and Metabolic Diseases
E-mail: qrding@@sibs.ac.cn (delete one @ to send email)
Education Background & Academic Experience:
Dr.Ding got her Bachelor degree from Nanjing University in 2004, and received her ph.D degree from the Institute for Nutritional Sciences, Chinese Academy of Sciences in 2010. From 2010 to 2014, she did her postdoctoral training at Harvard department of Stem Cell and Regenerative Biology and Harvard Stem Cell Institute. She joined the faculty of Institute for Nutritional Sciences at SIBS, CAS in 2014.
The wealth of data being generated by human genetics nowadays is providing new opportunities to discover novel genetic contributors to many human diseases. Our goal is to convert these novel genetic findings into the knowledge needed to develop new therapies for human metabolic diseases. The approach we have developed is 1) to use genome editing tools to introduce disease-associated gene mutations into human pluripotent stem cells (hPSCs) and to differentiate and engineer hPSCs into cell/tissue types relevant to disease in order to develop ex vivo models of disease; 2) to use genome editing tools to introduce disease-associated gene mutations into mice to generate genetic modified mouse models; 3) to transplant human stem cell derived somatic cell types into immunodeficient mice to generate humanized mouse disease models.
- Wei Y, Chen Y, Qiu Y, Zhao H, Liu G, Zhang Y, Meng Q, Wu G, Chen Y, Cai X, Wang H, Ying H, Zhou B, Liu M, Li D, Ding Q (2016). Prevention of muscle wasting by CRISPR/Cas9-mediated disruption of myostatin in vivo. Mol Ther. In press.
- Wei Y, Qiu Y, Chen Y, Liu G, Zhang Y, Xu L, Ding Q (2016). CRISPR/Cas9 with single guide RNA expression driven by small tRNA promoters showed reduced editing efficiency compared to U6 promoter. RNA. 2016 Oct 14. pii: rna.057596.116. [Epub ahead of print]
- Chen Y, Liu X, Zhang Y, Wang H, Ying H, Liu M, Li D, Lui K, Ding Q (2016). A self- restricted CRISPR system to reduce off-target effects. Mol Ther. 24(9):1508-10.
- Wang X, Raghavan A, Chen T, Qiao L, Zhang Y, Ding Q#, Musunuru K# (2016). CRISPR-Cas9 Targeting of PCSK9 in Human Hepatocytes In Vivo. Arterioscler Thromb Vasc Biol 143(9):1475-81 (#co-corresponding)
- Veres A, Gosis BS, Ding Q, Collins R, Ragavendran A, Brand H, Erdin S, Talkowski ME, Musunuru K (2014). Low Incidence of Off-Target Mutations in Individual CRISPR-Cas9 and TALEN Targeted Human Stem Cell Clones Detected by Whole-Genome Sequencing. Cell Stem Cell 15(1);27-30.
- Ding Q, Strong A, Patel KM, Ng SL, Gosis BS, Regan SN, Rader DJ, Musunuru K (2014). Permanent alteration of PCSK9 with in vivo CRISPR-Cas9 genome editing. Circ Res 115:488-492.
#Seleted as "Best of 2014" by Circulation Research and "Top cardiovascular disease research advances in 2014" by American Heart Association
- Ding Q, Regan SN, Xia Y, Oostrom LA, Cowan CA, Musunuru K (2013) Enhanced efficiency of human pluripotent stem cell genome editing through replacing TALENs with CRISPRs. Cell Stem Cell 12(4);393-4.
- Ding Q*, Lee YK*, Schaefer EA*, Peters DT, Veres A, Kim K, Kuperwasser N, Motola DL, Meissner TB, Hendriks WT, Trevisan M, Gupta RM, Moisan A, Banks E, Friesen M, Schinzel RT, Xia F, Tang A, Xia Y, Figueroa E, Wann A, Ahfeldt T, Daheron L, Zhang F, Rubin LL, Peng LF, Chung RT, Musunuru K, Cowan CA (2013) A TALEN genome-editing system for generating human stem cell-based disease models. Cell Stem Cell 12(2);238-51. (*equal contribution)
#Selected as "Best of 2013" by Cell Stem Cell
- Ding Q, Cowan CA (2013) Liver in a dish. Cell Res 23(11);1242-3.
- Strong A, Ding Q, Edmondson AC, Millar JS, Sachs KV, Li X, Kumaravel A, Wang MY, Ai D, Guo L, Alexander ET, Nguyen D, Lund-Katz S, Phillips MC, Morales CR, Tall AR, Kathiresan S, Fisher EA, Musunuru K, Rader DJ (2012) Hepatic sortilin regulates both apolipoprotein B secretion and LDL catabolism. J Clin Invest 122(8):2807-16.
- Jin T*, Ding Q*, Huang H, Xu D, Jiang Y, Zhou B, Li Z, Jiang X, He J, Liu W, Zhang Y, Pan Y, Wang Z, Thomas WG, Chen Y (2012) PAQR10 and PAQR11 mediate Ras signaling in the Golgi apparatus. Cell Res 22(4); 661-76. (*equal contribution)