Product Pathways - PI3K / Akt Signaling
ATP6V1B2 (D2F9R) Rabbit mAb #14617
ATPase. H+ transporting. lysosomal 56/58kDa. V1 subunit B2 Endomembrane proton pump 58 kDa subunit H+ transporting two-sector ATPase HO57 V-ATPase B2 subunit V-ATPase subunit B 2 V-type proton ATPase subunit B. brain isoform vacuolar H+-ATPase 56.000 subunit Vacuolar proton pump subunit B 2 VATB VATB2 Vma2 VPP3
|14617S||100 µl ( 10 western blots )||￥3,250.00 现货查询||购买询价|
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Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting,
Specificity / Sensitivity
ATP6V1B2 (D2F9R) Rabbit mAb recognizes endogenous levels of total ATP6V1B2 protein. This antibody does not cross-react with ATP6V1B1 protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human ATP6V1B2 protein.
Eukaryotic cells contain ATP-driven proton pumps known as vacuolar H+-ATPases (V-ATPases) that acidify intracellular compartments and translocate protons across the plasma membrane (1,2). Intracellular v-ATPases play an important role in endocytosis and intracellular membrane trafficking, while plasma membrane v-ATPases are important in processes such as urinary acidification and bone resorption (1,2). Vacuolar ATPase enzymes are large, heteromultimeric protein complexes with component proteins found in either the V1 peripheral domain or the V0 integral domain (2). The cytoplasmic V1 domain contains a hexamer of A and B catalytic subunits, as well as a number of other protein subunits required for ATPase assembly and ATP hydrolysis. The integral V0 v-ATPase domain exhibits protein translocase activity and is responsible for transport of protons across the membrane (2). Research studies show that the v-ATPases ATP6V0c, ATP6V0d1, ATP6V1A, ATP6V1B2, and ATP6V1D interact with the Ragulator protein complex and are essential for amino acid induced activation of mTORC1 on the surface of lysosomes (3).
Two isoforms of the B subunit are found in humans, ATP6V1B1 and ATP6V1B2. The ATP6V1B1 protein is expressed primarily in the kidney, with mutations in the corresponding gene responsible for a form of renal tubular acidosis associated with progressive hearing loss (4,5). ATP6V1B2 protein exhibits a broader range of expression, localized to kidney, brain, pancreas, and other tissues (4).
- Marshansky, V. and Futai, M. (2008) Curr Opin Cell Biol 20, 415-26.
- Jefferies, K.C. et al. (2008) Arch Biochem Biophys 476, 33-42.
- Zoncu, R. et al. (2011) Science 334, 678-83.
- van Hille, B. et al. (1994) Biochem J 303 ( Pt 1), 191-8.
- Karet, F.E. et al. (1999) Nat Genet 21, 84-90.
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