Professor | Li Baojie | Asia Growth Partners

Name	Li Baojie
Contact Information	libj.bio@gmail.com
Language ability	Chinese, English
Province	Shanghai

Name

Li Baojie

Contact Information

libj.bio@gmail.com

Language ability

Chinese, English

Province

Shanghai

University/Lab Affiliation and Title	Shanghai Jiao Tong University
Faculty	Life Sciences
Academic Background & Achievements	Bachelor's Degree: Beijing Normal University PhD: Albert Einstein College of Medicine, USA Postdoctoral Research: Columbia University Recipient of Shanghai 'Pujiang Talent' Program 2009 Key Project Leader in 863 Program for 'Whole Genome Association Analysis Platform Technology'
Work Experience	2001-2009 - Institute of Molecular and Cell Biology, Singapore - PI, Senior PI 2009-present - Shanghai Jiao Tong University - Distinguished Professor

University/Lab Affiliation and Title

Shanghai Jiao Tong University

Faculty

Life Sciences

Academic Background & Achievements

Bachelor's Degree: Beijing Normal University
PhD: Albert Einstein College of Medicine, USA
Postdoctoral Research: Columbia University
Recipient of Shanghai 'Pujiang Talent' Program 2009
Key Project Leader in 863 Program for 'Whole Genome Association Analysis Platform Technology'

Work Experience

2001-2009 - Institute of Molecular and Cell Biology, Singapore - PI, Senior PI
2009-present - Shanghai Jiao Tong University - Distinguished Professor

Areas of Focus	Mesenchymal stem cell in vivo self-renewal, differentiation, and aging regulation mechanisms Bone development, bone metabolism, and pathogenesis of osteoporosis DNA damage response, aging, and tumor development
Publications	A positive role for c-Abl in Atm and Atr activation in DNA damage response, Li B et al., 2011 S6K1 is a multifaceted regulator of Mdm2 that connects nutrient status and DNA damage response, Li B et al., 2010 Atm deficient mice: an osteoporosis model with defective osteoblast differentiation and increased osteoblastogenesis, Li B et al., 2006 p53 represses the expression of transcription factor osterix and functions as a negative regulator of osteoblastogenesis and bone formation, Li B et al., 2006 Distinct roles for c-Abl and Atm in Prx I induction by modulating expression of protein kinase C, Li B et al., 2004 Activation of p38MAPK is required for osteoblast differentiation, Li B et al., 2003 c-Abl knockout mice are osteoporotic and show defects in osteoblast maturation, Li B et al., 2000

Areas of Focus

Mesenchymal stem cell in vivo self-renewal, differentiation, and aging regulation mechanisms
Bone development, bone metabolism, and pathogenesis of osteoporosis
DNA damage response, aging, and tumor development

Publications

A positive role for c-Abl in Atm and Atr activation in DNA damage response, Li B et al., 2011
S6K1 is a multifaceted regulator of Mdm2 that connects nutrient status and DNA damage response, Li B et al., 2010
Atm deficient mice: an osteoporosis model with defective osteoblast differentiation and increased osteoblastogenesis, Li B et al., 2006
p53 represses the expression of transcription factor osterix and functions as a negative regulator of osteoblastogenesis and bone formation, Li B et al., 2006
Distinct roles for c-Abl and Atm in Prx I induction by modulating expression of protein kinase C, Li B et al., 2004
Activation of p38MAPK is required for osteoblast differentiation, Li B et al., 2003
c-Abl knockout mice are osteoporotic and show defects in osteoblast maturation, Li B et al., 2000

Stem Cells Self-Renewal Differentiation Aging Bone Development Bone Metabolism Osteoporosis Dna Damage Tumor Development Signal Transduction

Han Song Deng - Tongji University

Zhiyong Mao - Tongji University

Fanglin Sun - Tongji University

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