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.
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.
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