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gluconeogenic inhibitor 3 mpa  (MedChemExpress)
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METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and <t>siMETTL3+3-MPA</t> group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01
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METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and <t>siMETTL3+3-MPA</t> group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01
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mercaptopropionic acid mpa  (Aladdin Scientific Corporation)
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METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and <t>siMETTL3+3-MPA</t> group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01
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METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and <t>siMETTL3+3-MPA</t> group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01
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METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and <t>siMETTL3+3-MPA</t> group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01
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mpa solution (3- thiopropionic acid)  (Macklin Inc)
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Macklin Inc mpa solution (3- thiopropionic acid)
METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and <t>siMETTL3+3-MPA</t> group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01
Mpa Solution (3 Thiopropionic Acid), supplied by Macklin Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and siMETTL3+3-MPA group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01

Journal: Journal of Animal Science and Biotechnology

Article Title: METTL3 regulates Leydig cell proliferation via miR-145-PCK1 mediated gluconeogenesis in goats

doi: 10.1186/s40104-025-01307-5

Figure Lengend Snippet: METTL3 regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with siMETTL3 and siMETTL3+3-MPA group ( n = 5). B LCs were treated with siMETTL3 and siMETTL3+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Lactic acid level of LCs treated with siNC and siMETTL3+3-MPA for 24 h ( n = 4). D Glucose level of LCs treated with siMETTL3 and siMETTL3+3-MPA for 24 h ( n = 4). E Glucose uptake ability of LCs treated with siMETTL3 and siMETTL3+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. F – G Changes in mitochondrial membrane potential in LCs treated with siMETTL3 and siMETTL3+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. H The relative mRNA expression levels of METTL3 , PCK1 , CCNB1 and CCNE2 treated with siMETTL3 and siMETTL3+3-MPA ( n = 3). I – J The levels of METTL3, PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01

Article Snippet: To determine whether METTL3 induces proliferation through the gluconeogenic pathway, a 10 μmol/L dose of the gluconeogenic inhibitor 3-MPA (MCE, UK) was added 12 h after transfection along with siMETTL3, forming the siMETTL3 + 3-MPA group.

Techniques: Immunofluorescence, Membrane, Staining, Fluorescence, Expressing, Western Blot

miR-145-3p regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with Mimics-NC and Mimics-145-3p ( n = 5). B LCs were treated with Mimics-NC and Mimics-145-3p, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Glucose level of LCs treated with Mimics-NC and Mimics-145-3p ( n = 4). D Lactic acid level of LCs treated with Mimics-NC and Mimics-145-3p ( n = 4). E – F Glucose uptake ability of LCs treated with Mimics-NC and Mimics-145-3p, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. G – H Changes in mitochondrial membrane potential in LCs treated with Mimics-NC and Mimics-145-3p were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. I The relative mRNA expression levels of PCK1 , CCNB1 and CCNE2 treated with Mimics-NC and Mimics-145-3p ( n = 3). J – K The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). L Cell viability of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 5). M LCs were treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. N Glucose level of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 4). O Lactic acid level of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 4). P – Q Glucose uptake ability of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. R – S Changes in mitochondrial membrane potential in LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. T The relative mRNA expression levels of CCNB1 and CCNE2 treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 3). U – V The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01

Journal: Journal of Animal Science and Biotechnology

Article Title: METTL3 regulates Leydig cell proliferation via miR-145-PCK1 mediated gluconeogenesis in goats

doi: 10.1186/s40104-025-01307-5

Figure Lengend Snippet: miR-145-3p regulates goat LC proliferation through the glyconeogenesis pathway. A Cell viability of LCs treated with Mimics-NC and Mimics-145-3p ( n = 5). B LCs were treated with Mimics-NC and Mimics-145-3p, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. C Glucose level of LCs treated with Mimics-NC and Mimics-145-3p ( n = 4). D Lactic acid level of LCs treated with Mimics-NC and Mimics-145-3p ( n = 4). E – F Glucose uptake ability of LCs treated with Mimics-NC and Mimics-145-3p, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. G – H Changes in mitochondrial membrane potential in LCs treated with Mimics-NC and Mimics-145-3p were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. I The relative mRNA expression levels of PCK1 , CCNB1 and CCNE2 treated with Mimics-NC and Mimics-145-3p ( n = 3). J – K The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). L Cell viability of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 5). M LCs were treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. N Glucose level of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 4). O Lactic acid level of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 4). P – Q Glucose uptake ability of LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. R – S Changes in mitochondrial membrane potential in LCs treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. T The relative mRNA expression levels of CCNB1 and CCNE2 treated with Inhibitor-145-3p and Inhibitor-145-3p+3-MPA ( n = 3). U – V The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01

