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mtor activator mhy1485 (MedChemExpress)

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MedChemExpress mtor activator mhy1485

(A) Experimental timeline showing intravitreal injections of vehicle (1% DMSO), insulin + rapamycin (0.2 mg/mL and 20 µM, respectively), or <t>MHY1485</t> (100 µM) at 2, 3, and 4 days post-injury (dpi). Dendritic morphology and optic tectum reinnervation are quantified at 6 dpi. (B) Schematic of the insulin signaling pathway and pharmacological manipulations. Insulin activates mTORC2 and, via Akt signaling, mTORC1. Rapamycin selectively inhibits mTORC1, while MHY1485 selectively activates it. Green arrows indicate activation, and red blunt-ended lines indicate inhibition. (C) Representative sagittal retinal cryosections stained for phospho-S6 (pS6, Ser235/Ser236) and DAPI show comparable S6 phosphorylation in MHY1485-treated and vehicle-treated retinas at 3 dpi. Combined insulin and rapamycin treatment sharply reduces S6 phosphorylation in the retina. Scale bar = 25 µm. (D) Quantification of pS6–positive cells in the ganglion cell layer (GCL) shows a comparable percentage of pS6-positive cells in MHY1485-treated and vehicle-treated retinas, whereas combined insulin and rapamycin treatment results in almost no pS6-positive cells in the GCL. (E) Representative dendritic reconstructions at 6 dpi of cells from retinas treated with vehicle, combined insulin and rapamycin, or MHY1485. Combined insulin and rapamycin treatment results in dendritic complexity comparable to vehicle controls, whereas MHY1485-treated RGCs show increased dendritic complexity relative to vehicle-treated cells. Scale bar = 100 µm. (F) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) reveals that MHY1485 increases dendritic complexity relative to vehicle, whereas insulin + rapamycin does not significantly alter dendritic complexity compared with vehicle. (G) Representative coronal optic tectum sections following anterograde biocytin tracing. Biocytin visualization shows decreased tectal reinnervation after both combined insulin and rapamycin treatment or MHY1485 treatment compared with vehicle controls at 6 dpi. Scale bar = 200 µm. (H) Quantification of biocytin-positive area in the optic tectum disclose that both insulin plus rapamycin and MHY1485 treatments delay tectal reinnervation relative to vehicle. Data presented as median ± 95% confidence interval (D) or mean ± SD (F). Each dot represents one cell (D; N=52-63 cells sampled from n = 7 fish per group) or one fish (D; n = 4-5) (F; n = 7). One-way Kruskal-Wallis ANOVA with Tukey HSD post hoc tests (D, H) or one-way Welch ANOVA with Games–Howell multiple-comparisons test (F); exact p values are shown in the figure. Abbreviations: area under the curve (AUC); days post-injury (dpi); dorsal (D); insulin (Ins); ganglion cell layer (GCL); nasal (N); rapamycin (Rap); phospho-S6 (pS6, Ser235/Ser236); temporal (T); vehicle (Veh); ventral (V).

Mtor Activator Mhy1485, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 241 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 241 article reviews

mtor activator mhy1485 - by Bioz Stars, 2026-03

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1) Product Images from "Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration"

