Christopher E Turner, PhD

Christopher E Turner, PhD
Appointed 07/01/91
1297 Weiskotten Hall
766 Irving Ave.
Syracuse, NY 13210

315 464-8598

Current Appointments

Hospital Campus

  • Downtown

Research Programs and Affiliations

  • Biomedical Sciences Program
  • Cancer Research Institute
  • Cell and Developmental Biology
  • Research Pillars

Web Resources

Education & Fellowships

  • PhD: University of Oxford, England, 1986

Research Interests

  • Regulation of cell migration by focal adhesion adapter proteins and their role in cancer cell metastasis.

Web Resources

Publications

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Research Abstract

Abstract

The dynamic adhesion of cells to their surrounding extracellular matrix provides many of the environmental cues necessary for controlling cell migration and cell shape, survival, proliferation and differentiation. These fundamental events regulate an organism’s normal development, maintenance and recovery from injury and infection. Defects in the signaling pathways associated with cell adhesion provide the basis for cell transformation and cancer cell metastasis, various developmental defects and cardiovascular disease.

My lab uses a multi-faceted approach combining biochemistry, cell and molecular biology and various high-end microscopy techniques to determine the molecular organization of the proteins that are involved in cell adhesion and thereby understand how they each contribute to cell behavior. We are particularly interested in characterizing the function of the molecular scaffold/adapter proteins Paxillin and Hic-5 during tumor cell migration and invasion. We have found that these multi-domain proteins bind numerous structural and signaling proteins including kinases, phosphatases and Rho family GTPase regulators and effectors. We hypothesize that it is through these various interactions that the cell coordinates intracellular signaling and cytoskeletal reorganization to regulate adhesion and the cell migration machinery.

 

 

Selected References

Turner, C.E., (2000) Paxillin and focal adhesion signaling. Nature Cell Biol., 2 E231-6.

Turner, C.E., (2000) Paxillin interactions.  J. Cell Science, 113 4139-4140.

Brown, M.C. and Turner, C.E. (2004) Paxillin-Adapting to change.  Physiol. Revs. 84, 1315-1339.

Deakin, N.O., and Turner, C.E. Paxillin Comes of Age. (2008) J. Cell Sci 121, 2435-2444.

Deakin, N.O. and Turner. C.E. (2011) Paxillin and Hic-5 cooperate to regulate breast cancer cell plasticity, invasion and metastasis. Mol. Biol Cell 22 327-341.

Pignatelli, J., Tumbarello, D.A., Schmidt, R.P. and Turner, C.E. (2012) Hic-5 promotes invadopodia formation and invasion during TGF-β-induced epithelial-mesenchymal transition. J. Cell Biol.  197 421-437.

Deakin, N.O., Pignatelli, J., and Turner, C.E. (2012) Diverse Roles for the Paxillin Family of Proteins in Cancer. Genes and Cancer (in press).

 

Faculty Profile Shortcut: http://www.upstate.edu/faculty/turnerce

Faculty Honors

Dr. Dennis Stelzner has been elected a Fellow in the American Association of Anatomists. He was presented with a citation and plaque at the annual meeting of the American Association of Anatomists during the FASEB meeting on April 12, 2011 in Washington, DC.

The citation reads:
Spinal cord injury (SCI) has been studied during his entire career using neuroanatomical and ultrastructural methods. He showed that the ability of nerve tracts to regenerate or grow around partial SCI during development is dependent on their maturation at the time of injury.

Differences were also found in the ability of frog optic and tectal efferent axons to regenerate through the same diencephalic injury. The intrinsic cellular response needed for CNS axons to regenerate is the focus of his present work on propriospinal neurons using "molecular neuroanatomy" to determine factors underlying a maximal regenerative response after spinal cord injury.