Transmembrane protein 215 (TMEM215)

Transmembrane protein 215 (TMEM215) is a two-pass transmembrane protein localized mainly to the endoplasmic reticulum membrane and is highly expressed in endothelial cells as well as some neuronal tissues[1][2]. TMEM215 plays a critical, nonredundant role in regulating endothelial cell survival by inhibiting apoptosis: its knockdown results in pronounced endothelial cell death, leading to vessel regression and impaired angiogenesis[1][2]. Mechanistically, TMEM215 forms a complex with BiP and BIK to prevent excessive Ca2+ transfer from the ER to mitochondria via mitochondria-associated membranes (MAMs), thereby limiting mitochondrial Ca2+ overload and activation of apoptotic pathways[1]. In mouse models, loss of TMEM215 in endothelial cells disrupts vascular remodeling and inhibits tumor angiogenesis and metastasis by promoting endothelial apoptosis and reducing vessel density[1]. TMEM215 is not currently considered a pharmacological or clinical therapeutic target, and no drugs are known to modulate its function[1][2][3].

Other names

TMEM215transmembrane protein 215

modulation of endothelial apoptosis mediated by TMEM215 expression, via BiP and BIK interactions at the ER-mitochondria interface[1]