1.14.11.53: mRNA N6-methyladenine demethylase
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For detailed information about mRNA N6-methyladenine demethylase, go to the full flat file.
Word Map on EC 1.14.11.53
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1.14.11.53
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demethylation
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demethylases
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mettl14
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reader
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writer
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erasers
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ythdf1
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methyltransferases
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epitranscriptomic
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m6a-related
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fto-mediated
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m6a-dependent
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hnrnpa2b1
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methyltransferase-like
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hnrnpc
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lasso
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m6a-modified
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igf2bp1
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merip
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merip-seq
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m6a-binding
- 1.14.11.53
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demethylation
- demethylases
- mettl14
-
reader
-
writer
-
erasers
-
ythdf1
- methyltransferases
-
epitranscriptomic
-
m6a-related
-
fto-mediated
-
m6a-dependent
-
hnrnpa2b1
-
methyltransferase-like
-
hnrnpc
-
lasso
-
m6a-modified
-
igf2bp1
-
merip
-
merip-seq
-
m6a-binding
Reaction
Synonyms
AlkB homolog 5, ALKBH10B, ALKBH5, ALKBH5 demethylase, ALKBH9B, alkylation repair homolog protein 5, fat mass and obesity-associated enzyme, fat mass and obesity-associated protein, FTO, m6A mRNA demethylase, m6A RNA demethylase, m6A-RNA demethylase, N6-methyladenosine demethylase, RNA N6-methyladenine demethylase
ECTree
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analysis
development of a single-quantum-dot-based fluorescence resonance energy transfer (FRET) sensor for the identification of specific FTO demethylase inhibitors. The FTO-mediated demethylation of m6A can induce the cleavage of demethylated DNA to generate the biotinylated DNA fragments, which may function as capture probes to assemble the Cy5-labeled reporter probes onto the quantum dot surface, enabling the occurrence of FRET between the quantum dot and Cy5
medicine
synthesis
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visible-light-induced oxidation of m6ARNA is performed in live cells under atmospheric O2 by applying the metabolite flavin mononucleotide (FMN) as an efficient photosensitizer
FTO is up-regulated in human breast cancer. High level of FTO is significantly associated with lower survival rates in patients with breast cancer. FTO promotes breast cancer cell proliferation, colony formation and metastasis in vitro and in vivo. BNIP3, a pro-apoptosis gene, is a downstream target of FTO-mediated m6A modification. BNIP3 acts as a tumor suppressor and is negatively correlated with FTO expression in clinical breast cancer patients. BNIP3 dramatically alleviates FTO-dependent tumor growth retardation and metastasis
medicine
FTO level is increased in human melanoma. Knockdown of FTO increases m6A methylation in critical protumorigenic melanoma cell-intrinsic genes including PD-1, CXCR4, and SOX10, leading to increased RNA decay through the m6A reader YTHDF2. Knockdown of FTO sensitizes melanoma cells to interferon gamma
medicine
FTO mRNA and protein levels are overexpressed in non-small cell lung cancer tissues and cell lines, associated with a reduced m6A content. FTO loss-of-function mutations reduce the proliferation rate of cancer cells. FTO knockdown also inhibits the colony formation ability of lung cancer cells. FTO knockdown reduces lung cancer cells growth in vivo. FTO decreases the m6A level and increases mRNA stability of ubiquitin-specific protease (USP7), which relies on the demethylase activity of FTO. USP7 mRNA level is overexpressed in human lung cancer tissues and USP7 expression was positively correlated with FTO mRNA level
medicine
FTO nhances melanoma tumorigenesis in mice. Knockdown of FTO increases m6A methylation in critical protumorigenic melanoma cell-intrinsic genes including PD-1, CXCR4, and SOX10, leading to increased RNA decay through the m6A reader YTHDF2. Knockdown of FTO sensitizes melanoma cells to interferon gamma and sensitizes melanoma to anti-PD-1 treatment in mice
medicine
substrate NEAT1 is a potential binding long noncoding lncRNA of ALKBH5. NEAT1 is overexpressed in gastric cancer cells and tissue. Knockdown of NEAT1 significantly represses invasion and metastasis of gastric cancer cells. ALKBH5 affects the m6A level of NEAT1. The binding of ALKBH5 and NEAT1 influences the expression of EZH2 (a subunit of the polycomb repressive complex) and thus affects gastric cancer invasion and metastasis