Abstract
Studies form our laboratory and others show that the oncogenic tyrosine kinase and serine threonine kinase signaling pathways are essential for cone photoreceptor survival. These pathways are downregulated in mouse models of retinal degenerative diseases. In the present study, we found that activation mutants of mTOR delayed the death of cones in a mouse model of retinal degeneration. These studies suggest that oncogenic protein kinases may be useful as therapeutic agents to treat retinal degenerations that affect cones.
Keywords:
Cone photoreceptors; Insulin receptor; Oncogene; Protein kinases; Retinal degeneration; Retinitis pigmentosa; Survival; mTOR.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Basic-Leucine Zipper Transcription Factors / deficiency
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Cell Survival
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Disease Models, Animal
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Eye Proteins
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Genes, Synthetic
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Injections, Intraocular
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Mice
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Mice, Inbred BALB C
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Mice, Knockout
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Mice, Mutant Strains
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Promoter Regions, Genetic
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Receptor, Insulin / metabolism
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Recombinant Proteins / genetics
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Recombinant Proteins / therapeutic use
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Retinal Cone Photoreceptor Cells / drug effects*
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Retinitis Pigmentosa / therapy*
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TOR Serine-Threonine Kinases / genetics
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TOR Serine-Threonine Kinases / therapeutic use*
Substances
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Basic-Leucine Zipper Transcription Factors
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Eye Proteins
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Nrl protein, mouse
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Recombinant Proteins
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MTOR protein, human
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Receptor, Insulin
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TOR Serine-Threonine Kinases