N6-adenosine-methyltransferase subunit METTL14 (EC 2.1.1.62; UniProt Q9HCE5; also known as m6A methyltransferase METTL14, Methyltransferase-like protein 14) is encoded by the METTL14 (also known as KIAA1627) gene (Gene ID 57721) in human. N(6)-Methyladenosine (m(6)A) represents the most prevalent internal modification in messenger and long noncoding RNAs. This reversible modification is installed by the m(6)A methylation "writers" and remomved by demethylases that serve as "erasers. In addition, methyl-specific binding proteins, primarily of the YTH-domain family, function as "readers" and mediate the effect by binding to modified transcripts. METTL14 is a component of the nuclear methyltransferase complex (writers) composed of METTL3, METTL14, and WTAP. At least 2 demethylases (erasers), ALKBH5 and FTO, that can catalyze the reverse reaction. The roles of m(6)A in cell fates regulation and embryonic development highlight the existence of another layer of epigenetic regulation at the RNA level.
Specificity
The immunogen sequence is present in human METTL14 (UniProt Q9HCE5) and both of murine METTL14 spliced isoforms (Uniprot Q3UIK4).
Immunogen
KLH-conjugated linear peptide corresponding to an internal sequence from the C-terminal half of human METTL14.
Application
This Anti-METTL14 Antibody is validated for use in Western Blotting for the detection of METTL14.
Quality
Evaluated by Western Blotting in Raji nuclear extract.
Western Blotting Analysis: 0.5 µg/mL of this antibody detected METTL14 in 10 µg of Raji nuclear extract.
Target description
~56 kDa observed. 52.15 kDa (human), 52.12/40.72 kDa (mouse isoform 1/2) calculated. Uncharacterized band(s) may appear in some lysates.
Other Notes
Concentration: Please refer to lot specific datasheet.
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N6-methyladenosine (m6A) modification of RNA influences fundamental aspects of RNA metabolism and m6A dysregulation is implicated in various human diseases. In this study, we explored the potential role of RNA m6A modification in the pathogenesis of Alzheimer disease (AD). We
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