IndraLab

Statements

METTL3 activates USP4. 8 / 8
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"In prostate cancer, METTL3 remains the most studied m6A modification regulators, and METTL3 mediates m6A modification of USP4 mRNA at A2696 to promote prostate cancer invasion and metastasis (Chen et al., 2021[31])."
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"For example, metformin has been reported to improve the prognosis of patients with malignant tumours by inhibiting METTL3-mediated m A modification of THRAP3, RBM25, and USP4 mRNAs to repress their expression, hamper cell proliferation, and promote apoptosis (103)."
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"In androgen treatment-sensitive prostate cancer, METTL3 mediates m6A modification of USP4 mRNA at A2696, and m6A reader protein YTHDF2 binds to and induces degradation of USP4 mRNA, increasing the expression of Rho GDP dissociation inhibitor alpha (ARHGDIA) protein and promoting migration and invasion [182]."
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"METTL3 mediates m A modification of ubiquitin-specific peptidase 4 (USP4) mRNA at A2696, and m A reader protein YTHDF2 binds to and induces the degradation of USP4 mRNA by recruiting RNA-binding protein heterogeneous nuclear ribonucleoprotein D (HNRNPD) to the mRNA."
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"METTL3 promotes tumorigenesis and progression by m A modification of HDGF and ZMYM1 in GC, USP4 in GC, YAP in NSCLC, Notch1 in ESCC, Myc in BCa, BMI1 in OSCC, and CRB3 in CRC."
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"Mechanistically, METTL3 mediates the m A modification of the deubiquitinating enzyme USP4 RNA at A2696, which in turn promotes the binding of YTHDF2 and HNRNPD to USP4 RNA, leading to USP4 degradation."
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"It has been supposed that METTL3 writes m A modification at A2696 of USP4 mRNA, which is read by YTHDF2 and induces ubiquitin-specific peptidase 4 (USP4) mRNA degradation by recruiting the RNA-binding protein heterogeneous nuclear ribonucleoprotein D [HNRNPD]."
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"Chen et al. (Chen et al., 2021a) reported that YTHDF2 could recognize and degrade the abundance of m A-modified Ubiquitin Specific peptidase 4 (USP4) mRNA promoted by METTL3 in the PCa cells."
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