Eva-1 homolog A, regulator of programmed cell death (EVA1A)

Eva-1 homolog A, regulator of programmed cell death (EVA1A), is a highly conserved type I transmembrane protein encoded by the EVA1A gene and known by several aliases including TMEM166 and FAM176A[2][3][6]. EVA1A localizes mainly to the endoplasmic reticulum and lysosomes[1], where it functions as a dual regulator of autophagy and apoptosis[1][2]. It plays a critical role in autophagosome formation by interacting with the ATG16L1 protein complex through its C-terminal domain, acting downstream of the BECN1 complex[1]. EVA1A is expressed in a tissue- and cell-type specific manner and is notably downregulated in several human cancers, where its restoration inhibits tumor cell proliferation through the induction of autophagy and apoptosis, often making it a candidate tumor suppressor[1][2]. Gene therapy approaches using EVA1A (Ad5-EVA1A) have been explored for their anti-tumor activities in vivo and in vitro[2]. Beyond cancer, disruptions in EVA1A activity or expression are associated with neurodevelopmental and metabolic disorders, highlighting its broader biological significance[3].

Other names

Protein eva-1 homolog AFAM176ATMEM166Transmembrane protein 166SP24FLJ13391Protein FAM176AFamily with sequence similarity 176, member A

Induces autophagy and apoptosis in tumor cells (gene therapy approach); Promotes the recruitment of the ATG12–ATG5/ATG16L1 complex to autophagic membranes to stimulate autophagosome formation