Target intelligence / Profile preview

Methyltransferase-like protein 25 (METTL25)

Target
METTL25
Molecular classification
Enzyme (Methyltransferase; member of methyltransferase-like gene family), Other: Seven-beta-strand methyltransferase superfamily (based on protein structure)
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Overview

Methyltransferase-like protein 25 (METTL25) is a predicted protein methyltransferase in humans, encoded by the METTL25 gene (HGNC:26228). It belongs to the methyltransferase-like gene family, which is structurally defined by the presence of an S-adenosylmethionine (SAM)-binding domain and a characteristic seven-beta-strand motif[1][3][5][6][9]. METTL25 is phylogenetically related to METTL25B, an RNA-modifying enzyme that methylates rRNA. However, the precise biochemical substrate, cellular localization, and physiological function of METTL25 remain uncharacterized. It is predicted to participate in methylation reactions and may play a role in epigenetic regulation analogous to other METTL family members[1][3][5][6][9]. Disease associations are limited, with current annotations referencing immunodeficiency-centromeric instability-facial anomalies syndrome[3]. No specific drugs, biomarkers, or safety issues are reported for METTL25. Additional experimental investigations are necessary to clarify its function and relevance as a therapeutic target.

Other names
C12orf26FLJ22789Probable methyltransferase-like protein 25Putative methyltransferase-like protein 25Methyltransferase-like 25
02

Mechanism of action

Null. No established drugs, therefore mechanism of action is not known or characterized

03

Biological functions

Methylation (predicted enzymatic transfer of methyl groups to acceptor molecules)Likely involved in RNA methylation (inferred from phylogenetic similarity to METTL25B which methylates rRNA; exact function uncharacterized)Other: Epigenetic regulation (potential function inferred by analogy to other methyltransferases)
04

Disease associations

Immunodeficiency-centromeric instability-facial anomalies syndrome (disease association based on gene annotation)Other: No confirmed roles in other specific diseases, but gene family members often implicated in cancer, neurological, and developmental diseasesNo strong experimental evidence for direct disease causality to date

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