Target intelligence / Profile preview

Gamma-aminobutyric acid receptor-associated protein-like 1 (GABARAPL1)

Target
GABARAPL1
Molecular classification
Ubiquitin-like modifier, Autophagy-related protein, Trafficking-associated protein, Other
01

Overview

Gamma-aminobutyric acid receptor-associated protein-like 1 (GABARAPL1) is a ubiquitin-like protein involved in autophagy and receptor trafficking. Highly conserved across species, it belongs to the GABARAP/Atg8 protein family and is essential for autophagic vacuole formation and regulation of mitochondrial quality. GABARAPL1 interacts with the GABA(A) receptor and kappa opioid receptor, modulating their trafficking to the plasma membrane[1][2][3][4]. Experimentally, decreased GABARAPL1 impairs autophagic flux, increases cell proliferation and invasion (notably in breast cancer models), and disturbs mitochondrial homeostasis[1]. GABARAPL1 also plays a tumor suppressor role, and its reduced expression is linked to more aggressive cellular phenotypes and altered mitochondrial metabolism in certain cancers[1]. Additionally, changes in GABARAPL1 expression are observed in neurodegenerative and muscular diseases, reflecting its role in cellular response to stress and protein/organelle turnover[1][4]. No clinical drugs directly target GABARAPL1 at this time, but the protein represents a key node in autophagy regulation and disease-related cellular processes.

Other names
GEC1APG8LATG8LATG8BEarly estrogen-regulated proteinGABA(A) receptor-associated protein-like 1Glandular epithelial cell protein 1APG8-LIKEATG8GEC-1gec1
02

Mechanism of action

Not drug-targeted at present; biologically, modulates receptor trafficking and autophagic degradation

03

Biological functions

Autophagy (specifically macroautophagy and autophagic flux)Receptor trafficking (notably of GABA(A) and kappa opioid receptors)Regulation of cell proliferation and invasionMitochondrial homeostasis and metabolismMicrotubule binding and assembly
04

Disease associations

Cancer (tumor suppressor in breast cancer)Neurodegenerative disease (e.g., altered in Parkinson disease)Muscular disease (e.g., reduced in Duchenne muscular dystrophy)Other (potential roles in additional pathologies due to altered autophagy)
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Safety considerations

Not applicable due to lack of direct drug targeting; potential challenges if targeted could relate to perturbation of autophagy or mitochondrial homeostasis
06

Biomarkers

Low expression in breast cancer may indicate worse prognosisAltered expression in neurodegenerative and muscle diseases may serve as a marker

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