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Faculty Detail    
Name G M ANANTHARAMAIAH
 
Campus Address BDB 668 Zip 0012
Phone 205-934-1884
E-mail ananth@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Medicine  Med-Gerontology/Geriatrics/Palliative Care Professor
Secondary  Biochemistry & Molecular Genetics  Biochemistry & Molecular Genetics Associate Professor
Center  Center for Aging  COMPREHENSIVE CTR FOR HEALTHY AGING Professor
Center  Center for AIDS Research  Center for AIDS Research Professor
Center  Medicine  Comprehensive Diabetes Ctr Professor
Center  Medicine  Ctr Cardiovasc Bio Professor

Graduate Biomedical Sciences Affiliations
Biochemistry and Molecular Genetics Program 
Biochemistry and Structural Biology 
Cell, Molecular, & Developmental Biology 
Medical Scientist Training Program 
Microbiology 
Neuroscience 

Biographical Sketch 
Dr. Anantharamaiah joined UAB in 1982 and is a Professor in the Department of Medicine. His research is supported by grants from NIH.

Research/Clinical Interest
Title
Apolipoproteins, Amphipathic Helices and Atherosclerosis
Description
Two mechanisms have been proposed for the progression of atherosclerosis: 1) the cholesterol theory, increased plasma cholesterol levels increased the risk for atherosclerosis 2) injury and endothelial surface perturbation is the major cause of atherosclerosis, which is inhibited by the presence of high levels of good cholesterol (HDL). It has been shown that both apo E (the protein component of very low-density lipoproteins (VLDL) and apolipoprotein A-I (the major protein component of HDL) are antiatherogenic, but by two distinctly different mechanisms. Using the common structural motif present for the lipid associating domains in apolipoproteins, the amphipathic helix, we have been able to design peptide mimics for 1) the rapid removal of atherogenic lipoproteins from circulation in vivo, and 2) inhibit atherosclerosis in atherosclerosis sensitive mice without changing plasma cholesterol profile. Using cell culture studies, we have determined that the peptides that reduce plasma cholesterol levels do so by enhancing their removal by the proteoglycan-mediated pathway. Cell culture studies have also shown that the peptides that inhibit atherosclerosis without altering plasma cholesterol levels do so by “removing the seeding molecules” from atherogenic lipoproteins. The laboratory is now in the process of producing transgenic mice expressing these two types of molecules and determining the exact mechanism(s) of atherosclerotic plaque formation and avenues to inhibit this (these) process(es).