Article Title: Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration

Journal: bioRxiv

doi: 10.64898/2026.02.11.705324

(A) Experimental timeline showing intravitreal injections of vehicle (1% DMSO), insulin + rapamycin (0.2 mg/mL and 20 µM, respectively), or MHY1485 (100 µM) at 2, 3, and 4 days post-injury (dpi). Dendritic morphology and optic tectum reinnervation are quantified at 6 dpi. (B) Schematic of the insulin signaling pathway and pharmacological manipulations. Insulin activates mTORC2 and, via Akt signaling, mTORC1. Rapamycin selectively inhibits mTORC1, while MHY1485 selectively activates it. Green arrows indicate activation, and red blunt-ended lines indicate inhibition. (C) Representative sagittal retinal cryosections stained for phospho-S6 (pS6, Ser235/Ser236) and DAPI show comparable S6 phosphorylation in MHY1485-treated and vehicle-treated retinas at 3 dpi. Combined insulin and rapamycin treatment sharply reduces S6 phosphorylation in the retina. Scale bar = 25 µm. (D) Quantification of pS6–positive cells in the ganglion cell layer (GCL) shows a comparable percentage of pS6-positive cells in MHY1485-treated and vehicle-treated retinas, whereas combined insulin and rapamycin treatment results in almost no pS6-positive cells in the GCL. (E) Representative dendritic reconstructions at 6 dpi of cells from retinas treated with vehicle, combined insulin and rapamycin, or MHY1485. Combined insulin and rapamycin treatment results in dendritic complexity comparable to vehicle controls, whereas MHY1485-treated RGCs show increased dendritic complexity relative to vehicle-treated cells. Scale bar = 100 µm. (F) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) reveals that MHY1485 increases dendritic complexity relative to vehicle, whereas insulin + rapamycin does not significantly alter dendritic complexity compared with vehicle. (G) Representative coronal optic tectum sections following anterograde biocytin tracing. Biocytin visualization shows decreased tectal reinnervation after both combined insulin and rapamycin treatment or MHY1485 treatment compared with vehicle controls at 6 dpi. Scale bar = 200 µm. (H) Quantification of biocytin-positive area in the optic tectum disclose that both insulin plus rapamycin and MHY1485 treatments delay tectal reinnervation relative to vehicle. Data presented as median ± 95% confidence interval (D) or mean ± SD (F). Each dot represents one cell (D; N=52-63 cells sampled from n = 7 fish per group) or one fish (D; n = 4-5) (F; n = 7). One-way Kruskal-Wallis ANOVA with Tukey HSD post hoc tests (D, H) or one-way Welch ANOVA with Games–Howell multiple-comparisons test (F); exact p values are shown in the figure. Abbreviations: area under the curve (AUC); days post-injury (dpi); dorsal (D); insulin (Ins); ganglion cell layer (GCL); nasal (N); rapamycin (Rap); phospho-S6 (pS6, Ser235/Ser236); temporal (T); vehicle (Veh); ventral (V).

Figure Legend Snippet: (A) Experimental timeline showing intravitreal injections of vehicle (1% DMSO), insulin + rapamycin (0.2 mg/mL and 20 µM, respectively), or MHY1485 (100 µM) at 2, 3, and 4 days post-injury (dpi). Dendritic morphology and optic tectum reinnervation are quantified at 6 dpi. (B) Schematic of the insulin signaling pathway and pharmacological manipulations. Insulin activates mTORC2 and, via Akt signaling, mTORC1. Rapamycin selectively inhibits mTORC1, while MHY1485 selectively activates it. Green arrows indicate activation, and red blunt-ended lines indicate inhibition. (C) Representative sagittal retinal cryosections stained for phospho-S6 (pS6, Ser235/Ser236) and DAPI show comparable S6 phosphorylation in MHY1485-treated and vehicle-treated retinas at 3 dpi. Combined insulin and rapamycin treatment sharply reduces S6 phosphorylation in the retina. Scale bar = 25 µm. (D) Quantification of pS6–positive cells in the ganglion cell layer (GCL) shows a comparable percentage of pS6-positive cells in MHY1485-treated and vehicle-treated retinas, whereas combined insulin and rapamycin treatment results in almost no pS6-positive cells in the GCL. (E) Representative dendritic reconstructions at 6 dpi of cells from retinas treated with vehicle, combined insulin and rapamycin, or MHY1485. Combined insulin and rapamycin treatment results in dendritic complexity comparable to vehicle controls, whereas MHY1485-treated RGCs show increased dendritic complexity relative to vehicle-treated cells. Scale bar = 100 µm. (F) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) reveals that MHY1485 increases dendritic complexity relative to vehicle, whereas insulin + rapamycin does not significantly alter dendritic complexity compared with vehicle. (G) Representative coronal optic tectum sections following anterograde biocytin tracing. Biocytin visualization shows decreased tectal reinnervation after both combined insulin and rapamycin treatment or MHY1485 treatment compared with vehicle controls at 6 dpi. Scale bar = 200 µm. (H) Quantification of biocytin-positive area in the optic tectum disclose that both insulin plus rapamycin and MHY1485 treatments delay tectal reinnervation relative to vehicle. Data presented as median ± 95% confidence interval (D) or mean ± SD (F). Each dot represents one cell (D; N=52-63 cells sampled from n = 7 fish per group) or one fish (D; n = 4-5) (F; n = 7). One-way Kruskal-Wallis ANOVA with Tukey HSD post hoc tests (D, H) or one-way Welch ANOVA with Games–Howell multiple-comparisons test (F); exact p values are shown in the figure. Abbreviations: area under the curve (AUC); days post-injury (dpi); dorsal (D); insulin (Ins); ganglion cell layer (GCL); nasal (N); rapamycin (Rap); phospho-S6 (pS6, Ser235/Ser236); temporal (T); vehicle (Veh); ventral (V).

