Target intelligence / Profile preview

Ras-related protein Rab-24 (RAB24)

Target
RAB24
Molecular classification
Small GTPase, Enzyme, Ras superfamily, Rab family
01

Overview

Ras-related protein Rab-24 (RAB24) is an atypical small GTPase of the Rab family within the Ras superfamily, located on chromosome 5[1][5]. RAB24 is involved in the regulation of intracellular vesicle trafficking, with a particularly important role in the clearance of late autophagic vacuoles and regulation of basal autophagy[2][5]. It differs from other Rab proteins in its low GTPase activity and preference for the GTP-bound state, and has unique post-translational modification properties[4]. RAB24 is implicated in membrane trafficking events necessary for cellular homeostasis and is associated with diseases such as cancer, ataxia, and infections[2][3][5]. It interacts with several proteins involved in membrane fusion, suggesting roles in autophagosome-lysosome fusion and late endosome function[2]. No drugs are currently known to directly target RAB24, nor is it generally used as a clinical biomarker or associated with specific drug mechanism of action, but it is recognized as a therapeutic target in research settings given its roles in pathological states and essential cell processes[2][3][5].

Other names
RAB24rab24ras-related protein Rab-24
02

Mechanism of action

Not specifically characterized for drugs, but molecular mechanism involves GTP binding/hydrolysis to regulate autophagic and endosomal trafficking pathways

03

Biological functions

Intracellular protein traffickingAutophagy (especially clearance of late autophagic vacuoles)Endosomal degradationMembrane fusion events (putative)Basal autophagy regulation
04

Disease associations

Cancer (implicated in hepatocellular carcinoma, colorectal adenocarcinoma)AtaxiaTuberculosis (infection biology)Neurodegenerative disease (implicated in protein aggregate clearance)Q feverCeroid lipofuscinosis, neuronal, 6B
05

Safety considerations

Not specifically characterized, but perturbation of autophagy/endosomal pathways may have broad cellular impacts

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