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Jing QU, Ph. D.

Focusing on the rare diseases associated with aging, we establish human stem cells in aging research model. We aim at revealing the molecular mechanism of organism aging and aging diseases in genetic and epigenetic level, and exploring the molecular target and intervention strategies.

Staff: Jing Qu, Yanxia Ye, Ying Hao, Ruijun Bai
Postdoc: Wenlei Bao
Students: Zhiqing Diao, Zeming Wu, Xing Zhang, Hongkai Zhao

• QU Group website


  1.Model genetic and rare diseases using human pluripotent stem cells (hPSCs) derived cells.
  2.Introduce site-specific genetic changes in hPSCs, including gene correction and gene knockout in normal and disease hPSC lines.
  3. Generate genetic and rare disease-iPSC bank.
  4. Study the underlying mechanisms of human aging and its related diseases based on rare-disease hPSCs model.


Selected publications:

  1. Pan H, Guan D, Liu X, Li J, Wang L, Wu J, Zhou J, Zhang W, Ren R, Zhang W, Li Y, Yang J, Hao Y, Yuan T, Yuan G, Wang H, Ju Z, Mao Z, Li J, Qu J*, Tang F*, Liu GH*.SIRT6 safeguards human mesenchymal stem cells from oxidative stress by coactivating NRF2. Cell Res. 2016Jan 15. doi: 10.1038/cr.2016.4. [Epub ahead of print] (*Corresponding author)
  2. Duan S, Yuan G, Liu X, Ren R, Li J, Zhang W, Wu J, Xu X, Fu L, Li Y, Yang J, Zhang W, Bai R, Yi F, Suzuki K, Gao H, Esteban CR, Zhang C, Belmonte JC, Chen Z, Wang X, Jiang T, Qu J*, Tang F*, Liu GH*. PTEN deficiency reprograms human neuralstem cells towards a glioblastoma stem cell-like phenotype. Nat Commun. 2015. (*Corresponding author)
  3. Zhang W1, Li J1,Suzuki K1, Qu J1, Wang P, Zhou J, Liu X, Ren R, Xu X, Ocampo A, Yuan T, Yang J, Li Y, Shi L, Guan D, Pan H, Duan S, Ding Z, Li M, Yi F, Bai R, Wang Y, Chen C, Yang F, Li X, Wang Z, Aizawa E, Goebl A, Soligalla RD, Reddy P, Esteban CR, Tang F, Liu GH, Belmonte JC. A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging. Science. 2015 Apr 30. pii: aaa1356. (1equal contribution)
  4. Suzuki K1, Yu C1, Qu J1, Li M1, Yao X, Yuan T, Goebl A, Tang S, Ren R, Aizawa E, Zhang F, Xu X, Soligalla R, Chen F, Kim J, Kim NY, Liao HK, Benner C, Esteban CR, Jin Y, Liu GH*, Li Y* , Belmonte JC*. Targeted gene correction in human disease-specific induced pluripotent stem cells minimally impacts whole-genome mutational load. Cell Stem Cell. 2014. 2014; 15, 31–36. (1equal contribution)
  5. Liu GH1, Suzuki K1, Li M1, Qu J1, Montserrat N, Tarantino C, Gu Y, Yi F, Xu X, Zhang W, Ruiz S, Plongthongkum N, Zhang K, Masuda S, Nivet E, Tsunekawa Y, Soligalla R, Goebl A, Aizawa E, Kim N, Kim J, Dubova I, Li Y, Ren R, Benner C, del Sol A, Bueren J, Trujillo J, Surralles J, Esteban C, Izpisua Belmonte JC. Modeling Fanconi Anemia pathogenesis and therapeutics using integration-free patient-derived iPSCs. Nat Commun. 2014. DOI: 10.1038/ncomms5330. (1equal contribution)
  6. Yang J1, Cai N1, Yi F1, Liu GH*, Qu J*, Belmonte JC*. Gating pluripotency via nuclear pores. Trends Mol Med. 2014 Jan; 20(1):1-7. (*Corresponding author)(Cover story
  7. Liu GH1, Qu J1, Suzuki K1, Nivet E, Li M, Montserrat N, Yi F, Xu X, Ruiz S, Zhang W, Ren B, Wagner U, Kim A, Li Y, Goebl A, Kim J, Soligalla R, Dubova I, Thompson J, Yates JIII, Esteban C, Sancho-Martinez I, Belmonte JC. (2012) Progressive degeneration of human neural stem cells caused by pathogenic LRRK2. Nature, 2012, 491(7425):603-7. (1equal contribution) Highlighted by Nature Reviews Neurology (Nature Reviews Neurology | doi:10.1038/nrneurol.2012.230)
  8. Liu GH1, Suzuki K1, Qu J1, Sancho-Martinez I, Yi F, Li M, Kumar S, Nivet E, Kim J, Soligalla RD, Dubova I, Goebl A, Plongthongkum N, Fung HL, Zhang K, Loring J, Laurent L, and Belmonte JC. Targeted gene correction of laminopathy-associated LMNA mutations in patient-specific iPSCs. Cell Stem Cell, 2011,8(6):688-94. (1equal contribution). Highlighted by Nature (Nature 474, 8. doi:10.1038/474008c)Highlighted by Cell Stem Cell (Cell Stem Cell 9, 2: 93-94)
  9. Qu J1, Nakamura T1, Cao G, Mckercher S, Lipton S. S-Nitrosylation Activates Cdk5 and Contributes to Synaptic Spine Loss Induced by β-Amyloid Peptide. Proceedings of the National Academy of Sciences. 2011,108(34):14330-5. (1equal contribution)
  10. Liu GH, Barkho BZ, Ruiz S, Diep D, Qu J, Yang SL, Panopoulos AD, Suzuki K, Kurian L, Walsh C, Thompson J, Boue S, Fung HL, Sancho-Martinez I, Zhang K, Iii JY, Belmonte JC. Recapitulation of premature ageing with iPSCs from Hutchinson-Gilford progeria syndrome. Nature. 2011;14;472: 221-5