Techniques Used: Activation Assay, Inhibition, Staining, Phospho-proteomics

A) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) at 6dpi following vehicle, combined insulin and rapamycin or MHY1485 treatment. Cells treated with insulin and rapamycin exhibit a dendritic complexity comparable to vehicle controls across all morphotypes. MHY1485-treated cells showed preservation of dendritic complexity relative to vehicle controls at 6 dpi, particularly in the number of bifurcations across all morphotypes. Data presented as median ±95% confidence interval. Each dot represents one cell (N=52-63 cells sampled from n = 7 fish per group). One-way Kruskal-Wallis ANOVA with multiple comparisons followed by Mann–Whitney post hoc tests; p values are shown in the figure. Abbreviations: Area under the curve (AUC); days post-injury (dpi); insulin (Ins); rapamycin (Rap); vehicle (Veh)

Figure Legend Snippet: A) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) at 6dpi following vehicle, combined insulin and rapamycin or MHY1485 treatment. Cells treated with insulin and rapamycin exhibit a dendritic complexity comparable to vehicle controls across all morphotypes. MHY1485-treated cells showed preservation of dendritic complexity relative to vehicle controls at 6 dpi, particularly in the number of bifurcations across all morphotypes. Data presented as median ±95% confidence interval. Each dot represents one cell (N=52-63 cells sampled from n = 7 fish per group). One-way Kruskal-Wallis ANOVA with multiple comparisons followed by Mann–Whitney post hoc tests; p values are shown in the figure. Abbreviations: Area under the curve (AUC); days post-injury (dpi); insulin (Ins); rapamycin (Rap); vehicle (Veh)

Techniques Used: Preserving, MANN-WHITNEY

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Journal: bioRxiv

Article Title: Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration

doi: 10.64898/2026.02.11.705324

Figure Lengend Snippet: (A) Experimental timeline showing intravitreal injections of vehicle (1% DMSO), insulin + rapamycin (0.2 mg/mL and 20 µM, respectively), or MHY1485 (100 µM) at 2, 3, and 4 days post-injury (dpi). Dendritic morphology and optic tectum reinnervation are quantified at 6 dpi. (B) Schematic of the insulin signaling pathway and pharmacological manipulations. Insulin activates mTORC2 and, via Akt signaling, mTORC1. Rapamycin selectively inhibits mTORC1, while MHY1485 selectively activates it. Green arrows indicate activation, and red blunt-ended lines indicate inhibition. (C) Representative sagittal retinal cryosections stained for phospho-S6 (pS6, Ser235/Ser236) and DAPI show comparable S6 phosphorylation in MHY1485-treated and vehicle-treated retinas at 3 dpi. Combined insulin and rapamycin treatment sharply reduces S6 phosphorylation in the retina. Scale bar = 25 µm. (D) Quantification of pS6–positive cells in the ganglion cell layer (GCL) shows a comparable percentage of pS6-positive cells in MHY1485-treated and vehicle-treated retinas, whereas combined insulin and rapamycin treatment results in almost no pS6-positive cells in the GCL. (E) Representative dendritic reconstructions at 6 dpi of cells from retinas treated with vehicle, combined insulin and rapamycin, or MHY1485. Combined insulin and rapamycin treatment results in dendritic complexity comparable to vehicle controls, whereas MHY1485-treated RGCs show increased dendritic complexity relative to vehicle-treated cells. Scale bar = 100 µm. (F) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) reveals that MHY1485 increases dendritic complexity relative to vehicle, whereas insulin + rapamycin does not significantly alter dendritic complexity compared with vehicle. (G) Representative coronal optic tectum sections following anterograde biocytin tracing. Biocytin visualization shows decreased tectal reinnervation after both combined insulin and rapamycin treatment or MHY1485 treatment compared with vehicle controls at 6 dpi. Scale bar = 200 µm. (H) Quantification of biocytin-positive area in the optic tectum disclose that both insulin plus rapamycin and MHY1485 treatments delay tectal reinnervation relative to vehicle. Data presented as median ± 95% confidence interval (D) or mean ± SD (F). Each dot represents one cell (D; N=52-63 cells sampled from n = 7 fish per group) or one fish (D; n = 4-5) (F; n = 7). One-way Kruskal-Wallis ANOVA with Tukey HSD post hoc tests (D, H) or one-way Welch ANOVA with Games–Howell multiple-comparisons test (F); exact p values are shown in the figure. Abbreviations: area under the curve (AUC); days post-injury (dpi); dorsal (D); insulin (Ins); ganglion cell layer (GCL); nasal (N); rapamycin (Rap); phospho-S6 (pS6, Ser235/Ser236); temporal (T); vehicle (Veh); ventral (V).

