Target intelligence / Profile preview

ADP-ribosylation factor-like protein 8B (ARL8B)

Target
ARL8B
Molecular classification
Small GTPase, Ras small GTPases superfamily, Vesicular transport protein, Intracellular signaling peptide/protein
01

Overview

ADP-ribosylation factor-like protein 8B (ARL8B) is a conserved small GTPase localized predominantly to lysosomal membranes, serving as a master regulator of lysosomal positioning, trafficking, and fusion. ARL8B acts by recruiting motor-protein complexes (notably kinesin 1 via the effector SKIP) to mediate microtubule-dependent lysosome transport toward the cell periphery. This function is critical for diverse biological contexts, including immune responses (by facilitating antigen presentation and cytolytic granule exocytosis), neuronal presynaptic assembly, and intracellular cargo delivery. ARL8B-dependent lysosome movement is implicated in cancer progression through enhanced lysosomal secretion of proteases and facilitation of matrix remodeling, as well as in host defense and infection pathways. Loss of ARL8B impairs these processes, leading to decreased cell invasion, metabolism, and immune efficacy[1][2][3][4][5].

Other names
ARF like GTPase 8BARL8BARL10CGIE1FLJ10702Gie1ADP-ribosylation factor-like protein 10CADP-ribosylation factor-like protein 8BGTPase indispensable for equal segregation of chromosomes 1novel small G protein indispensable for equal chromosome segregation 1ADP ribosylation factor like GTPase 8BADP-ribosylation factor-like 10C
02

Mechanism of action

Drugs targeting ARL8B would likely inhibit lysosome positioning, protease secretion, and trafficking, thereby affecting cancer cell invasion and proliferation[3][4].

03

Biological functions

Lysosomal positioningLysosome trafficking and fusionCytosolic transportAntigen processing and presentationVesicle fusionAnterograde axonal long-range transportCargo delivery to lysosomesChromosome segregation
04

Disease associations

Cancer (invasion, progression, metabolism)[3]Spondylometaphyseal dysplasia, Sedaghatian type[2]Hermansky-Pudlak syndrome[2]Infection (notably viral infection such as SARS-CoV-2, tuberculosis)[2]
05

Safety considerations

Disruption may impair immune cell functions (NK cell cytotoxicity, antigen presentation)[5]May alter lysosome-dependent processes including degradation, signaling, and cellular metabolism—risks of broad intracellular dysregulation[3][5]
06

Interacting drugs

No specific drugs currently approved or commonly reported to directly target ARL8B[2][3][4]; however, it is emerging as a candidate for anti-cancer drug development[3].
07

Biomarkers

Tumor lysosome localization and secretion phenotypesExpression and localization of ARL8B in malignant tissuesCellular invasive potential correlated with ARL8B expression[3]

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