Target intelligence / Profile preview

Sorting nexin 13 (SNX13)

Target
SNX13
Molecular classification
Sorting nexin family (SNX), Regulator of G protein signaling (RGS) family, PX domain–containing protein, RGS domain–containing protein
01

Overview

Sorting nexin 13 (SNX13) is a multifunctional protein containing both PX (phosphoinositide-binding) and RGS (regulator of G protein signaling) domains, classifying it in both the sorting nexin and RGS protein families[1][2][3][5]. SNX13 acts as a molecular brake on cholesterol export from lysosomes and structures ER–lysosome contacts, contributing to the regulation of lipid homeostasis in cells[1]. It also serves as a GTPase activating protein specifically for Gαs, thus linking G protein–mediated signaling to vesicular trafficking processes[1][2]. SNX13 delays epidermal growth factor receptor degradation by regulating lysosomal trafficking, indicating a role in receptor sorting and lysosomal targeting[1][3]. Genetic deletion of SNX13 in mice leads to severe developmental abnormalities and embryonic lethality, primarily due to disrupted endosomal-lysosomal trafficking and nutrient uptake[3]. While SNX13 is critical to cellular homeostasis and development, there are currently no known drugs or clinical biomarkers that target or utilize this molecule[1][2][3].

Other names
RGS-PX1KIAA0713sorting nexin-13RGS domain- and PHOX domain-containing proteinSNX13
02

Mechanism of action

Not applicable (no drugs directly targeting SNX13 are described)

03

Biological functions

Intracellular traffickingEndosome homeostasisRegulation of endocytic traffickingRegulation of receptor degradation (e.g., epidermal growth factor receptor)GTPase activating activity for Gαs (a G protein subunit)Modulation of ER–lysosome membrane contact sitesNegative regulation of cholesterol egress from lysosomesPossible roles in negative regulation of cardiac muscle cell apoptosis (ortholog studies)
04

Disease associations

Developmental disorders (lethality in knockout mice due to defects in nutrient transport, neural tube closure, vasculogenesis, and placenta formation)Spinocerebellar Ataxia, Autosomal Recessive 20Dermatosis Papulosa NigraPotential involvement in disorders of lipid/cholesterol homeostasis
05

Safety considerations

Essential for embryonic development (systemic knockout is embryonically lethal in mice, suggesting that complete inhibition would have major developmental toxicity)Potential impact on endosomal/lysosomal trafficking and cell nutrient uptake if altered pharmacologically

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