Western Blotting (WB), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p))
Purification
This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis
Immunogène
This GCAP1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 160-191 amino acids from the C-terminal region of human GCAP1.
GUCA1A
Reactivité: Souris, Rat
ELISA, WB, IHC (p), IHC (fro)
Hôte: Lapin
Polyclonal
Biotin
Indications d'application
For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:50~100
Restrictions
For Research Use only
Format
Liquid
Buffer
Supplied in PBS with 0.09 % (W/V) sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
4 °C,-20 °C
Stockage commentaire
Store at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Guanylate cyclase-activating protein is a l Ca(2+)-binding protein that upregulates synthesis of cGMP in photoreceptors. The known mammalian GCAPs are more than 90 % similar, consisting of 201 to 205 amino acids, and containing 3 identically conserved Ca(2+)-binding sites. The GUCA1A gene, also termed GCAP1, is transcribed into a single 1.7-kb mRNA species detectable only in the retina. In a 4-generation British family with typical clinical features of autosomal dominant cone dystrophy a tyr99-to-cys mutation) in the GUCA1A gene has been identified. Another family with a pro50-to-leu mutation in GUCA1A demonstrated phenotypic variability ranging from mild photophobia to rod-cone dystrophy. The mutant protein could activate guanylate cyclase 1 (GUCY2D) and displayed similar calcium sensitivity to wildtype protein. However, there was a marked increase in the susceptibility to protease degradation and a reduction in the thermal stability of the pro50-to-leu mutation, which may depress cellular concentration and thereby contribute to retinal cell mortality.