Article Snippet: To determine whether METTL3 induces proliferation through the gluconeogenic pathway, a 10 μmol/L dose of the gluconeogenic inhibitor 3-MPA (MCE, UK) was added 12 h after transfection along with siMETTL3, forming the siMETTL3 + 3-MPA group.

Techniques: Immunofluorescence, Membrane, Staining, Fluorescence, Expressing, Western Blot

PCK1 regulates goat Leydig cell proliferation through the gluconeogenesis pathway. A The relative mRNA expression levels of PCK1 , CCNB1 and CCNE2 treated with OE-NC and OE-PCK1 ( n = 3). B – C The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). D The relative mRNA expression levels of PCK1 , CCNB1 and CCNE2 treated with siNC and siPCK1 ( n = 3). E – F The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). G Cell viability of LCs treated with OE-PCK1 and OE-PCK1+3-MPA group ( n = 5). H LCs were treated with OE-PCK1 and OE-PCK1+3-MPA group, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. I Glucose level of LCs treated with OE-PCK1 and OE-PCK1+3-MPA ( n = 4). J Lactic acid of LCs treated with OE-PCK1 and OE-PCK1+3-MPA ( n = 4). K–L Glucose uptake ability of LCs treated with OE-PCK1 and OE-PCK1+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. M–N Changes in mitochondrial membrane potential in LCs treated with OE-PCK1 and OE-PCK1+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. O The relative mRNA expression levels of CCNB1 and CCNE2 treated with OE-PCK1 and OE-PCK1+3-MPA ( n = 3). P – Q The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01

Journal: Journal of Animal Science and Biotechnology

Article Title: METTL3 regulates Leydig cell proliferation via miR-145-PCK1 mediated gluconeogenesis in goats

doi: 10.1186/s40104-025-01307-5

Figure Lengend Snippet: PCK1 regulates goat Leydig cell proliferation through the gluconeogenesis pathway. A The relative mRNA expression levels of PCK1 , CCNB1 and CCNE2 treated with OE-NC and OE-PCK1 ( n = 3). B – C The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). D The relative mRNA expression levels of PCK1 , CCNB1 and CCNE2 treated with siNC and siPCK1 ( n = 3). E – F The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). G Cell viability of LCs treated with OE-PCK1 and OE-PCK1+3-MPA group ( n = 5). H LCs were treated with OE-PCK1 and OE-PCK1+3-MPA group, and EdU (green) was used to label the proliferating cells. The cell nuclei were counterstained with DAPI ( n = 4). Scale bar: 100 μm. I Glucose level of LCs treated with OE-PCK1 and OE-PCK1+3-MPA ( n = 4). J Lactic acid of LCs treated with OE-PCK1 and OE-PCK1+3-MPA ( n = 4). K–L Glucose uptake ability of LCs treated with OE-PCK1 and OE-PCK1+3-MPA, assessed using immunofluorescence and quantitative analysis ( n = 4). Scale bar: 100 μm. M–N Changes in mitochondrial membrane potential in LCs treated with OE-PCK1 and OE-PCK1+3-MPA were analyzed by JC-1 staining and the fluorescence intensity of JC-1 aggregates/monomers was quantified ( n = 4). Scale bar: 100 μm. O The relative mRNA expression levels of CCNB1 and CCNE2 treated with OE-PCK1 and OE-PCK1+3-MPA ( n = 3). P – Q The levels of PCK1, CCNB1, CCNE2 and β-actin were assessed via Western blotting. Relative protein levels were analysed via gray scanning ( n = 3). * P < 0.05, ** P < 0.01

Article Snippet: To determine whether METTL3 induces proliferation through the gluconeogenic pathway, a 10 μmol/L dose of the gluconeogenic inhibitor 3-MPA (MCE, UK) was added 12 h after transfection along with siMETTL3, forming the siMETTL3 + 3-MPA group.

Techniques: Expressing, Western Blot, Immunofluorescence, Membrane, Staining, Fluorescence