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Associate Professor of Biochemistry & Molecular Biology
PO Box 980614
Richmond, VA 23298-0614
Email: cjchen@vcu.edu
Telephone: (804) 828-9762
Education
- B.S., 1985, Tunghai University, Taiwan
- M.S., 1987, National Taiwan University, Taiwan
- Ph.D., 1995, University of Washington
Post-Doc
1996-2000, California Institute of Technology
Research
We use biochemical, electrophysiological, and genetic tools to study the biology of
vertebrate retinal photoreceptors. These post-mitotic and highly differentiated cells
transduce visible light into electrical signals. Two types of morphologically
distinctive photoreceptors are found in the retina. Rod photoreceptors, responsible for
dim light vision due to their higher sensitivity, transduce light relatively slower.
Cone photoreceptors, responsible for daytime vision and color vision, are less sensitive
but transduce light much faster than rods. The biochemical reactions linking photon
absorption to the generation of neural signals is a canonical G-protein signal
transduction pathway called phototransduction, in which rod and cone photoreceptors use
cGMP as a second messenger. Certain proteins are used by both photoreceptors but each
type of cells expresses distinct sets of proteins for the task. Our long-term goal is to
recount the molecular basis of the differences in sensitivity and response kinetics in
rod and cone phototransduction. Our short-term aims are to determine the rate-limiting
steps in the recovery of rod phototransduction pathway and to delineate the function of
GRK7, a seventh member of the G-protein coupled receptor kinase family found in cone
photoreceptors of several mammalian species including human.
Individuals whose photoreceptors sustain genetic or environmental insults suffer from
photoreceptor degeneration, a clinical condition with very limited treatment options.
Unlike other inherited degenerative diseases of the central nervous system, in which
mutations occur with common structural features (as in the trinucleotide repeat
expansion disease) or in groups of genes with related functions (as in Alzheimer’s
disease), the degeneration of photoreceptors can be triggered by mutations in a wide
variety of genes. As of May of 2005, 158 genetic loci are linked to retinal diseases and
among them 110 genes are identified. A good portion of these genes are expressed in a
photoreceptor-specific fashion while several others are ubiquitously expressed. Many
animal models mimicking the phenotypic expression of mutations in human are identified
or made by targeted genetics. None of the pathologic mechanisms in these models is
known, but it is widely accepted that programmed cell death is centrally involved. We
hypothesize that these multiple individual forms of photoreceptor degeneration converge
down to just a few preapoptotic pathways. We will test the hypothesis by conditional
targeted genetic approaches in mice. Our short-term aims are to determine the roles of
caspase activation as well as the involvement of apoptosis-inducing factor (AIF) during
photoreceptor degeneration. The long-term goal is to identify novel therapeutic and
pharmaceutical modalities to diagnose/prevent/treat the degeneration of retinal
photoreceptors.
Publications
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1101 E Marshall St | PO Box 980614 | Richmond, VA 23298 | ph 804.828.9762 | fax 804.828.1473
Site Update July 20, 2008, Responsible Unit - Department of Biochemistry & Molecular Biology, biochemgrad@mail.vcu.edu
Virginia Commonwealth University,
VCU School of Medicine
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