Methyltransferase-like protein 17 (METTL17)

Methyltransferase-like protein 17 (METTL17) is a mitochondrial protein and member of the methyltransferase superfamily, mainly acting as a ribosome assembly factor for the mitochondrial small ribosomal subunit. It binds 4Fe-4S clusters and interacts with mitochondrial 12S rRNA and small ribosomal subunit proteins, playing a vital role in methylation modifications on mitochondrial RNAs (such as m^4C, m^5C on rRNA; m^3C, m^7G on tRNA; and m^6A on mRNA), which are crucial for efficient mitochondrial translation and respiratory chain activity[1][2][4][5]. METTL17 has also been reported to function as a transcriptional coactivator for estrogen receptors (ERα and ERβ) in breast cancer cells, enhancing transcriptional activity and promoting cancer cell proliferation[1]. Loss of METTL17 impairs mitochondrial protein translation, disrupts energy metabolism, increases susceptibility to ferroptosis, and inhibits tumor growth in colorectal cancer, making it a promising therapeutic target for cancer intervention[1][3]. Evidence suggests METTL17 may have lost classical methyltransferase activity but retains S-adenosylmethionine binding and ribosome assembly functions[2][4]. **Note:** No drugs, actionable biomarkers, or directly reported safety concerns are currently associated with METTL17. It is best classified as a mitochondrial assembly factor and epigenetic regulator with emerging implications in cancer biology and ferroptosis resistance.

Other names

METT11D1FLJ20859Methyltransferase 11 domain-containing protein 1False p73 target gene proteinProtein RSM22 homolog (mitochondrial)Ribosome assembly protein METTL17 (mitochondrial)