Background:  The Nirs (Nir1, Nir2, and Nir3), human homologues of Drosophila retinal degeneration B (rdgB), have been considered candidate genes for human inherited retinal degeneration diseases. The three Nir proteins are highly expressed in the developing retina, each exhibiting a distinct distribution profile. Nir1, also known as CORD5, RDGBA3 or PITPNM3, is a 974 amino acid peripheral membrane protein that belongs to the PtdIns transfer protein family. Nir1 is expressed in the brain and spleen, and at low levels in ovary. Nir1 interacts with PYK2 via its C-terminus and catalyzes the transfer of phosphatidylinositol and phosphatidylcholine between membranes. Defects in Nir1 are the cause of cone-rod dystrophy type 5 (CORD5). CORDs are inherited retinal dystrophies belonging to the group of pigmentary retinopathies. CORDs are characterized by retinal pigment deposits visible on fundus examination, predominantly in the macular region, and initial loss of cone photoreceptors followed by rod degeneration, which leads to decreased visual acuity and sensitivity in the central visual field, followed by loss of peripheral vision.

Description: Rabbit polyclonal to NIR1

Immunogen: KLH conjugated synthetic peptide derived from NIR1

Specificity:  ·Reacts with Human, Mouse, Pig and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 107 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.