Qiang (John) Ding, PhD

Pulm_Div_Ding

Associate Professor of Medicine and Cell Biology

Division of Pulmonary, Allergy & Critical Care Medicine
1530 3rd Avenue So, THT-422
University of Alabama at Birmingham
Birmingham, AL 35294

Contact Information

Campus Address:

 THT 422

Academic Office location:

 THT 437

Office Phone:

 (205) 996-2512

Office Fax (Academic):

 (205) 934-1721

Email Address:

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Brief Bio

Dr. Qiang Ding completed his Ph.D. degree at the University of Alabama at Birmingham. Following his postdoctoral fellow training in Department of Pathology at the University of Alabama at Birmingham, he spent six years in department of Medicine at the University of Alabama at Birmingham where he rose to the rank of Associate Professor of Medicine.

Academic & Research Interests

The long term goal in Dr. Ding's laboratory is to understand the signaling proteins and molecular mechanisms by which tissue injury and repair are regulated. One of the areas in Dr. Ding's laboratory is investigating the role of fibroblast migration and myofibroblast differentiation in the development of lung fibrosis, and the molecular mechanisms contributing the fibroblast migration and myofibroblast differentiation. Focal adhesion kinase (FAK) plays an important role in regulation of fibroblast migration, differentiation, and proliferation. Dr. Ding has found that FAK regulates cell proliferation though regulation of the expression of extracellular matrix proteins and Cyclin D1.  FAK-related non-kinase (FRNK) is one cytoplasmic protein, and acts to limit FAK-dependent cell migration and proliferation. Data from his laboratory indicate that FRNK acts to limit myofibroblast differentiation induced by transforming growth factor beta-1 (TGF-beta-1), and can inhibit ERK and p38 activation induced by TGF-beta-1 in primary human lung fibroblasts. His laboratory is investigating the expression of FRNK and its downstream signaling pathways in primary cells isolated from fibrotic and control lung tissues.  TGF-beta-1 signaling is important in the development of lung fibrosis. Dr. Ding recently found that ERK and p38 MAPKs utilizes different signaling pathways regulate myofibroblast differentiation in primary lung fibroblasts. His laboratory is currently studying the downstream molecular mechanisms that MAPKs regulate the myofibroblast differentiation. 

Key Publications

Ding Q, Stewart J, Prince CW, Chang PL, Trikha M, Han X, Grammer J, and Gladson CL.  Promotion of Malignant Astrocytoma Cell Migration by Osteopontin Expressed in the Normal Brain: Differences in Integrin Signaling During Cell Adhesion to Osteopontin Versus Vitronectin.  Cancer Research. 2002 Sep 15; 62(18):5336-43.

Ding Q, Stewart J, Olman MA, Klobe MR, and Gladson CL.  The Pattern of Enhancement of Src Kinase Activity on PDGF Stimulation of Glioblastoma Cells Is Affected by The Integrin Engaged.  Journal of Biological Chemistry. 2003 Oct 10:278(41):39882-91.

Ding Q, Grammer JR, Nelson MA, Guan JL, Stewart JE, and Gladson CL. p27(Kip1) and Cyclin D1 Are Necessary for Focal Adhesion Kinase (FAK) Regulation of Cell Cycle Progression in Glioblastoma Cells Propagated In Vitro and In Vivo in the Scid Mouse Brain.  Journal of Biological Chemistry.  2005 Feb 25; 280(8):6802-15.

Cai G, Zheng A, Tang Q, White ES, Chou C, Gladson CL, Olman MA, and Ding Q.  Downregulation of FAK-Related Non-Kinase Mediates the Migratory Phenotype of Human Fibrotic Lung Fibroblasts. Exp. Cell Res. 316, 1600-1609.

Ding Q, Gladson, CL, Wu, H, Hayasaka, H, and Olman MA. FAK-related non-kinase inhibits myofibroblast differentiation through differential MAPK activation in a FAK-dependent manner. J Biol Chem. 2008 Oct 3; 283(40): 26839-49. Epub 2008 Jul 31.


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