Ramareddy Guntaka, PhD
Professor
858 Madison Ave.
101 H Molecular Science Building
Memphis, TN 38163
Email: rguntaka@uthsc.edu
Phone: 901.448.8230
Fax: 901.448.7360
Education
- BSc, 1963 (April) Chemistry and Biology, A.N.R. College, Gudivada (Affiliated to the Andhra University, A.P., India)
- MSc,1965 (December) Microbiology, U.P. Agricultural University, Pantnagar, U.P., India (Thesis: Relationship between sporulation and antibiotic production in Bacillus licheniformis)
- PhD,1970 (January) Microbiology, Kansas State University, Manhattan, Kansas (Thesis: Mechanism of thymineless death in Bacillus subtilis)
Research Interests
Currently there are three ongoing projects in my laboratory: (i) Control of Fibrosis by Collagen Gene-Specific Oligonucleotides; ii) Cloning and characterization of Hepatitis C Virus and iii) Studies on the Y-box protein YB. In the first project, we are applying a novel triplex strategy to intervene reactive fibrosis, which is responsible for the damage of various organs. This fibrosis is mainly due to abnormal deposition of high levels of type I collagen. We have found that a triplex-forming oligonucleotide (TFO) specifically forms triplexes (see figure below) with the polypurine/polypyrimidine tract located in the promoter region of type I collagen gene and inhibits collagen gene transcription. Currently we are carrying out experiments using animal models of fibrosis to determine the effect of this TFO on fibrosis. In particular we are working on experiments to specifically target this TFO to stellate cells of the liver. In the second project, we are characterizing the genome of Hepatitis C virus (Indian strain) in order to determine genetic variation in the envelope gene of this virus. The ultimate goal is develop a vaccine and/or antiviral agents to control this deadly infection, which is the cause of hepatitis, cirrhosis and hepatocellular carcinoma. Earlier we have shown by knocking out one allele of the YB-1 transcription factor gene in a pre-B cell line that this factor plays an essential role in cell proliferation. It appears that YB-1 blocks some step(s) at the post-synthetic phase of cell cycle probably by interacting with the tumor suppressor gene p53. We are currently focusing on identifying these events in this third ongoing project.