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Jeffrey Harrison, Ph.D.

Harrison_Jeffrey_1Professor
Phone: 352-627-9208
Office: R5-254 Academic Research Bldg.
Email: jharriso@ufl.edu

Publications: Search PubMed

 

Research Interests – part I:

Our laboratory is interested in understanding the functional significance of chemokine networks in the central nervous system with a recent focus on determining roles for these molecules in brain cancer. We study mechanisms involved in tumor-immune cell interactions as well as direct effects of chemokines on glioma initiating cells. Experimental approaches encompass in vitro and in vivo methods and include use of chemokine receptor selective pharmacological agents.

Selected publications:

Davis, C.D., V. Zujovic, and J.K. Harrison. Viral macrophage inflammatory protein-II and fractalkine (CX3CL1) chimeras identify molecular determinants of affinity, efficacy, and selectivity at CX3CR1. Mol Pharmacol 66:1431-1439, 2004.

Chen, S., D.L. Tuttle, J.T. Oshier, H.J. Knot, W.J. Streit, M.M. Goodenow, and J.K. Harrison. Transforming growth factor-b 1 increases CXCR4 expression, stromal derived factor-1α-stimulated signaling and human immunodeficiency virus-1 entry in human monocyte-derived macrophages. Immunology 114:565-574, 2005.

Davis, C.D. and J.K. Harrison. Pro326 in the C-terminus of murine CX3CR1 prevents G-protein and PI3-kinase dependent stimulation of Akt and ERK in CHO cells. J Pharmacol Exp Ther 316:356-367, 2006.

Liu, C, D. Luo, W.J. Streit, and J.K. Harrison. CX3CL1 and CX3CR1 in the GL261 murine model of glioma: CX3CR1 deficiency does not impact tumor growth or infiltration of microglia and lymphocytes. J. Neuroimmunol. 198:98-105, 2008.

Liu, C., D. Luo, B.A. Reynolds, G. Meher, A. Katritzky, B. Lu, C. Gerard, C. Bhadha, and J.K. Harrison. Chemokine receptor CXCR3 promotes growth of glioma. Carcinogenesis32:129-137, 2011.

Research Interests – part II:

An additional area of investigation that has received considerable attention by our group relates to the characterization of a unique molecule called HN1 (hemopoietic- and neurologic-expressed sequence 1). HN1 is highly expressed during development, and is up-regulated in injured motoneurons that normally undergo efficient repair of their severed axons, and successfully reinnervate target skeletal muscle tissue. This gene is also highly expressed in a variety of cancer cell lines and in vivo tumor models, including glioblastoma and melanoma. Experiments in the lab are directed toward understanding the function of this gene in development and disease, and include cellular and animal models.

Selected publications:

Zujovic, V., D. Luo, H.V. Baker, M.C. Lopez, K.R. Miller, W.J. Streit, and J.K. Harrison. The facial motor nucleus transcriptional program in response to peripheral nerve injury identifies Hn1 as a regeneration associated gene. J Neurosci Res 82:581-591, 2005.

Laughlin, K.M., D. Luo, C. Liu, G. Shaw, K.J. Warrington, Jr., B.K. Law, and J.K. Harrison. Hematopoietic- and neurologic-expressed sequence 1 (Hn1) depletion in B16.F10 melanoma cells promotes a differentiated phenotype that includes increased melanogenesis and cell cycle arrest. Differentiation 78:35-44, 2009

. Laughlin, K.M., D. Luo, C. Liu, G. Shaw, K.H. Warrington, Jr., J. Qiu, A.T. Yachnis, and J.K. Harrison. Hematopoietic- and neurologic-expressed sequence 1 expression in the murine GL261 and human high grade gliomas. Pathol. Oncol. Res. 15:437-444, 2009.