4.5 Review

m6A modification and its role in neural development and neurological diseases

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SPI1-induced downregulation of FTO promotes GBM progression by regulating pri-miR-10a processing in an m6A-dependent manner

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Ziying Yu et al.

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The RNA m6A writer METTL14 in cancers: Roles, structures, and applications

Huimin Zhou et al.

Summary: m(6)A modification is the most abundant and diverse epigenetic modification of mRNAs in eukaryotes, regulating biological metabolism, cell differentiation, and responses to diseases. METTL3 and METTL14 are key components of the m(6)A writer complex, with METTL14 crucial for complex integrity and recognizing special RNA substrates, and its roles in cancer are currently being extensively reviewed.

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The m6A RNA Demethylase ALKBH5 Promotes Radioresistance and Invasion Capability of Glioma Stem Cells

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METTL3-dependent RNA m6A dysregulation contributes to neurodegeneration in Alzheimer's disease through aberrant cell cycle events

Fanpeng Zhao et al.

Summary: The study revealed that decreased m(6)A levels and reduced expression of METTL3 in AD brains led to memory deficits, synaptic loss, neuronal death, and multiple cellular alterations. Restoring m(6)A modification by inhibiting demethylation or overexpressing METTL3 rescued synaptic damage, cognitive impairment, and neuronal deficits in AD models.

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Genome-Wide Detection of m6A-Associated Genetic Polymorphisms Associated with Ischemic Stroke

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Identification of IGF2BP3 as an Adverse Prognostic Biomarker of Gliomas

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Small-Molecule Inhibitors of the RNA M6A Demethylases FTO Potently Support the Survival of Dopamine Neurons

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METTL3 enhances the stability of MALAT1 with the assistance of HuR via m6A modification and activates NF-κB to promote the malignant progression of IDH-wildtype glioma

Yu-Zhou Chang et al.

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m6A modification of RNA and its role in cancer, with a special focus on lung cancer

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Conditional deficiency of m6A methyltransferase Mettl14 in substantia nigra alters dopaminergic neuron function

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YTHDF2 facilitates UBXN1 mRNA decay by recognizing METTL3-mediated m6A modification to activate NE-κB and promote the malignant progression of glioma

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