Retinal rods utilize a prototypical G-protein signaling cascade to encode our visual scene under dim light. Often, defects in the molecular components of this cascade, or their over-stimulation by bright light, cause blinding disorders in humans.
The first aim will investigate biochemical cascades in rods following bright light exposure that may slow dark adaptation.
The second aim i s to investigate the induction of endoplasmic stress by bright light exposure and mis-folded rhodopsin with the goal towards manipulation of these pathways to prolong photoreceptor cell survival. The long term objective of this proposal is to understand phototransduction in normal function and dysfunction so that this knowledge can be used to devise strategies for the treatment of human visual disorders.

Public Health Relevance

Photoreceptor cells utilize a prototypical G-protein signaling cascade to convey the presence of light. Genetic mutations and environmental factors that affect the performance of this signaling cascade cause many different forms of blinding diseases through mechanisms that are not well defined. A thorough understanding of these mechanisms will help in the design of treatment options.

National Institute of Health (NIH)
National Eye Institute (NEI)
Research Project (R01)
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Biology and Diseases of the Posterior Eye Study Section (BDPE)
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Neuhold, Lisa
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University of Southern California
Anatomy/Cell Biology
Schools of Medicine
Los Angeles
United States
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Song, Xiufeng; Seo, Jungwon; Baameur, Faiza et al. (2013) Rapid degeneration of rod photoreceptors expressing self-association-deficient arrestin-1 mutant. Cell Signal 25:2613-24

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