Target intelligence / Profile preview

Ras-related protein Rab-11B (RAB11B)

Target
RAB11B
Molecular classification
Small GTPase, Ras superfamily member, Membrane trafficking protein, Vesicle transport regulator
01

Overview

Ras-related protein Rab-11B (RAB11B) is a member of the Rab subfamily of the Ras superfamily of small GTPases, involved in regulating intracellular membrane trafficking including vesicle budding, movement, tethering, and fusion[1][3][6]. RAB11B primarily functions in the recycling of proteins from endosomes to the plasma membrane and is distinguished from the closely related RAB11A by its tissue expression (most abundant in brain, heart, and testes) and unique vesicular compartment localization[1][3]. It regulates exocytosis, endocytosis, and the degradation and recycling of multiple membrane channels and transporters, such as CFTR and L-type calcium channels[2][3]. In gut epithelial cells, RAB11B plays a critical role in maintaining mitochondrial structure and function; its absence leads to impaired mitochondrial integrity and activity[5]. Mutations or dysfunction in RAB11B are associated with rare neurodevelopmental disorders and cellular physiological defects[3][5].

Other names
RAB11BYPT3H-YPT3GTP-binding protein YPT3Ras-related protein Rab-11B
02

Mechanism of action

Small GTPase cycling (GDP/GTP-bound switching) regulating recruitment of effectors for vesicle formation, tethering, and fusion Modulation of membrane protein degradation and recycling (e.g., Ca_v_1.2 L-type Ca^2+ channel, CFTR, ENaC) Regulation of mitochondrial protein targeting and integrity in epithelial cells

03

Biological functions

Regulation of intracellular membrane traffickingEndocytosis and exocytosisRecycling of proteins from endosomes to plasma membraneVesicle budding, tethering, and fusionRegulation of mitochondrial integrity and functionPolarized transport in epithelial cellsRegulation of channel protein surface expressionSecretion and exocytosis
04

Disease associations

Neurodevelopmental disorder (e.g., Neurodevelopmental disorder with ataxic gait, absent speech, and decreased cortical white matter)LissencephalyPotential roles in cardiac/cellular metabolic disorders (based on mitochondrial function)Other (implications in cell survival, potentially cancer via vesicular trafficking)
05

Safety considerations

None directly known; disruption in RAB11B function leads to severe mitochondrial defects and impaired epithelial cell mitochondrial function, with possible systemic consequences[5]

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