Dr. Giridhar R. Akkaraju
Texas Christian University Biology Department
Assistant Professor of Biology

(817) 257-6125
(817) 257-7165 (Biology Departmental Office)
Box 298930
Fort Worth, TX 76129
"Not all those who wander are lost" J.R.R. Tolkien

Education:
B.Sc. (1985) University of Bombay, Mumbai, India.
Ph.D. (1997) University of Pittsburgh, Pittsburgh, PA.

Research Interests:
My first project in graduate school involved studying the regulation of protein synthesis initiation. Specifically, we looked at the control of eukaryotic initiation factor 2 a by phosphorylation. The significance is that eIF-2a is the rate limiting step that determines whether translation should proceed or not. The cell blocks translation during virus infection. This is done by activating a protein, known as double stranded RNA dependent protein kinase (PKR) that phosphorylates eIF-2a, blocks translation in the infected cell and eventually killing it.

My second project also in graduate school was to study the feasibility of gene therapy for Duchenne Muscular Dystrophy (DMD). The idea was to insert the dmd gene cDNA into a viral vector, we used Herpes simplex virus type I (HSV I) and infect cells and animals deficient in Dystrophin — the protein product of the dmd gene.

My third project, as a post-doctoral fellow, was to look at apoptosis regulation by Protein kinase d in cancer cells. As a model, we looked at cervical cancer and breast cancer cell lines.

During my second post-doctoral fellowship, I studied the regulation of gene expression during viral infection. I focused on the activation of NF-kB following viral infection and the formation of an enhanceosome consisting of a three different transcription factors in addition to NF-kB. This process may or may not involve PKR, an issue that is still under some debate.

The research in my laboratory involves studying the control of PKR by cellular and viral factors, and the effect of viral infection on gene expression. Another one of the projects in my lab involves the study of Hepatitis C virus. In particular we are trying to understand how is manages to be such a successful pathogen. We are currently focusing on the HCV protein NS5A and its ability to inhibit antiviral gene expression as well as apoptosis.

In essence I have come a full circle since my first days of graduate school, proving, unnecessarily, again that everything in the universe is cyclical.

Courses:
Principles of Life Sciences: (Biol 10504), Fall, Molecular genetics
Cell, Molecular and Developmental Biology: (Biol 30603), Spring, Molecular and Developmental Biology.
Virology: (BIOL 40970) Spring, Even Years, Survey of molecular virology and gene therapy.
Molecular Biology of Eukaryotes (BIOL 40133) Spring, Odd Years, Molecular Biology, Current topics, Readings of
related journal Articles. Biology.

Selected Publications:

  • Akkaraju, G. R., Huard, J. Cohen, J, Goins, W. F. and Glorioso, J.C. Herpes simplex virus vector-mediated dystrophin gene transfer and expression in mdx mouse skeletal muscle (1999) J. of Gene Medicine, 1, 280–289.
  • Akkaraju, G. R. and Basu, A. Overexpression of Protein kinase C-eta attenuates caspase activation and Tumor Necrosis Factor-a-induced cell death. (2000) Biochem. Biophys. Res. Comm., 279, 103–107.
  • Wang, C., Deng, L., Hong, M., Akkaraju, G. R., Inoue, J.-I. and Chen, Z. J. TAK1 is a ubiquitin-dependent kinase of MKK and IKK. (2001) Nature, 412, 346–351.
  • Frederickson, B., Akkaraju, G. R., Foy, E., Wang, C., Pflugheber, J., Chen, Z. J. and Gale, M. Activation of the Interferon-beta promoter during Hepatitis C virus RNA replication. (2002) Viral Immunology, 15, 29–40.
  • Basu, A., Lu, D., Sun, B., Moor, A. N., Akkaraju, G. R. and Huang, J. Proteolytic activation of protein kinase C-epsilon by caspase-mediated processing and transduction of anti-apoptotic signals. (2002) Journal of Biological Chemistry, 277, 41850–41856.

Links:
Molecular Biology Tools
National Center for Biotechnology Information
Sierra Club
Union of Concerned Scientists
Outdoor Recreation Guide

 
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