Anti Calbindin (D-28K) pAb (Rabbit, Affinity Purified)

Cosmo Bio USA

Anti Calbindin (D-28K) pAb (Rabbit, Affinity Purified)

16

Research Use Only

Background Neurodegenerative diseases such as Alzheimers disease and Parkinsons disease have been increasing rapidly and have become a serious social problem. In recent years, new causative genes have been discovered for amyotrophic lateral sclerosis (ALS) and other intractable neurological diseases opening new avenues for research on pathogenesis. It has been suggested that aggregation and accumulation of specific proteins cause neurotoxicity and the formation of lesions, but the onset and progression mechanisms are still unclear. Neuropathological diagnostic and experimental model biomarkers are needed for drug construction, drug discovery, and therapeutic development. Vitamin D-dependent 28 kDa calcium-binding protein (calbindin D 28k or CB) is a member of the calmodulin superfamily of calcium binding proteins discovered in 1966 by Wasserman and Taylor. The protein has a distinct distribution in the brain and sensory system and is abundant in specific neuronal cell types. Calbindin D-28k constitutes as much as 0.1-1.5 % of the total soluble protein in brain and it may be present at intracellular concentrations up to 1 mM. Several recent studies have shown that calbindin D can protect cells from degeneration and ischemic injury under extracellular stress. In particular, this is demonstrated in the brain of Alzheimer and quotes disease patients. Cells containing calbindin D have a considerably lower plaque and tangles burden than those lacking this 28 kDa protein. Applications Western Blotting (WB): 0.1 ug/ml Immunofluorescence (IF) : 1 ug/ml Immunoprecipitation (IP) : assay dependent Enzyme-linked immunosorbent assay (ELISA) : assay dependent Immunohistochemistry (Paraffin) (IHC (P)) : assay dependent Product description References: Zhu YY, Takashi M, Miyake K, Kato K. (1991) Sensitive enzyme immunoassay for human 28 kDa calbindin-D. Clin Chim Acta. 1991 201:183-92.

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