Tmem150a, also known as TM6P1 and damage-regulated autophagy modulator 5, is a transmembrane protein that plays a crucial role in regulating phosphatidylinositol (4,5)-bisphosphate [PI(4,5)P2] production at the plasma membrane. It modifies the composition of the phosphatidylinositol 4-kinase enzyme complex, and this regulation is part of the Toll-like receptor 4 (TLR4) signaling pathway, which is important for the body's immune response [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 cellular homeostasis [1]. In glioblastoma multiforme (GBM), overexpression of Tmem150a was observed in cancerous tissues. Suppressing its expression inhibited GBM cell proliferation, migration, and invasion. Also, Tmem150a overexpression was associated with stromal, immune, and estimate scores, immune cells, cell markers, and RNA modifications, indicating its potential as a biomarker for poor prognosis in GBM [2].

In conclusion, Tmem150a is essential for maintaining PI(4,5)P2 homeostasis and cellular cytokine regulation. Gene knockdown models have revealed its significance in immune-related cytokine regulation and in the context of glioblastoma multiforme. Understanding Tmem150a function through these models provides insights into disease mechanisms and potential therapeutic targets for diseases such as GBM.