Rabbit anti-Human RALBP1 Monoclonal Antibody

Uniprot Id

Q15311

Target Species

Human

Target Name

RALBP1

Target Full Name

RalA-binding protein 1

Target Function

Multifunctional protein that functions as a downstream effector of RALA and RALB. As a GTPase-activating protein/GAP can inactivate CDC42 and RAC1 by stimulating their GTPase activity. As part of the Ral signaling pathway, may also regulate ligand-dependent EGF and insulin receptors-mediated endocytosis. During mitosis, may act as a scaffold protein in the phosphorylation of EPSIN/EPN1 by the mitotic kinase cyclin B-CDK1, preventing endocytosis during that phase of the cell cycle. During mitosis, also controls mitochondrial fission as an effector of RALA. Recruited to mitochondrion by RALA, acts as a scaffold to foster the mitotic kinase cyclin B-CDK1-mediated phosphorylation and activation of DNM1L.; Could also function as a primary ATP-dependent active transporter for glutathione conjugates of electrophiles. May also actively catalyze the efflux of a wide range of substrates including xenobiotics like doxorubicin (DOX) contributing to cell multidrug resistance.

Target Subcellular Location

Cell membrane; Peripheral membrane protein. Cytoplasm, cytosol. Cytoplasm, cytoskeleton, spindle pole. Nucleus. Mitochondrion.

Target Tissue Specificity

Expressed ubiquitously but at low levels. Shows a strong expression in the erythrocytes.

Target Synonyms

RLIP1; 76 kDa Ral-interacting protein; 76-kDa Ral-interacting protein; Dinitrophenyl S-glutathione ATPase; DNP-SG ATPase; Ral-interacting protein 1; Ral-interacting protein 1, 76-KD; RalA-binding protein 1; RalBP1; RBP1_HUMAN; RIP1; RLIP1; RLIP76

Target Background

RALBP1 plays a role in receptor-mediated endocytosis and is a downstream effector of the small GTP-binding protein RAL (see RALA; MIM 179550). Small G proteins, such as RAL, have GDP-bound inactive and GTP-bound active forms, which shift from the inactive to the active state through the action of RALGDS (MIM 601619), which in turn is activated by RAS (see HRAS; MIM 190020) (summary by Feig, 2003 [PubMed 12888294]).