Additional file 1 of METTL3-mediated m6A modification of SIRT1 mRNA inhibits progression of endometriosis by cellular senescence enhancing
This study identified primers and siRNA sequences used to investigate METTL3-mediated m6A modification of SIRT1 mRNA and its role in inhibiting endometriosis progression through cellular senescence enhancement.
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References (43)
- Abnormal activation of the sonic hedgehog signaling pathway in endometriosis and its diagnostic potency via openalex
- Association between endometriosis and gynecological cancers: a critical review of the literature via openalex
- CPEB3, an RNA-Binding Protein, Modulates the Behavior of Endometriosis-Derived Stromal Cells via Regulating CXCL12 via openalex
- Cross-Talk between N6-Methyladenosine and Their Related RNAs Defined a Signature and Confirmed m6A Regulators for Diagnosis of Endometriosis via openalex
- Endometriosis via openalex
- Experimental Endometriosis via openalex
- FTO-dependent N(6)-Methyladenosine regulates the progression of endometriosis via the ATG5/PKM2 Axis via openalex
- Inhibition of METTL3/m6A/<i>miR126</i> promotes the migration and invasion of endometrial stromal cells in endometriosis via openalex
- Pathogenesis of endometriosis: Interaction between Endocrine and inflammatory pathways via openalex
- Pathogenesis of endometriosis: the genetic/epigenetic theory via openalex
- Role of SIRT1 and Progesterone Resistance in Normal and Abnormal Endometrium via openalex
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- last seen: 2026-05-11T08:33:08.643147+00:00