Article Snippet: To enhance mTOR signaling activation, the mTOR activator MHY1485 (MCE, Cat# HY-B0795) , was administered by intravitreal injection at 2, 3, and 4 dpi using the same procedure described above, at a final injection concentration of 100 μM.

Techniques: Activation Assay, Inhibition, Staining, Phospho-proteomics

Journal: bioRxiv

Article Title: Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration

doi: 10.64898/2026.02.11.705324

Figure Lengend Snippet: A) Quantification of dendritic morphometrics (Sholl AUC, dendritic area, total dendritic length, and number of bifurcations) at 6dpi following vehicle, combined insulin and rapamycin or MHY1485 treatment. Cells treated with insulin and rapamycin exhibit a dendritic complexity comparable to vehicle controls across all morphotypes. MHY1485-treated cells showed preservation of dendritic complexity relative to vehicle controls at 6 dpi, particularly in the number of bifurcations across all morphotypes. Data presented as median ±95% confidence interval. Each dot represents one cell (N=52-63 cells sampled from n = 7 fish per group). One-way Kruskal-Wallis ANOVA with multiple comparisons followed by Mann–Whitney post hoc tests; p values are shown in the figure. Abbreviations: Area under the curve (AUC); days post-injury (dpi); insulin (Ins); rapamycin (Rap); vehicle (Veh)

Techniques: Preserving, MANN-WHITNEY

Effects of Gln and RAPA on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Journal: Frontiers in Oncology

Article Title: Glutamine alleviates radiation-induced intestinal injury in rats via the mTOR/Notch1 axis

doi: 10.3389/fonc.2026.1735401

Figure Lengend Snippet: Effects of Gln and RAPA on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: To investigate the role of mTOR/notch1 pathway on Gln radio-resistance effects in colon, HT-29 cells were treated with the 10 μmol/L Jagged-1 (MCE, USA) , which activates the Notch1 receptor.

Techniques: Expressing, Immunofluorescence

Effects of Gln and Jagged-1 on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Journal: Frontiers in Oncology

Article Title: Glutamine alleviates radiation-induced intestinal injury in rats via the mTOR/Notch1 axis

doi: 10.3389/fonc.2026.1735401

Figure Lengend Snippet: Effects of Gln and Jagged-1 on the mTOR/Notch1 axis and MUC2 expression in HT-29 cells. (A) The expression of mTOR, p-mTOR, Notch1, and GAPDH. (B) Immunofluorescence analysis of MUC2 in HT-29 cells (800×). Data are presented as mean ± SD (n = 3). One-way ANOVA was carried out followed by Tukey’s test. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Techniques: Expressing, Immunofluorescence

AKT/mTOR pathway inhibition by GEM and SSD combination therapy. (A) Immunocytochemistry staining of AKT/mTOR signaling proteins in MIA PaCa-2 and AsPC-1 cells treated with Ctrl, G0.25, S4 or the combination (G0.25 + S4; magnification, ×40; insets show phosphoprotein details). Scale bar, 50 µm. (B) Western blot analysis of p-AKT (60 kDa), AKT (56 kDa), p-mTOR (289 kDa), mTOR (289 kDa) and β-actin (42 kDa). Semi-quantification of phosphorylation ratios in (C) MIA PaCa-2 and (D) AsPC-1 cells. In the figure, GEM represents 0.25 µmol/l GEM and SSD represents 4 µmol/l SSD. Data are presented as the mean ± SD (n=5). Compared with GEM monotherapy, the G0.25 + S4 combination led to a greater reduction in both p-AKT/AKT and p-mTOR/mTOR ratios (both P adj <0.0001), with large effect sizes (η 2 =0.73 and 0.81, respectively). All P-values are Benjamini-Hochberg-adjusted. ****P<0.0001 for G0.25 + S4 vs. Ctrl; ## P<0.01, ### P<0.001 for G0.25 + S4 vs. G0.25. Statistical analysis was performed using one-way ANOVA with Tukey's post hoc test. Ctrl, control; GEM, gemcitabine; SSD, Saikosaponin D; p-, phosphorylated.

