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Transmembrane protein 164 (TMEM164)
- Target
- TMEM164
- Molecular classification
- Transmembrane protein, Other
01
Overview
Transmembrane protein 164 (TMEM164) is a conserved protein localized to various cellular membranes. It acts as a positive regulator of ferroptosis by selectively mediating the formation of ATG5-dependent autophagosomes under ferroptosis-inducing (but not starvation) conditions. TMEM164 facilitates the autophagic degradation of ferritin, GPX4, and lipid droplets, which increases intracellular iron levels and lipid peroxidation, ultimately promoting ferroptotic cell death. This protein has emerging importance in cancer biology, where high expression correlates with better survival and immune infiltration in pancreatic ductal adenocarcinoma. TMEM164 is also implicated in genetic syndromes involving Xq22.3q23 microdeletion and may play a role in tissue-specific pathology. No drugs currently target TMEM164 directly, but its activity modulates cellular sensitivity to ferroptosis-inducing reagents.
02
Mechanism of action
Promotion of ferroptosis via autophagy-dependent degradation of GPX4, ferritin, and lipid droplets; Enhancement of ATG5-dependent autophagosome assembly under ferroptosis-inducing conditions
03
Biological functions
Positive regulation of ferroptosisPromotion of ATG5-dependent autophagosome formation (during ferroptosis)Regulation of iron accumulation and lipid peroxidationSelective degradation of ferritin, GPX4, and lipid droplets (during ferroptosis)
04
Disease associations
Cancer (notably pancreatic ductal adenocarcinoma)Genetic disorders (associated with Xq22.3q23 microdeletions causing syndromic diseases including intellectual disability, midfacial hypoplasia, elliptocytosis, and Alport syndrome)
05
Safety considerations
Potential issues if targeted therapeutically may include unintended enhancement or inhibition of cell death pathways across multiple tissues, especially given TMEM164’s tissue expression (including pancreas and others). Clinical safety profile for modulation is unknown.
06
Interacting drugs
No approved drugs specifically target TMEM164; however, cells lacking TMEM164 show resistance to SLC7A11 inhibitors (erastin, sulfasalazine, sorafenib) and GPX4 inhibitors (RSL3, ML162, ML210). These drugs are primarily used as research tools to trigger ferroptosis, especially in cancer models.
07
Biomarkers
High TMEM164 mRNA expression serves as a biomarker for improved survival and increased immune cell infiltration in pancreatic ductal adenocarcinoma
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