Anti-RAB11B Antibody Picoband® Fluoro488 Conjugated

Ras-related protein Rab-11B is a protein that in humans is encoded by the RAB11B gene. It is mapped to 19p13.2. The Ras superfamily of small GTP-binding proteins, which includes the Ras, Ral, Rho, Rap, and Rab families, is involved in controlling a diverse set of essential cellular functions. The Rab family, including RAB11B, appears to play a critical role in regulating exocytotic and endocytotic pathways.

A synthetic peptide corresponding to a sequence at the C-terminus of human RAB11B, which shares 97.4% and 100% amino acid (aa) sequence identity with mouse and rat RAB11B, respectively.

Angiogenesis, Cancer, Cardiovascular, Growth Factors, Growth Factors/Hormones, Invasion/Microenvironment, Neurogenesis, Neurology Process, Neuroscience, Signal Transduction

The small GTPases Rab are key regulators of intracellular membrane trafficking, from the formation of transport vesicles to their fusion with membranes. Rabs cycle between an inactive GDP-bound form and an active GTP-bound form that is able to recruit to membranes different set of downstream effectors ly responsible for vesicle formation, movement, tethering and fusion. That Rab plays a role in endocytic recycling, regulating apical recycling of several transmembrane proteins including cystic fibrosis transmembrane conductance regulator/CFTR, epithelial sodium channel/ENaC, potassium voltage-gated channel, and voltage-dependent L-type calcium channel. May also regulate constitutive and regulated secretion, like insulin granule exocytosis. Required for melanosome transport and release from melanocytes. Also regulates V-ATPase intracellular transport in response to extracellular acidosis.

1. Gross, M. B. Personal Communication. Baltimore, Md. 7/25/2014. 2. Lamers, I. J. C., Reijnders, M. R. F., Venselaar, H., Kraus, A., DDD Study, Jansen, S., de Vries, B. B. A., Houge, G., Gradek, G. A., Seo, J., Choi, M., Chae, J.-H., and 11 others. Recurrent de novo mutations disturbing the GTP/GDP binding pocket of RAB11B cause intellectual disability and a distinctive brain phenotype. Am. J. Hum. Genet. 101: 824-832, 2017. 3. Zhu, A. X., Zhao, Y., Flier, J. S. Molecular cloning of two small GTP-binding proteins from human skeletal muscle. Biochem. Biophys. Res. Commun. 205: 1875-1882, 1994.