Journal: Oncology Reports

Article Title: Saikosaponin D overcomes gemcitabine resistance in pancreatic cancer via AKT/mTOR pathway inhibition and synergistic induction of apoptosis and autophagy

doi: 10.3892/or.2025.9033

Figure Lengend Snippet: AKT/mTOR pathway inhibition by GEM and SSD combination therapy. (A) Immunocytochemistry staining of AKT/mTOR signaling proteins in MIA PaCa-2 and AsPC-1 cells treated with Ctrl, G0.25, S4 or the combination (G0.25 + S4; magnification, ×40; insets show phosphoprotein details). Scale bar, 50 µm. (B) Western blot analysis of p-AKT (60 kDa), AKT (56 kDa), p-mTOR (289 kDa), mTOR (289 kDa) and β-actin (42 kDa). Semi-quantification of phosphorylation ratios in (C) MIA PaCa-2 and (D) AsPC-1 cells. In the figure, GEM represents 0.25 µmol/l GEM and SSD represents 4 µmol/l SSD. Data are presented as the mean ± SD (n=5). Compared with GEM monotherapy, the G0.25 + S4 combination led to a greater reduction in both p-AKT/AKT and p-mTOR/mTOR ratios (both P adj <0.0001), with large effect sizes (η 2 =0.73 and 0.81, respectively). All P-values are Benjamini-Hochberg-adjusted. ****P<0.0001 for G0.25 + S4 vs. Ctrl; ## P<0.01, ### P<0.001 for G0.25 + S4 vs. G0.25. Statistical analysis was performed using one-way ANOVA with Tukey's post hoc test. Ctrl, control; GEM, gemcitabine; SSD, Saikosaponin D; p-, phosphorylated.

Article Snippet: The following antibodies were purchased from Proteintech Group, Inc.: Mouse monoclonal antibodies against mTOR (1:500; cat. no. 66888-1-Ig), phosphorylated (p-)mTOR (Ser2448) (1:2,000; cat. no. 67778-1-Ig), p-AKT (Ser473) (1:500; cat. no. 66444-1-Ig), caspase-3 (1:2,000; cat. no. 66470-2-Ig), cleaved caspase-3 (1:1,000; cat. no. 66470-2-Ig), Bax (1:500; cat. no. 60267-1-Ig), AKT (1:500; cat. no. 60203-2-Ig) and β-actin (1:2,000; cat. no. 66009-1-Ig); as well as rabbit antibodies, including polyclonal antibodies against Bcl-2 (1:1,000; cat. no. 12789-1-AP), Beclin 1 (1:1,000; cat. no. 11306-1-AP) and LC3 (1:1,000; cat. no. 14600-1-AP).

Techniques: Inhibition, Immunocytochemistry, Staining, Western Blot, Phospho-proteomics, Control

Proposed mechanism of GEM and SSD combination therapy. Co-treatment with GEM and SSD synergistically inhibits the AKT/mTOR pathway, concurrently inducing apoptosis (via Bax/Bcl-2 modulation and caspase-3 activation) and autophagy (via Beclin 1 activation and LC3 conversion), thereby overcoming GEM resistance in pancreatic cancer cells. GEM, gemcitabine; P, phosphorylated; SSD, Saikosaponin D.

Journal: Oncology Reports

Article Title: Saikosaponin D overcomes gemcitabine resistance in pancreatic cancer via AKT/mTOR pathway inhibition and synergistic induction of apoptosis and autophagy

doi: 10.3892/or.2025.9033

Figure Lengend Snippet: Proposed mechanism of GEM and SSD combination therapy. Co-treatment with GEM and SSD synergistically inhibits the AKT/mTOR pathway, concurrently inducing apoptosis (via Bax/Bcl-2 modulation and caspase-3 activation) and autophagy (via Beclin 1 activation and LC3 conversion), thereby overcoming GEM resistance in pancreatic cancer cells. GEM, gemcitabine; P, phosphorylated; SSD, Saikosaponin D.

