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>>Zhenyu Ju, Ph.D.

1. Personal Details

Name: Zhenyu Ju
Gender: Male
Academic title: M.D./Ph.D
Current Position: Investigator
Date of birth: Dec. 22nd, 1974
Institution: Institute of Laboratory Animal Sciences and Max-Planck-Partner-Group on Stem Cell Aging, Chinese Academy of Medical Sciences
Address:  Panjiayuan Nanli 5, Chaoyang, Beijing 100021, China
Telephone:  0086-10-67776051
Fax:   0086-10-67776838
Nationality: Chinese

2. Education:

2004--2007 PhD, at Dept. Gastroenterology, Hepatology & Endocrinology, Medical School of Hannover 
1998 --2001   Master of Medicine at China Medical University
1992 --1997   Study of medicine at Medical School of Shandong University

3. Experiences:

2010-- Investigator, Institute of Laboratory Animal Sciences and Max-Planck-Partner-Group on Stem Cell Aging, Chinese Academy of Medical Sciences
2007-- 2009 Associate Investigator, Institute of Laboratory Animal Sciences and Max-Planck-Partner-Group on Stem Cell Aging, Chinese Academy of Medical Sciences
2007   Posdoc Fellow at Department of Molecular Medicine and Max-Planck-Research-Group on Stem Cell Aging, Ulm University
2005 Guest scientist at Laboratory of Stem Cell Therapy, Institute of Medical Science, University of Tokyo
2003-- 2004  Visiting Scientist at Gene Mapping Center, Max Delbrščck Center, Berlin, Germany
2001-- 2003 Research Assistant, Sino-German Laboratory for Molecular Medicine, Fu Wai Hospital & Cardiovascular Institute, Peking Union Medical College, Chinese Academy of Medical Sciences
1997 --1998  Resident Physician, Youjian Hospital, Shangdong, China

4. Research Interests:

My research interest is using genetically modified mouse to study the DNA damage checkpoints in stem cells during aging. The decline of stem cell function is one of the characteristics of aging. Telomere shortening induces cell intrinsic DNA damage checkpoints and cell extrinsic alterations that impair the stem cell function and maintenance during aging of telomere dysfunctional mice. Further understanding of the DNA damage checkpoints induced by telomere dysfunction during aging will lend support to develop therapeutic approaches to slow down aging process and improve old organ functions.

5. Award:


6. Selected Publications:

Peer-Reviewed Papers
1.Songa Z, Wang J, Guachalla LM, Terszowskif G, Ju Z(co-corresponding), Rudolph KL. Alterations of the systemic environment are the primary cause of impaired B- and T-lymphopoiesis in telomere dysfunctional mice. Blood 2009 in press.
2.Guachalla LM, Ju Z, Koziel R, Figura G, Song Z, Fusser M, Epe B, Jansen-Dűrr P, Rudolph KL. Sod2 haploinsufficiency does not accelerate aging of telomere dysfunctional mice. AGING 2009, Mar 1(3).
3.Yang Z, Huang X, Jiang H, Zhang Y, Liu H, Qin C, Eisner GM, Jose PA, Rudolph KL, Ju Z(corresponding). Short Telomeres and Prognosis of Hypertension in a Chinese Population. Hypertension 2009 Mar 2.
4.Jiang H, Schiffer E, Song Z, Wang J, Zščrbig P, Thedieck K, Moes S, Bantel H, Saal N, Jantos J, Brecht M, Jenö P, Hall MN, Hager K, Manns MP, Hecker H, Ganser A, Döhner K, Bartke A, Meissner C, Mischak H, Ju Z, Rudolph KL. Proteins induced by telomere dysfunction and DNA damage represent biomarkers of human aging and disease. Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11299-304.
5.Schaetzlein S, Kodandaramireddy NR, Ju Z, Lechel A, Stepczynska A, Lilli DR, Clark AB, Rudolph C, Wei K, Schlegelberger B, Schirmacher P, Kunkel TA, Greenberg RA, Edelmann W, Rudolph KL.Exonuclease-1 deletion impairs DNA damage signaling and prolongs lifespan of telomere-dysfunctional mice. Cell 2007 Sep 7;130(5):863-77.
6.Ju Z, Hong J, Jaworski M, Gompf A, Rathinam C, Klein C, Trumpp A, Rudolph KL. Telomere dysfunction induces environmental defects limiting hematopoietic stem cell function and engraftment. Nature Medicine 2007 Jun;13(6):742-7.
7.Roy Choudhury A, Ju Z(co-first), Djojosubroto MW, Schienke A, Lechel A, Schaetzlein S, Jiang H, Stepczynska A, Wang C, Buer J, Lee HW, von Zglinicki T, Ganser A, Schirmacher, P., Nakauchi, H & Rudolph, K.L. Cdkn1a deletion improves stem cell function and lifespan of mice with dysfunctional telomeres without accelerating cancer formation. Nature Genetics 2007, 39(1):99-105.

Book Chapter
1.Huang X, Ju Z(corresponding). Mouse model: Telomeres and telomerase in stem cell and cancer. Telomeres and Telomerase in Cancer. The Humana Press. In Press
2.Guachalla L, Ju Z(corresponding). Telomere shortening induces checkpoints of stem cells. Telomeres and Telomerase in Ageing, Disease, and Cancer. Springer-Verlag, ISBN 978-3-540-73708-7, 2008, 161-180.
3.Ju Z, Rudolph KL. Telomeres and telomerase in stem cells during aging and disease. Genome and Disease. S. Karger, ISBN 3-8055-8029-0, 2006, Vol 1: 84-103
1.Song Z, Ju Z, Rudolph KL. Cell intrinsic and extrinsic mechanisms of stem cell aging depend on telomere status. Exp Gerontol. 2009 Jan-Feb;44(1-2):75-82.
2.Ju Z, Rudolph Kl. Telomere dysfunction and stem cell ageing. Biochimie. 2008 Jan;90(1):24-32.
3.Jiang H, Ju Z, Rudolph KL. Telomere shortening and ageing. Z Gerontol Geriatr 2007 Oct;40(5):314-24.
4.Ju Z, Roy Choudhury A, Rudolph, KL, The dual role of p21 in stem cell aging. Ann N Y Acad Sci. 2007 Apr;1100:333-44.
5.Ju Z, Rudolph, KL. Telomeres and telomerase in cancer stem cells. European Journal of Cancer. 2006, 42(9): 1197-1203


Resource Exploitation and Deve
Sino-German Laboratory
R&D for QA/QC system in Labora
Infectious Disease Animal Mode