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Rhodopsin Antibody

Mouse monoclonal antibody

     
  • IHC - Rhodopsin  Antibody AN1166
    Immunohistochemical staining of mouse retinal section showing specificimmunolabeling of the rhodopsin protein in the rod spherules. Photo courtesyof Mary Raven, University of California, Santa Barbara, CA.
    detail
  • SPECIFICATION
  • CITATIONS
  • PROTOCOLS
  • BACKGROUND
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immunoelectronmicroscopy
  • EIA=Enzyme Immunoassay
IHC
Primary Accession P02699
Reactivity Human, Mouse, Rat
Host Mouse
Clonality monoclonal
Isotype IgG1
Clone Names 1D4
Calculated MW 39 KDa
Additional Information
Gene ID 509933
Gene Name RHO
Other Names Rhodopsin, RHO
Target/Specificity Purified native bovine rhodopsin.
Dilution IHC~~ 1:100
Format Protein G purified culture supernatant.
Antibody Specificity Specific for the ~ 39k rhodopsin protein.
StorageMaintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.
PrecautionsRhodopsin Antibody is for research use only and not for use in diagnostic or therapeutic procedures.
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Research Areas
Citations (0)
citation

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Background

Rhodopsin is a photoreceptor protein found in retinal rods. It is a complex formed by the binding of retinaldehyde, the oxidized form of retinol, to the protein opsin and undergoes a series of complex reactions in response to visible light resulting in the transmission of nerve impulses to the brain. Mutation of the rhodopsin gene is a major contributor to various retinopathies such as retinitis pigmentosa. The disease-causing protein generally aggregates with ubiquitin in inclusion bodies, disrupts the intermediate filament network and impairs the ability of the cell to degrade non-functioning proteins which leads to photoreceptor apoptosis (Berson et al., 1991). Other mutations on rhodopsin lead to X-linked congenital stationary night blindness, mainly due to constitutive activation, when the mutations occur around the chromophore binding pocket of rhodopsin (Dryja et al.,1993). Several other pathological states relating to rhodopsin have been discovered including poor post-Golgi trafficking, dysregulative activation, rod outer segment instability and arrestin binding.

References

Berson EL, Rosner B, Sandberg MA, Dryja TP
(1991). "Ocular findings in patients with
autosomal dominant retinitis pigmentosa and a rhodopsin gene defect (Pro-23-His)".
Arch.
Ophthalmol.
109
(1): 92–101.
Dryja TP, Berson EL, Rao VR, Oprian DD (1993) Heterozygous missense mutation in the
rhodopsin gene as a cause of congenital stationary night blindness. Nature Genet. 4:280-283.
Molday RS, MacKenzie D. (1983) Monoclonal ant
ibodies to rhodopsin: characterization, cross-
reactivity, and application as structural probes. Biochemistry. 22(3):653-60.

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$ 365.00
Cat# AN1166
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