Tmem150a, also known as TM6P1 and damage-regulated autophagy modulator 5, is a transmembrane protein. It is involved in regulating phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P2] production at the plasma membrane by modifying the composition of the phosphatidylinositol 4-kinase enzyme complex, which is related to Toll-like receptor 4 (TLR4) signaling pathway and is important for cellular homeostasis [1,3,4].

Knockdown of Tmem150a in TLR4-expressing epithelial cells led to increased levels of lipopolysaccharide (LPS)-induced cytokine secretion and transcript levels. In a lung epithelial cell line (H292), Tmem150a knockdown also increased cytokine levels in unstimulated conditions, suggesting its role in maintaining cellular balance [1]. In glioblastoma multiforme (GBM), overexpression of Tmem150a was observed in cancerous tissues, correlated with poor prognostic indicators. Suppressing Tmem150a expression in vitro inhibited GBM cell proliferation, migration, and invasion, and was associated with immune status and RNA modifications [2].

In conclusion, Tmem150a plays a crucial role in regulating PI(4,5)P2 production and cellular homeostasis. Studies with Tmem150a knockdown models have revealed its significance in cytokine regulation and in GBM, providing insights into its role in disease-related biological processes. This helps in understanding the underlying mechanisms and may offer potential targets for disease treatment [1,2].