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Faculty Detail    
Name PETER H KING
 
Campus Address SC 260C Zip 0017
Phone 205-975-8116
E-mail pking@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Neurology   Neurology Chair Office Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  General Clinical Research Center  Comprehensive Neuroscience Center Professor
Center  Ctr for Glial Bio in Med  Ctr for Glial Bio in Med Professor
Center  Medicine  Ctr Cardiovasc Bio Professor

Graduate Biomedical Sciences Affiliations
Cancer Biology 
Hughes Med-Grad Fellowship Program 
Integrative Biomedical Sciences 
Medical Scientist Training Program 
Neuroscience 
Neuroscience Graduate Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
I was born in Canton, Ohio in 1959. I graduated from Duke University with a BA in zoology in 1981 and Duke University Medical School in 1985. I did a one year research fellowship in Dr. James McNamara’s laboratory in epilepsy research in 1984. My medical training included an internship (internal medicine) at Case Western Reserve University (1985-1986) and a residency in Neurology at Duke University (1987-1990). I completed a molecular biology fellowship in Dr. Jack Keene’s laboratory (1990-1991) studying basic RNA biology and a clinical neuromuscular fellowship at the Cleveland Clinic (1991-1992). I became Assistant Professor of Neurology in 1992 and Assistant Professor of Physiology and Biophysics in 1994. I was later promoted to Associate Professor (1998). I was appointed Chief of Neurology at the Birmingham Veterans Administration Medical Center in 2000.

Society Memberships
Organization Name Position Held Org Link
American Association of Cancer Research  Member   
American Neurological Association  Associate   

Research/Clinical Interest
Title
Mechanisms of Growth Factor mRNA Stabilization in Cancer
Description
My laboratory interests have centered on mechanisms of growth factor mRNA stabilization in malignant gliomas and amyotrophic lateral sclerosis (ALS). In the former disease, growth factor mRNAs such as VEGF and IL-8 are stabilized by cellular factors and upregulated to promote tumor cell growth and angiogenesis. In contrast, ALS linked to mutations of superoxide dismutase leads to motor neuron degeneration and VEGF mRNA destabilization. These two models provide excellent platforms to study the impact of posttranscriptional RNA regulation on human disease. Our long term goal is to characterize mechanisms involved in this level of gene regulation to identify potential therapeutic targets. For ALS, augmenting RNA stabilization of neuroprotective growth factors would promote motor neuron survival. For malignant gliomas, on the other hand, augmenting RNA destabilization of the very same factors would suppress tumor growth.

Selected Publications 
Publication PUBMEDID
Suswam, E., Li, Y, Gillespie, G.Y., Zhang, X., Shacka, J., Li, X. Lu, L., Zheng, L., and King, P.H. Expression of RNA Destabilizer Tristetraprolin in Malignant Gliomas Negatively Regulates Angiogenic Growth Factors IL-8 and VEGF. Cancer Res. 2008;68: 674-682.

 
 
Lu, L., Zheng, L., Viera, L., Suswam, E., Li, Y., Li, X., Estevez, A.G. and King, P.H. Mutant Cu/Zn-Superoxide Dismutase associated with Amyotrophic Lateral Sclerosis Destabilizes VEGF mRNA and Downregulates its Expression. J. Neurosci. 2007;27: 7929-7938.   
Suswam, E.A., Li, Grace, Mahtani, H., and King, P.H. Novel DNA-binding Properties of the RNA-binding protein TIAR. Nuc. Acids Res. 2005; 33:4507-4518.   
Suswam, E.A., Nabors, L.B., Huang, Y, Yang, X., and King, P.H. 2004. Interleukin-1 Induces stabilization of Interleukin-8 mRNA in Malignant Breast Cancer Cells via the 3’ Untranslated Region: Involvement of Divergent RNA-binding Factors HuR, KSRP, and TIAR. Int. J .Cancer, 2005; 113:911-919.   
Nabors, L.N., Suswam, E., Huang, Y.,Yang, X., Johnson, M.J., King, P.H. Tumor Necrosis Factor- induces angiogenic factor upregulation in malignant glioma cells: a role for RNA stabilization and HuR. Cancer Res., 2003; 63: 4181-4187.   
Dixon, D.A., Tolley, N.D., King, P.H., Harkins, L., McIntyre, T.M., Zimmerman, G.A. and Prescott, S.M. Altered Expression of the mRNA Stability Factor HuR Promotes Overexpression of Cyclooxygenase-2 in Human Colon Cancer. J. Clin. Inv., 2001;108:1657-1665.   
Nabors, L.B., Gillespie, Y., Harkins, L. and King, P.H. HuR, a RNA Stability Factor, is expressed in malignant brain tumors and binds to adenine- and uridine-rich elements within the 3’ untranslated regions of cytokine and angiogenic factor mRNAs. Cancer Res., 2001; 61:2154-2161.   
Meng, Z., King, P.H., Emanuel, P.D., Blume, S.W. The ELAV RNA-stability factor binds the 5’-untranslated region of the human IGF-IR transcript and negatively regulates translational efficiency. Nuc. Acids Res., 2005; 33:2962-2979.   
   
   

Keywords
RNA stability; AU-rich elements; angiogenic growth factors; glioblastoma; amyotrophic lateral sclerosis