Tmem150a, also known as TM6P1 and damage-regulated autophagy modulator 5, is a transmembrane protein. It plays a crucial role 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. This function is related to Toll-like receptor 4 (TLR4) signaling pathways, and thus has implications for cellular homeostasis and immune-related processes [1,3,4]. Genetic models, such as gene knockout (KO) models, are valuable for studying its functions.

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, indicating its importance in cellular homeostasis [1]. In glioblastoma multiforme (GBM), overexpression of Tmem150a was observed in cancerous tissues. Suppressing Tmem150a expression in vitro inhibited GBM cell proliferation, migration, and invasion, suggesting its potential as a biomarker for poor prognosis in GBM patients [2].

In conclusion, Tmem150a is essential for regulating PI(4,5)P2 production and maintaining cellular homeostasis. Studies using KO or knockdown models have revealed its roles in cytokine regulation in epithelial cells and in the progression of glioblastoma multiforme. These findings contribute to our understanding of immune-related processes and cancer biology, potentially providing new directions for disease treatment and biomarker discovery.