Background:  Appears to be a potent inhibitor of regeneration following spinal cord injury.Nogo is an oligodendrocyte-specific member of the Reticulon family and is a component of CNS white matter that inhibits axon outgrowth, induces collapse of growth cones of chick dorsal root ganglion cells, and inhibits the spreading of 3T3 fibroblasts. Nogo is expressed by oligodendrocytes but not by Schwann cells, and associates primarily with the endoplasmic reticulum. Nogo exists in three different splice forms, Nogo-A, -B and -C. NIMP (NOGO-interacting mitochondrial protein), also known as RTN4IP1 (Reticulon-4-interacting protein 1), is a 396 amino acid mitochondrial protein that contains a C-terminal oxidoreductaselike domain and numerous sites for phosphorylation. NIMP is expressed in mitochondrial-rich tissue such as kidney, heart, skeletal muscle and specific regions within the nervous system. Through interaction with Nogo, it is likely that NIMP plays a role in Nogo-induced inhibition of neurite growth. There are three isoforms of NIMP that are produced as a result of alternative splicing events.

Description: Rabbit polyclonal to NIMP

Immunogen: KLH conjugated synthetic peptide derived from NIMP

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 44 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.