TMEM164 (F2M4W) Rabbit mAb #25484

Transmembrane protein 164 (TMEM164) is a member of the TMEM family of proteins that span the lipid bilayer of the plasma membrane and other cellular organelles (1). TMEM164 has been shown to act as a positive regulator of ferroptosis by selectively mediating autophagy-related 5 (Atg5)-dependent autophagosome formation during ferroptosis, rather than starvation. Induced by ferroptosis activators, such as RSL3, this TMEM164-dependent autophagosome formation results in the selective degradation of anti-ferroptosis regulators, including GPX4, FTH1, and lipid droplets (2). Additionally, TMEM164 has been identified as an acyltransferase involved in the synthesis of specific ether phospholipids which also contribute to ferroptosis (3).

High TMEM164 expression is associated with improved survival and increased immune cell infiltration in patients with pancreatic cancer (2), whereas expression is downregulated in lung cancer and associated with poor prognosis (4). Therefore, upregulation of TMEM164 as a therapeutic target can significantly inhibit cell proliferation, migration, and invasion. Notably, high TMEM164 expression combined with anti-PD-1 antibodies demonstrated synergistic anti-tumor effects in mouse models (4,5). TMEM164 overexpression was also shown to prevent the induction of neurotoxic reactive astrocytes, amyloid β deposition, neurodegeneration, and memory decline in the 5XFAD Alzheimer's disease mouse model (6).