Target intelligence / Profile preview

Transmembrane protein 242 (TMEM242)

Target
TMEM242
Molecular classification
Transmembrane protein, mitochondrial membrane protein, protein containing domain of unknown function (DUF1358)
01

Overview

Transmembrane protein 242 is a small mitochondrial protein, 141 amino acids in length, encoded by the TMEM242 gene located on chromosome 6q25.3[1]. TMEM242 has two transmembrane domains formed by alpha helices buried in the membrane, and the protein is highly expressed in several tissues, especially in the brain, heart, adrenal gland, and thyroid[1]. It localizes uniquely to the mitochondrial inner membrane and is involved in the assembly of ATP synthase by aiding the formation and integration of the c₈-ring and the incorporation of additional subunits (ATP6, ATP8, j, k) required for ATP synthase function[2]. TMEM242 also interacts with the mitochondrial complex I assembly (MCIA) complex, supporting the assembly of the membrane arm of complex I—another critical component of cellular respiration[2]. Although essential for efficient assembly of ATP synthase and complex I, TMEM242 is not itself considered a direct therapeutic target, nor have specific disease roles, drug interactions, or biomarker applications been documented in scientific literature to date[2]. The scientific community does not yet fully understand the biological function and regulatory mechanisms of TMEM242, nor is it currently established as a primary clinical target. TMEM242 remains a protein of interest for studying mitochondrial function, assembly of major respiratory complexes, and their role in organismal metabolism.

Other names
TMEM242C6orf35BM033HSPC287UPF0463 transmembrane protein C6orf35transmembrane protein 242
02

Biological functions

Assembly of mitochondrial ATP synthase (complex V)Assembly of mitochondrial respiratory complex IMitochondrial inner membrane integrationRegulation of proton motive force via ATP synthase assembly
03

Disease associations

Other (TMEM242 is implicated indirectly via dysfunction of ATP synthase or mitochondrial complex I, which are linked to mitochondrial diseases, but no direct disease association for TMEM242 has been established in current literature)

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