Faculty & Staff at TUC
Greg Gayer
College: COM
Department: Basic Sciences
Title: Associate Professor and Chair
Phone: (707) 638-5209
Fax: (707) 638-5255
E-Mail: ggayer@touro.edu
Office: Administration & Faculty 1, Rm. 224
Institution | Degree | Field of Study | Obtained |
University of California, San Francisco | PhD | Pharmacology | 1992 |
Course Coordinator and Principle Lecturer: Pharmacology, College of Osteopathic Medicine.
1999-present
Course Coordinator: Integrated System-Cardiovascular Respiratory, Renal. College of
Osteopathic Medicine
Lecturer: Pharmacology and Pathophysiology, College of Pharmacy
Research Overview
Research Project While at TU-CA
1) DNA-micro array analysis of reward pathways: 2001-2002
Former project at the Ernest Gallo Clinic & Research Center (EGCRC), at the University
of California San Francisco (UCSF). I worked on a project with Dr. Michael Miles.
In this lab we studied the underlying molecular changes that produce the process of
sensitization in the nucleus accumbens upon exposure to drugs of abuse. Using DNA-chip-array
technology genes that are regulated by administration of cocaine and alcohol to mice
were evaluated.
My role in this project is to help with an ongoing effort by providing my time and
molecular biology expertise as well as my knowledge regarding ethanol-induced gene
expression changes.
Lipton P. A. Gayer G. G. Wang L., Miles M.F. Time course of effects of chronic cocaine
administration expression in mice Society of Neuroscience,. Abstract, 977.15, 2001.
2)Dynorphinergic and enkephalinergic neuronal pathways 2003-2006
Dr. Robert Messing (Ernest and Gallo Research Center, Co-Director, UCSF) and I collaborated
on a project to better elucidate that molecular events that occur in reward centers
like the nucleus accumbens when exposed to acute and chronic treatments to drugs with
high abuse potential. I developed DNA expression vectors that contain green-fluorescent
protein directed by pdynorphin (pdyn-GFP) and penkephalin (pENK-EYFP) tissue specific
promoter elements. These constructs were developed to make transgenic mice that would
enable the visualization of enkephalenergic and dynorphenergic neurons, a simple gene
expression assay, and provide a visual identification for the capture of events produced
by acute or chronic use of cocaine, heroine, and ethanol, etc. in brain areas hard
to identify microscopically. Elucidating the connections in these meso-limbic reward
pathways would provide important insights into drugs of abuse. Once these vectors
were constructed, it was confirmed that they were functional by transfecting promoter-reporter
constructs into tissue culture cells. Expression was confirmed by the population of
fluorescent cells. Next, the expression vectors were injected into mouse embryo cells
and transgenic mouse strains were analyzed.
3)Angiotensin II receptor function and glycation 2006-Future
I have received a $24,000 intramural grant to study the regulation of pathways central
to many pathologic processes observed in diabetic patients. Specifically, angiotensin-II-AT1
receptor function will be observed under various environmental conditions that occur
in patients with diabetes. (see attached grant proposal for details). Briefly, it
involves measuring the AT1 receptor function under conditions that promote receptor-glycation.
This grant proposal received the highest possible rating.
Research Project Prior to Employment at TUCA
At UCSF, EGCRC, I designed and conducted an innovative research project on a neurophysiological
component of alcoholism. I was awarded for my efforts a National Institute of Health
grant to research causes of alcoholism with potential for future development and use
in the treatment of alcoholism and alcohol abuse. This work produced the discovery
that chronic ethanol exposure to a neuronal cell culture system led to increases in
Tyrosine Hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis,
protein and mRNA levels. It was further discovered that these increases in gene expression
were at the translational level and independent of known ethanol-induced changes receptor
function and second messenger cascades. The TH enhancer/promoter transcriptional activation
region responsible for ethanol-induced increases was identified (see bold publications
below).
