• Dr. Qiang Ding is an Associate Professor of Medicine in the Division of Pulmonary, Allergy, and Critical Care Medicine. Dr. Ding received his PhD degree in molecular and cellular pathology at the University of Alabama at Birmingham. After completing his postdoctoral fellowship training in the UAB Department of Pathology, Dr. Ding joined the UAB Division of Pulmonary, Allergy, and Critical Care medicine at the rank of Assistant Professor. Dr. Ding is actively involved in education and service for the medical community. He holds a secondary appointment in the Department of Cell, Developmental, and Integrative Biology (CDIB), is a member of the Intellectual and Developmental Disabilities Research Center (IDDRC), and is a faculty member of the Graduate Biomedical Science PhD program at UAB.
  • Selected Publications

    Academic Article

    Year Title Altmetric
    2018 Correction: Hepatitis C virus NS4B induces the degradation of TRIF to inhibit TLR3-mediated interferon signaling pathway.PLoS Pathogens.  14:e1007455. 2018
    2018 Germline mutations in DNA repair genes are associated with bladder cancer risk and unfavourable prognosis.BJU International.  122:808-813. 2018
    2018 Overexpression of low density lipoprotein receptor-related protein 1 (LRP1) is associated with worsened prognosis and decreased cancer immunity in clear-cell renal cell carcinoma.Biochemical and Biophysical Research Communications.  503:1537-1543. 2018
    2018 Review of grid dispatching considering thermal power and large-scale wind power integrationDianli Xitong Baohu Yu Kongzhi.  46:162-170. 2018
    2018 HOXA9, PCDH17, POU4F2, and ONECUT2 as a Urinary Biomarker Combination for the Detection of Bladder Cancer in Chinese Patients with HematuriaEuropean urology focus2018
    2018 NOS3 895G>T and CBR3 730G>A Are Associated with Recurrence Risk in Non-Muscle-Invasive Bladder Cancer with Intravesical Instillations of THP.Chemotherapy.  63:191-197. 2018
    2017 Angiotensin-converting enzyme defines matrikine-regulated inflammation and fibrosis.JCI insight.  2. 2017
    2017 Focal adhesion kinase signaling determines the fate of lung epithelial cells in response to TGF-β.AJP - Lung Cellular and Molecular Physiology.  312:L926-L935. 2017
    2013 FAK-related nonkinase is a multifunctional negative regulator of pulmonary fibrosis.American Journal of Pathology.  182:1572-1584. 2013
    2008 Focal adhesion kinase (FAK)-related non-kinase inhibits myofibroblast differentiation through differential MAPK activation in a FAK-dependent manner.Journal of Biological Chemistry.  283:26839-26849. 2008


    Year Title Altmetric
    2019 Mouse Models for Studying HCV Vaccines and Therapeutic Antibodies..  481-503. 2019

    Research Overview

  • Dr. Ding's research focuses on cellular and extracellular environment interaction in various diseases and how such interaction affects the molecular mechanisms contributing to tissue injury and disregulated tissue repairing.

    Dr. Ding's laboratory is currently investigating the role of fibroblast migration and myofibroblast differentiation in the development of lung fibrosis, and the molecular mechanisms which contribute to fibroblast migration and myfibroblast differentiation.

    Focal adhesion kinase (FAK) plays an important role in regulation of fibroblast migration, differentiation, and proliferation. The Ding Lab has found that focal adhesion kinase (FAK) regulates cell proliferation through regulation of the expression of extracellular matrix proteins and Cyclin D1. The cytoplasmic protein FAK-related non-kinase (FRNK) acts to limit FAK-dependent cell migration and proliferation. Data from this laboratory indicates that FRNK acts to limit myofibroblast differentiation induced by transforming growth factor beta-1 (TGF-beta-1), a core signaling process in the development of lung fibrosis.

    The Ding Lab is also interested in exploring the expression of FRNK, its signaling pathways, and how that signaling regulates the pro-fibrotic phenotype and plasticity of the cell types involved. Recently, the lab investigated post-transcriptional regulation and its role in pathogenesis, along with examining the therapeutic potentials of small molecular inhibitors of involved signaling pathways in treating pulmonary fibrosis, cancer, and excessive tissue injury.
  • Education And Training

  • University of Alabama at Birmingham, Other
  • University of Alabama at Birmingham, Postdoctoral Research
  • Bachelor's Level Degree in Biochemistry, Biophysics and Molecular Biology, Fudan University
  • Doctor of Philosophy in Pathology Residency Program, University of Alabama at Birmingham
  • Full Name

  • Qiang Ding
  • Fax

  • 205-934-1721