| Overview |
| bs-8506R-A488 |
| OSTM1 Polyclonal Antibody, ALEXA FLUOR® 488 Conjugated |
| WB, FCM, IF(IHC-P), IF(IHC-F), IF(ICC) |
| Human, Mouse, Rat |
| Pig |
| Specifications |
| ALEXA FLUOR® 488 |
| Rabbit |
| KLH conjugated synthetic peptide derived from human OSTM1 |
| 21-120/334 |
| Polyclonal |
| IgG |
| 1ug/ul |
| Purified by Protein A. |
| Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. |
| Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles. |
| Target |
| 28962 |
| Q86WC4 |
| Cell membrane |
| GL; GIPN; OPTB5; HSPC019; Osteopetrosis-associated transmembrane protein 1; Chloride channel 7 beta subunit; OSTM1; UNQ6098/PRO21201 |
| OSTM1 (osteopetrosis associated transmembrane protein 1), also known as gl (gray-lethal) or HSPC019, is a 338 amino acid single-pass type I membrane protein that is expressed primarily in osteoclasts and melanocytes as well as brain, kidney and spleen. Bone autosomal recessive osteopetrosis (ARO) is the most severe form of hereditary bone disease whose cellular basis is in the osteoclast and is characterized by abnormally dense bone, due to defective resorption of immature bone. ARO is suggested to be caused by mutations in the OSTM1 gene. The disorder occurs in two forms: a severe autosomal recessive form occurring in utero, infancy, or childhood, and a benign autosomal dominant form occurring in adolescence or adulthood. Defects in the OSTM1 gene are also the cause of the spontaneous gl mutant, which is responsible for a coat color defect in mice. |
| Application Dilution |
| WB |
1:300-5000 |
| FCM |
1:20-100 |
| IF(IHC-P) |
1:50-200 |
| IF(IHC-F) |
1:50-200 |
| IF(ICC) |
1:50-200 |
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