Background:  Retinal degeneration slow (rds) is a mouse neurological mutation that is characterized phenotypically by abnormal development of rod and cone photoreceptors followed by their slow degeneration. This phenotype resembles the pathologic abnormalities seen in retinitis pigmentosa. Mouse rds is due to a defect in a specific retinal protein which is photoreceptor-specific and is homologous in several respects to the rod outer segment protein-1. The human RDS protein is 92% homologous to its murine analog. The RDS protein is a membrane-associated glycoprotein restricted to photoreceptor outer segment discs and may function as an adhesion molecule involved in stabilization and compaction of outer segment discs. The association of the rds gene with a degenerative retinopathy in mice makes it an important candidate gene for human retinopathies. The gene which encodes RDS maps to human chromosome 6p21.2-12.3.

Description: Rabbit polyclonal to PRPH2

Immunogen: KLH conjugated synthetic peptide derived from PRPH2

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 39 kDa;

·Immunohistochemistry (Paraffin/frozen tissue section): 1/50-200;

·Immunocytochemistry/Immunofluorescence: 1/100;

·Immunoprecipitation: 1/50;

·ELISA: 1/500;

·Optimal working dilutions must be determined by the end user.