Techniques: Activation Assay

The protein expression of PI3K, AKT, mTOR and their respective phosphorylated forms detected by Western blotting

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Microbiota-gut-brain axis and neuroendocrine pathways underlie divergent mechanisms of intermittent and continuous theta-burst stimulation in autism spectrum disorder

doi: 10.1007/s00018-026-06096-2

Figure Lengend Snippet: The protein expression of PI3K, AKT, mTOR and their respective phosphorylated forms detected by Western blotting

Article Snippet: For immunofluorescence staining, free-floating hypothalamic sections were co-incubated with primary antibodies against somatostatin (SST) (1:100, rabbit, bs-37040R, Bioss) and growth hormone-releasing hormone (GHRH) (1:100, rabbit, bs-0205R, Bioss), while prefrontal cortical sections were incubated with primary antibodies targeting growth hormone (GH) (1:1000, rabbit, GB113303-100, Servicebio), phospho-AKT (1:100, rabbit, bs-0876R, Bioss), phospho-mTOR (1:100, rabbit, bs-3495R, Bioss), growth hormone receptor (GHR) (1:100, rabbit, bs-0654R, Bioss), and somatostatin receptor 2 (SSTR2) (1:100, rabbit, bs-10986R, Bioss).

Techniques: Expressing, Western Blot

Immunofluorescence analysis of GHR and SSTR2 in the prefrontal cortex. A Proposed signaling pathway of GH in regulating the PI3K/Akt/mTOR axis (KEGG Entry: map04935). B Quantitative analysis of the expression levels of GHR and SSTR2. C Representative immunofluorescence images of GHR and SSTR2 (50.0×, Scale bar: 20 μm). The data are presented as mean ± SD ( n = 3). ### p < 0.001 vs. control group; *** p < 0.001 vs. VPA group

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Microbiota-gut-brain axis and neuroendocrine pathways underlie divergent mechanisms of intermittent and continuous theta-burst stimulation in autism spectrum disorder

doi: 10.1007/s00018-026-06096-2

Figure Lengend Snippet: Immunofluorescence analysis of GHR and SSTR2 in the prefrontal cortex. A Proposed signaling pathway of GH in regulating the PI3K/Akt/mTOR axis (KEGG Entry: map04935). B Quantitative analysis of the expression levels of GHR and SSTR2. C Representative immunofluorescence images of GHR and SSTR2 (50.0×, Scale bar: 20 μm). The data are presented as mean ± SD ( n = 3). ### p < 0.001 vs. control group; *** p < 0.001 vs. VPA group

Techniques: Immunofluorescence, Expressing, Control

Immunofluorescence analysis of GH and p-AKT/GH and p-mTOR co-localization in the prefrontal cortex. A Representative immunofluorescence images of GH and p-Akt (50.0×, Scale bar: 20 μm). B Quantification of the Pearson’s correlation coefficient (R value) for GH and p-Akt co-localization. C Representative immunofluorescence images of GH and p-mTOR (50.0×, Scale bar: 20 μm). D Quantification of the Pearson’s correlation coefficient (R value) for GH and p-mTOR co-localization from. The data are presented as mean ± SD ( n = 3). ### p < 0.001 vs. control group; *** p < 0.001 vs. VPA group

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Microbiota-gut-brain axis and neuroendocrine pathways underlie divergent mechanisms of intermittent and continuous theta-burst stimulation in autism spectrum disorder

doi: 10.1007/s00018-026-06096-2

Figure Lengend Snippet: Immunofluorescence analysis of GH and p-AKT/GH and p-mTOR co-localization in the prefrontal cortex. A Representative immunofluorescence images of GH and p-Akt (50.0×, Scale bar: 20 μm). B Quantification of the Pearson’s correlation coefficient (R value) for GH and p-Akt co-localization. C Representative immunofluorescence images of GH and p-mTOR (50.0×, Scale bar: 20 μm). D Quantification of the Pearson’s correlation coefficient (R value) for GH and p-mTOR co-localization from. The data are presented as mean ± SD ( n = 3). ### p < 0.001 vs. control group; *** p < 0.001 vs. VPA group

Techniques: Immunofluorescence, Control

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