Chuanyue Wu, PhD
Professor of Pathology

Dr. Wu, Professor of Pathology and Lombardi and Shinozuka Experimental Pathology Research Chair, is a member of the Section of Laboratory Medicine.

Office Location:
S-707B Scaife Hall
University of Pittsburgh
3550 Terrace Street
Pittsburgh, PA 15261

Contact Information:
Office Telephone: 412-648-2350
Lab Telephone: (412) 624-2471


  • PhD - University of Pittsburgh, 1990

Awards and Honors

  • 2011 - Pitt Innovator Award, University of Pittsburgh
  • 2010 - Pitt Innovator Award, University of Pittsburgh
  • 1998 - V Foundation Scholar, V Foundation for Cancer Research
  • 1996 - Edward Livingston Trudeau Scholar, American Lung Association
  • 1996 - Parker B. Francis Fellow
  • 1996 - Edward C. Kendall Alumni Award for Meritorious Research, Mayo Foundation

Research Interests

Cell-extracellular matrix adhesion is a fundamental process that regulates cell shape, proliferation and differentiation. Abnormalities in cell-matrix adhesion and extracellular matrix assembly are closely associated with the pathogenesis of a variety of human diseases. The goals of my research are:

  • To elucidate the molecular mechanism underlying cell-extracellular matrix adhesion and signaling
  • To determine the role of integrin-linked kinase signaling in the pathogenesis of diabetic nephropathy

To achieve these goals, we are employing a wide variety of molecular and cell biological techniques including molecular cloning, mutagenesis, gene transfer, protein expression, yeast two-hybrid and other protein-protein interaction assays, hybridoma production, cell culture, cell adhesion, cell migration, immunofluorescence microscopy, immunoprecipitation, Northern, Southern and Western blotting, cell proliferation, apoptosis, and immunohistochemistry in our research. We have demonstrated that a protein complex consisting of PINCH-1, integrin-linked kinase (ILK) and parvin is crucial for cell-matrix adhesion, migration and survival signaling. Alterations of the PINCH-1-ILK-parvin complex are involved in the pathogenesis of diabetic nephropathy. Furthermore, we have identified a critical role of kindlin-2 in regulation of integrin activation and cell-matrix adhesion. Our studies shed new light on the molecular basis underlying cell-matrix and cell-cell communications as well as their roles in the pathogenesis of human diseases including diabetic nephropathy and cancer.

NIH Research

View Dr. Wu's NIH RePORT on

Selected Publications

View Dr. Wu's publications on PubMed

  • Li, H., Deng, Y., Sun, K., Yang, H., Liu,J., Wang, M., Zhang, Z., Lin, J., Wu, C.*, Wei, Z.*, Yu, C.* Structural basis of kindlin-mediated integrin recognition and activation Proc. Natl. Acad. Sci USA 2017 Aug 29;114(35):9349-9354 (*Co-correspondence authors). PMC5584418
  • Sun, Y., Guo, C., Ma, P., Lai, Y., Yang, F., Cai, J., Cheng, Z., Zhang, K., Liu, Z., Tian, Y., Sheng, Y., Tian, R., Deng, Y., Xiao, G., Wu, C. Kindlin-2 association with RhoGDIα suppresses Rac1 activation and podocyte injury. J. Am. Soc. Nephrol.2017 Dec;28(12):3545-3562. PMC5698060
  • Guo, L., Cai, T., Chen, K., Wang, R., Wang, J., Cui, C., Yuan, J., Zhang, K., Liu, Z., Deng, Y., Xiao, G., Wu, C. Kindlin-2 regulates mesenchymal stem cell differentiation through control of YAP1/TAZ. J. Cell Biol. 2018 Apr 2;217(4):1431-1451. PMC5881491
  • Guo, L., Wang, X., Yuan, J., Zhu, M., XU, R.-H., Fu, X., Wu, C., and Wu, Y. TSA restores hair follicle-inductive capacity of skin-derived precursors, Sci. Rep. 2019Feb 27;9(1):2867
  • Guo, L., Cui, C., Zhang, K., Wang, J., Wang, Y., Lu, Y., Chen, K., Yuan, J., Xiao, G., Tang, B., Sun, Y., Wu, C. Kindlin-2 links mechano-environment to proline synthesis and tumor growth. Nat. Commun. 2019 Feb 19;10(1):845.
  • Sun, Y., Ding, Y., Guo, C., Liu, C., Ma, P., Ma, S., Wang, Z., Liu, J., Qian, T., Ma, L.,Deng, Y., Wu, C. α-parvin 1 promotes breast cancer progression and metastasis through interaction with G3BP2 and regulation of TWIST1 signaling. Oncogene.2019 Jun;38(24):4856-4874
  • Guo, L. and Wu, C. Mechano-regulation of proline metabolism and cancer progression by kindlin-2. Mol Cell Oncology. 2019 Apr 12;6(3):1596003. doi: 10.1080/23723556.2019.1596003. eCollection 2019. PMCID: PMC6512932
  • Guo, L., Wang, R., Zhang, K., Yuan, J., Wang, J., Wang, X., Ma, J., Wu, C. A PINCH-1-Smurf1 signaling axis mediates mechano-regulation of BMPR2 and stem cell differentiation. J. Cell Biol. 2019 Nov 4;218(11):3773-3794 (Recommended by F1000)
  • Wang, Y., Yan, Q., Zhao, Y., Liu, X., Lin, S., Zhang, P., Ma, L., Lai, Y., Bai, X., Liu, C., Wu, C., Feng, J.Q., Chen, D., Cao, H., Xiao, G. Focal adhesion proteins Pinch1 and Pinch2 regulate bone homeostasis in mice. JCI Insight. 2019 Nov 14;4(22). pii: 131692. doi: 10.1172/jci.insight.131692.
  • C., Sun, Y. PINCH-1 interacts with myoferlin to promote breast cancer progression and metastasis. Oncogene. 2019 Dec 4. doi: 10.1038/s41388-019-1135-5.
  • Zhu, K., Lai, Y., Cao, H., Bai, X., Liu, C., Yan, Q., Ma, L., Chen, D., Kanaporis, G., Wang, J., Li, L., Cheng, T., Wang, Y., Wu, C., Xiao, G. Kindlin-2 modulates MafA and β-catenin expression to regulate β-cell function and mass in mice. Nat Commun. 2020 Jan 24;11(1):484. doi: 10.1038/s41467-019-14186-y.