guanosine-5--o-(3-thiotriphosphate) and Retinal-Degeneration

guanosine-5--o-(3-thiotriphosphate) has been researched along with Retinal-Degeneration* in 2 studies

Other Studies

2 other study(ies) available for guanosine-5--o-(3-thiotriphosphate) and Retinal-Degeneration

Article	Year
Role for the target enzyme in deactivation of photoreceptor G protein in vivo. Science (New York, N.Y.), 1998, Oct-02, Volume: 282, Issue:5386 Heterotrimeric guanosine 5'-triphosphate (GTP)-binding proteins (G proteins) are deactivated by hydrolysis of the GTP that they bind when activated by transmembrane receptors. Transducin, the G protein that relays visual excitation from rhodopsin to the cyclic guanosine 3',5'-monophosphate phosphodiesterase (PDE) in retinal photoreceptors, must be deactivated for the light response to recover. A point mutation in the gamma subunit of PDE impaired transducin-PDE interactions and slowed the recovery rate of the flash response in transgenic mouse rods. These results indicate that the normal deactivation of transducin in vivo requires the G protein to interact with its target enzyme. Topics: 3',5'-Cyclic-GMP Phosphodiesterases; Animals; Cyclic Nucleotide Phosphodiesterases, Type 6; Electroretinography; Enzyme Activation; Female; Guanosine 5'-O-(3-Thiotriphosphate); Guanosine Triphosphate; Hydrolysis; Light; Male; Mice; Mice, Knockout; Mice, Transgenic; Point Mutation; Retina; Retinal Degeneration; Rod Cell Outer Segment; Transducin; Transgenes; Vision, Ocular	1998
Altered cAMP levels in retinas from transgenic mice expressing a rhodopsin mutant. Biochemical and biophysical research communications, 1995, Nov-22, Volume: 216, Issue:3 Transgenic mice expressing the rhodopsin mutant Pro347Ser (Serine 6) display retinal degeneration through apoptosis that is characteristic of the disease retinitis pigmentosa. By 5 weeks after birth, these mice have lost approximately 35% of their photoreceptor cells. Retinas from these mice showed higher levels of cAMP compared to the levels in retinas of normal mice. Our studies provide evidence that elevated cAMP is common to the apoptotic process that occurs in retinitis pigmentosa. In addition, in vitro studies demonstrate no differences in the ability of the mutant and the wild-type rhodopsin to activate transducin, the rod cell G protein, to be phosphorylated by rhodopsin kinase or to bind arrestin. Mutants of rhodopsin, including Pro347Ser, are mistargeted to the rod inner segment, raising the possibility that rhodopsin triggers apoptosis through activation of signaling pathways not normally under its control. Topics: Animals; Apoptosis; Cyclic AMP; Guanosine 5'-O-(3-Thiotriphosphate); Mice; Mice, Transgenic; Mutation; Photoreceptor Cells; Retina; Retinal Degeneration; Retinitis Pigmentosa; Rhodopsin; Serine; Signal Transduction	1995

Article

Year

Role for the target enzyme in deactivation of photoreceptor G protein in vivo.

Science (New York, N.Y.), 1998, Oct-02, Volume: 282, Issue:5386

Heterotrimeric guanosine 5'-triphosphate (GTP)-binding proteins (G proteins) are deactivated by hydrolysis of the GTP that they bind when activated by transmembrane receptors. Transducin, the G protein that relays visual excitation from rhodopsin to the cyclic guanosine 3',5'-monophosphate phosphodiesterase (PDE) in retinal photoreceptors, must be deactivated for the light response to recover. A point mutation in the gamma subunit of PDE impaired transducin-PDE interactions and slowed the recovery rate of the flash response in transgenic mouse rods. These results indicate that the normal deactivation of transducin in vivo requires the G protein to interact with its target enzyme.

Topics: 3',5'-Cyclic-GMP Phosphodiesterases; Animals; Cyclic Nucleotide Phosphodiesterases, Type 6; Electroretinography; Enzyme Activation; Female; Guanosine 5'-O-(3-Thiotriphosphate); Guanosine Triphosphate; Hydrolysis; Light; Male; Mice; Mice, Knockout; Mice, Transgenic; Point Mutation; Retina; Retinal Degeneration; Rod Cell Outer Segment; Transducin; Transgenes; Vision, Ocular

1998

Altered cAMP levels in retinas from transgenic mice expressing a rhodopsin mutant.

Biochemical and biophysical research communications, 1995, Nov-22, Volume: 216, Issue:3

Transgenic mice expressing the rhodopsin mutant Pro347Ser (Serine 6) display retinal degeneration through apoptosis that is characteristic of the disease retinitis pigmentosa. By 5 weeks after birth, these mice have lost approximately 35% of their photoreceptor cells. Retinas from these mice showed higher levels of cAMP compared to the levels in retinas of normal mice. Our studies provide evidence that elevated cAMP is common to the apoptotic process that occurs in retinitis pigmentosa. In addition, in vitro studies demonstrate no differences in the ability of the mutant and the wild-type rhodopsin to activate transducin, the rod cell G protein, to be phosphorylated by rhodopsin kinase or to bind arrestin. Mutants of rhodopsin, including Pro347Ser, are mistargeted to the rod inner segment, raising the possibility that rhodopsin triggers apoptosis through activation of signaling pathways not normally under its control.

Topics: Animals; Apoptosis; Cyclic AMP; Guanosine 5'-O-(3-Thiotriphosphate); Mice; Mice, Transgenic; Mutation; Photoreceptor Cells; Retina; Retinal Degeneration; Retinitis Pigmentosa; Rhodopsin; Serine; Signal Transduction

1995