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Last update 08 May 2025

SNX10

Last update 08 May 2025

Basic Info

Synonyms

SNX10, sorting nexin 10, Sorting nexin-10

Introduction

Probable phosphoinositide-binding protein involved in protein sorting and membrane trafficking in endosomes. Plays a role in cilium biogenesis through regulation of the transport and the localization of proteins to the cilium. Required for the localization to the cilium of V-ATPase subunit ATP6V1D and ATP6V0D1, and RAB8A. Involved in osteoclast differentiation and therefore bone resorption.

Drugs associated with SNX10

DC-SX029

Target

PIKFYVE x SNX10

Mechanism

PIKFYVE inhibitors [+1]

Active Org.

Fudan University

Originator Org.

Fudan University

Active Indication

Inflammatory Bowel Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SNX10

100 Translational Medicine associated with SNX10

0 Patents (Medical) associated with SNX10

Literatures (Medical) associated with SNX10

02 Jun 2025·Journal of Cell Biology

Sorting nexin 10 regulates lysosomal ionic homeostasis via ClC-7 by controlling PI(3,5)P2

Article

Author: Pemberton, Joshua G. ; Freeman, Spencer A. ; Sasaki, Junko ; Bablani, Priya ; Grinstein, Sergio ; Sasaki, Takehiko ; Wu, Jing Ze ; Morioka, Shin ; Balla, Tamas

Mutations or ablation of Snx10 are associated with neurodegeneration, blindness, and osteopetrosis. The similarities between osteoclasts and macrophages prompted us to analyze the role of Snx10 in phagocytosis. Deletion of Snx10 impaired phagosome resolution. Defective resolution was caused by reduced Cl− accumulation within (phago)lysosomes, replicating the phenotype reported in macrophages lacking ClC-7, a lysosomal 2Cl−/H+ antiporter. Delivery of ClC-7 to (phago)lysosomes was unaffected by ablation of Snx10, but its activity was markedly depressed. Snx10 was found to regulate ClC-7 activity indirectly by controlling the availability of phosphatidylinositol 3,5-bisphosphate (PI[3,5]P2), which inhibits ClC-7. By limiting the formation of PI(3,5)P2, Snx10 enables the accumulation of luminal Cl− in phagosomes and lysosomes, which is required for their optimal degradative function. Our data suggest that Snx10 regulates the delivery of PI 3-phosphate (PI[3]P), the precursor of PI(3,5)P2, from earlier endocytic compartments to (phago)lysosomes. By controlling the traffic of phosphoinositides, Snx10 regulates phagosomal resolution and possibly accounts for the impaired bone resorption in Snx10-deficient osteoclasts.

05 May 2025·Journal of Cell Biology

SNX10 functions as a modulator of piecemeal mitophagy and mitochondrial bioenergetics

Article

Author: Simonsen, Anne ; Singh, Sakshi ; Pankiv, Serhiy ; Asp, Nagham Theres ; Mathai, Benan John ; Lapao, Ana ; Veroni, Chiara ; Schultz, Sebastian W. ; Trachsel-Moncho, Laura

We here identify the endosomal protein SNX10 as a negative regulator of piecemeal mitophagy of OXPHOS machinery components. In control conditions, SNX10 localizes to early endocytic compartments in a PtdIns3P-dependent manner and modulates endosomal trafficking but also shows dynamic connections with mitochondria. Upon hypoxia-mimicking conditions, SNX10 localizes to late endosomal structures containing selected mitochondrial proteins, including COX-IV and SAMM50, and the autophagy proteins SQSTM1/p62 and LC3B. The turnover of COX-IV was enhanced in SNX10-depleted cells, with a corresponding reduced mitochondrial respiration and citrate synthase activity. Importantly, zebrafish larvae lacking Snx10 show reduced levels of Cox-IV, as well as elevated ROS levels and ROS-mediated cell death in the brain, demonstrating the in vivo relevance of SNX10-mediated modulation of mitochondrial bioenergetics.

22 Apr 2025·Proceedings of the National Academy of Sciences

SNX10 deficiency impairs sensitivity to anti-HER2 antibody–drug conjugates via altering HER2 trafficking in HER2-positive breast cancer

Article

Author: Zhou, Yu-Jie ; Shao, Zhi-Ming ; Yu, Ke-Da ; Zhang, Qing-Hua ; Zhang, Zhong-Wei ; Liu, Cui-Cui ; Chen, Yu-Fei

Antibody–drug conjugates (ADCs) are a rapidly developing therapeutic approach in cancer treatment that has shown remarkable efficacy in breast cancer. Despite the promising efficacy of anti-HER2 ADCs, many patients are still experiencing disease progression under treatment. Here, by analyzing the transcriptome data from patient-derived organoid models, I-SPY2 trial, and resistant cell lines, we identified that SNX10 deficiency conferred anti-HER2 ADCs resistance in HER2-positive breast cancer. Low levels of SNX10 attenuated HER2 recycling and promoted HER2 trafficking into lysosomes. Furthermore, we found the underlying mechanism of SNX10 in HER2 traffic by regulating the endosomal RAB11A. We propose that SNX10 deficiency contributes to the inhibition of HER2 recycling as well as the decrease of cell-surface HER2 and causes anti-HER2 ADC resistance.

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