Major scientific achievements:
  1. Reveal the role of S-nitrosylation in different pathological conditions (PLoS One. 2009; PNAS, 2011; PRION, 2012; J Neurosci, 2014; Nucleic Acids Res. 2007; J Cell Sci. 2009).
2. Establish the first safe and efficient gene engineering approach to genetically correct mutated gene(s) in patient-specific iPSCs, evaluation of the mutation load attributable to genome editing technologies at single base pair level by Whole Genome Sequencing, and generation of HDAdV-TALEN hybrid vector for highly efficient gene editing (Cell Stem Cell 2011;2014).
3. Establish the platform for multiple human diseases studies and drug discovery (including Fanconi Anemia, Parkinson’s diseases, Artherosclerosis etc.) by a combination of human induced pluripotent stem cell and genome editing technologies. (Nature Communication, 2014; Nature 2012; Cell Res 2011; Nature 2011)
4. Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficiency. We generate a human WS model in human embryonic stem cells (ESCs). Differentiation of WRN-null ESCs to mesenchymal stem cells (MSCs) recapitulates features of premature cellular aging. Using the platform, our observations uncover a role for WRN in maintaining heterochromatin stability and highlight heterochromatin disorganization as a potential determinant of human aging (Science 2015).
5. Generate a novel model of PTEN knock-out human NSCs, which can serve as  the first “proof-of-concept” platform to study  NSC transformation, which may lead to the development of personalized treatment of glioblastomaNature Communication 2015.
6. Provide first evidence that SIRT6 is a key gatekeeper for human adult stem cell homeostasis, and highlight that SIRT6-NRF2 pathway is a novel target for preventing aging-associated stem cell attrition (Cell Research 2016).