Cited by 4,106RNA modifications and cancerEpigenetics and DNA MethylationRNA regulation and disease

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N6-Methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO

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Jia, Guifang, Fu, Ye, Zhao, Xu, Dai, Qing, Zheng, Guanqun, Yang, Ying, Yi, Chengqi, Lindahl, Tomas, Pan, Tao, Yang, Yun-Gui, He, Chuan·2011·Nature Chemical Biology

DOI 10.1038/nchembio.687PMC PMC3218240

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Abstract

We report here that fat mass and obesity-associated protein (FTO) has efficient oxidative demethylation activity targeting the abundant N6-methyladenosine (m(6)A) residues in RNA in vitro. FTO knockdown with siRNA led to increased amounts of m(6)A in mRNA, whereas overexpression of FTO resulted in decreased amounts of m(6)A in human cells. We further show the partial colocalization of FTO with nuclear speckles, which supports the notion that m(6)A in nuclear RNA is a major physiological substrate of FTO.

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“Actually, our previous work showed that FTO, the first identified m 6 A demethylase (Jia et al, 2011), is strongly associated with obesity and metabolic disorders (Church et al, 2009; Fischer et al, 2009).”
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Self-citation
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“Here we describe a novel HTS approach to identify inhibitors of RNA-modifying enzymes, and the use of this assay to identify inhibitors of fat mass and obesity-associated protein (FTO), an enzyme that exhibits m6A-demethylating activity (Jia et al., 2011).”
BackgroundMethodResultInfluential
Structural Chemistry of Human RNA Methyltransferases
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Mettl14 is required for mouse postimplantation development by facilitating epiblast maturation
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“…(FTO) and ALKBH5 have been shown to act as m 6 A demethylases, it is commonly accepted that m 6 A modifications are reversible in mammalian cells (Jia et al., 2011; Zheng et al., 2013), evoking the biological implications of the dynamic m 6 A modification, which is incompletely understood in…”
Self-citation
Meclofenamic Acid Reduces Reactive Oxygen Species Accumulation and Apoptosis, Inhibits Excessive Autophagy, and Protects Hair Cell-Like HEI-OC1 Cells From Cisplatin-Induced Damage
Li, H., Song, Y., He, Z., Chen, X., Wu, X., Li, X., Bai, X., Liú, W., Li, B., Wang, S., et al. (2018) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2018.00139 · Cited by 89
“…demethylation of nucleotide bases, and the knockdown of FTO leads to increased amounts of m6A in mRNA, whereas overexpression of FTO results in Frontiers in Cellular Neuroscience | www.frontiersin.org 10 May 2018 | Volume 12 | Article 139 decreased amounts of m6A in human cells (Jia et al., 2011).”
MTCH2 promotes adipogenesis in intramuscular preadipocytes via an m 6 A‐YTHDF1‐dependent mechanism
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Metal–Organic Framework Showing Selective and Sensitive Detection of Exogenous and Endogenous Formaldehyde
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The N 6 ‐methyladenosine (m 6 A) erasers alkylation repair homologue 5 (ALKBH5) and fat mass and obesity‐associated protein (FTO) are prognostic biomarkers in patients with clear cell renal carcinoma
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Decreased ALKBH5, FTO, and YTHDF2 in Peripheral Blood Are as Risk Factors for Rheumatoid Arthritis
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The role of M6A modification in the regulation of tumor-related lncRNAs
Lan, Y., Liu, B., & Guo, H. (2021) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2021.04.002 · Cited by 86

Authors: Jia, G., Fu, Y., Zhao, X., Dai, Q., Zheng, G., Yang, Y., Yi, C., Lindahl, T., Pan, T., Yang, Y.-G., & He, C.
Affiliations: University of Chicago (US)
Chinese Academy of Sciences (CN)
Cancer Research UK (GB)
Corresponding author: He, Chuan
ORCID: Jia, Guifang
Fu, Ye
Dai, Qing
Yang, Ying
Yi, Chengqi
Lindahl, Tomas
Pan, Tao
Yang, Yun-Gui
He, Chuan
Venue: Nature Chemical Biology
Publisher: Springer Science and Business Media LLC
Published: 2011-10-16
Volume: 7
Issue: 12
Pages: 885-887
ISSN: 1552-4450 (ISSN-L)
1552-4469
DOI: 10.1038/nchembio.687
PMC: PMC3218240
OpenAlex: W2071930821
Cited by: 4,106
References: 27
Citations by year: 2026: 272 · 2025: 416 · 2024: 473 · 2023: 489 · 2022: 546 · 2021: 544 · 2020: 341 · 2019: 217 · 2018: 218 · 2017: 159 · 2016: 109 · 2015: 107 · 2014: 94 · 2013: 67 · 2012: 45
FWCI: 26.98
Type: journal article
Language: en
Update notices: erratum (2012-11-26)
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Nature Chemical Biology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute of General Medical Sciences (GM071440, R01GM071440, R01GM088599, GM088599)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA modifications and cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA regulation and disease
Keywords: N6-methyladenosine, m6A demethylation, FTO, nuclear RNA, RNA modification, oxidative demethylation, nuclear speckles, obesity, RNA metabolism
MeSH terms: Alpha-Ketoglutarate-Dependent Dioxygenase FTO, Adenosine, Cell Nucleus, HeLa Cells, Humans, Methylation, Obesity, Oxidation-Reduction, Proteins, RNA, Messenger, Substrate Specificity

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N6-Methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO

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