I followed graduate work I was recipient of a Howard Hughes post-doctoral fellowship
to investigate neural development with Dr. Richard Scheller, a pioneer in the field
of molecular biology and the study of synapse function. Investigated the underlying
biochemical mechanisms involved in how extracellular matrix proteins aid in developing
neural muscular synapse. This project involved designing recombinant gene expression
systems for analysis of rat agrin isoforms. I determined the role of the agrin y-splice
variant in binding specificity to heparin and the dystrophin glycoprotein complex
(see bold publication below and attached, note authors contributed equally on this
project). In addition, I performed immunohistochemical localization of agrin splice
variants during rat embryo development using florescence microscopy.
TU-CA: The effects of glycation on AT1 receptor function ($24,000) 2006
Publications Lipton P. A. Gayer G. G. Wang L., Miles M.F. Time course of effects of
chronic cocaine administration expression in mice Society of Neuroscience,. Abstract,
977.15, 2001
Wilke N; Sganga M.W.; Gayer G.G.; Hsieh K; Miles M.F. (2000) Characterization of promoter
elements mediating ethanol regulation of hsc70 gene transcription. JPET, vol 292 pp.
173-180, 2000
Gayer G.G.; Campanelli, J.T.; Scheller, R.T. (1996) Regulation of membrane protein
organization at the neuromuscular junction. In “The plasma membrane-cytoskeleton interface:
Template for protein domains, vesicle trafficking and signal transduction (A volume
of current topics in membranes).” Ed. Nelson, J.N. Academic Press
Campanelli, N.T; Gayer, G.G.; Scheller, R.H. (1996) Alternative RNA splicing that
determines agrin activity regulates binding to heparin and dystroglycan. Development,
Vol. 122. pp. 1663-1672
Miles, M.F., Gayer, G. and Sganga, M. (1993) Regulation of neuronal gene expression
by ethanol. Alcohol, Cell Membranes, and Signal Transduction in Brain. Ed. C. Alling
and G. Sun, Eds. Plenum Publishing Corporation, New York. Pp. 283-298
Gayer, G.G; Gordon, A.S.; Miles, M.F. (1991) Ethanol increases tyrosine hydroxylase
gene expression in N1E-115 neuroblastoma cells. Journal Biological Chemistry, Vol.
266. pp. 22279-22284
Gayer G.G.; Gordon A.S.; Miles, M.F. (1991) Ethanol regulates tyrosine hydroxylase
gene expression in N1E-115 neuroblastoma cells. Society of Neuroscience, Vol. 17,
Part 2. Abstract, pp. 1432
Gayer, G.G.; Gordon A.S.; Miles, M.F. (1991) Chronic ethanol exposure causes increased
tyrosine hydroxylase gene expression in N1E-115 neuroblastoma cells. Journal of Cellular
Biochemistry, Vol. 15B. pp. 189
Miles, M.F.; Gayer, G.G.; Gordon A.S.; Diaz, J.E.; Chin W.; Barhite, S.; and Wilke,
N. (1991) Regulation of gene expression by ethanol in neural cell cultures. Journal
of Cellular Biochemistry, Vol. 16A. p. 102
Faculty Collegiality Award (Faculty) 2000-2001
Most Organized Department (Class of 2003)
Student Advocate Award (Class of 2003)
Most Organized Department (Class of 2004) 2001-2002
Golden Apple Award (Class of 2004)
Most Entertaining Lecturer Award (Class of 2004)
Most Organized Department (Class of 2005) 2002-2003
Most Likely to Have Full Attendance in Lecture (Class of 2005)
Best Sense of Humor (Class of 2006) 2003-2004
Best at Turning Tedious Topics Tolerable (Class of 2006)
Faculty Collegiality Award (Faculty)
Who’s Who Among America’s Teachers 2004
Founding Fathers Award 2005
White Coat Presenter Class 2008 2006
Best Lecturer Award 2007
Most Approachable Professor 2007
Employer | Title | From - To |
TUCA-CA | Associate Professor | 1999-present |
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