pi3k agonist 740 y p  (MedChemExpress)

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can activate the PI3K/AKT pathway by inhibiting the expression of PTEN in glioma cells.Western blotting was used to detect the expression of PTEN in U87 and U251 cell lines (A); the CCK-8 assay was used to measure the viability of U87 and U251 glioma cells treated with different concentrations of LY294002 and 740 Y-P (B); Western blotting was also used to detect the expression of PI3K, p-AKT/AKT in U87 and U251 cell lines (C).*P < 0.05 vs si-NC，@P < 0.05 vs si-NC+Agonist，#P < 0.05 vs si-TNKS1，&P < 0.05 vs OE-TNKS1.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Expressing, Western Blot, CCK-8 Assay

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the proliferation and glycolysis of glioma cells by mediating the PTEN-PI3K/AKT pathway.Cell viability of various groups in U87 and U251 cell lines (A); detection of glucose (GLU) and lactate (LA) levels in the culture supernatant of various groups in U87 and U251 cell lines using biochemical assay kits (B); qPCR was used to detect the mRNA levels of GLUT1 and HK2 in various groups of U87 and U251 cell lines (C). Statistical significance *p < 0.05, **p < 0.01, ***p < 0.001, **** p < 0.0001,"ns" P ≥ 0.05.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques:

Journal: IBRO Neuroscience Reports

Article Title: TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas

doi: 10.1016/j.ibneur.2026.01.007

Figure Lengend Snippet: TNKS1 can regulate the PTEN-PI3K/AKT pathway in glioma xenografts.Western blotting was used to detect the protein expression levels of PTEN, PI3K, p-AKT, and AKT in cells from each group.* P < 0.05 vs TNKS1-siRNA NC, @ P < 0.05 vs TNKS1-siRNA，# P < 0.05 vs Inhibitor.

Article Snippet: The cells were then cultured in the incubator for another 12 h. Subsequently, the cells in each well were randomly divided into groups: the si-NC+agonist group, the si-TNKS1 +agonist group, and the OE-TNKS1 +inhibitor group were treated with PI3K agonist 740 Y-P (HY-P0175, MCE, USA) and PI3K inhibitor LY294002 (HY-10108, MCE, USA) and continued to be cultured for 24 h. The TNKS1-siRNA empty vector group (si-NC), the TNKS1-siRNA group (si-TNKS1), and the TNKS1 overexpression group (OE-TNKS1) were treated with an equivalent amount of diluent and continued to be cultured for 24 h.

Techniques: Western Blot, Expressing

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The mRNA expression of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2 , and Caspase 3 in E.tenella host cells.

Article Snippet: p-PI3K Rabbit Ab , Abmart , P76365R4 , 1: 1500.

Techniques: Expressing

Journal: Poultry Science

Article Title: Pathogenic mechanism of Eimeria tenella Et MIC2 promotes Eimeria tenella invasion and inhibits host cell apoptosis through binding to the ITGAV receptor

doi: 10.1016/j.psj.2026.106922

Figure Lengend Snippet: The protein activity changes of ITGAV, FAK, PLC, PKC, p65, ERK, JNK, p38, PI3K, Akt, Bax, Bcl2, and Caspase 3 in E.tenella host cells.

Article Snippet: p-PI3K Rabbit Ab , Abmart , P76365R4 , 1: 1500.

Techniques: Activity Assay

Journal: Bioactive Materials

Article Title: Integrated cryopreservation-thawing-transplantation platform for neural stem cell-based spinal cord injury repair

doi: 10.1016/j.bioactmat.2026.01.024

Figure Lengend Snippet: Mechanisms of NSC Differentiation into Neurons Promoted by Composite In Vitro. A) Schematic of the interactive system with NSCs and the composites. B) Representative confocal images of NSCs treated with distinct groups for 72 h. NSCs were stained with Tuj-1 (red), GFAP (green), and DAPI (blue). Scale bar: 50 μm. C-D) Quantitative analysis of Tuj-1 (C) and GFAP (D) fluorescence intensity in each group (n = 4). E) Western blot bands of Tuj-1 and GFAP protein expression in NSCs treated with separate groups. F-G) Quantitative analysis of Tuj-1/GAPDH (F) and GFAP/GAPDH (G) ratios in each group (n = 3). H) Volcano plots of DEGs in the hUCMSC-Exo + PM vs. control. DEGs are defined as |log2FC| ≥ 1 with q < 0.05. I-J) GO and KEGG pathway enrichment analysis of DEGs in NSCs after intervention with hUCMSC-Exo + PM. K) Heatmap showing the expression levels of significantly altered genes in the hUCMSC-Exo + PM and Control. L) GSEA showing pathways significantly positively correlated with DEGs in the hUCMSC-Exo + PM group. Enrichment scores (ES), P values, and false discovery rates (FDR) values are indicated for each pathway. M) Western blot bands of p-CaMK II, CaMK II, p-CREB, CREB, p-PI3K, PI3K, p-AKT, and AKT protein expression in NSCs treated with distinct groups. N) Quantitative analysis of p-CaMK II/CaMK II, p-CREB/CREB, p-PI3K/PI3K, and p-AKT/AKT ratios (n = 3). All data are presented as the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: The primary antibodies used in this research are listed below: CD68 (Abcam, Cambridge, UK), CD206 (Abcam, Cambridge, UK), GFAP (Bioss, Beijing, China), iNOS (Abcam, Cambridge, UK), Tuj-1 (Abcam, Cambridge, UK), NF-200 (Invitrogen, CA, USA), MBP (Abcam, Cambridge, UK), HIF-1α (Abcam, Cambridge, UK), VEGFA (Abcam, Cambridge, UK), P-CaMKII (Abcam, Cambridge, UK), CaMKII (Abcam, Cambridge, UK), P-CREB (Cell Signaling Technology, USA), CREB (Cell Signaling Technology, USA), P-PI3K (Cell Signaling Technology, USA), PI3K (Cell Signaling Technology, USA), P-AKT (Cell Signaling Technology, USA), AKT (Cell Signaling Technology, USA), Cleaved-Caspase3 (Cell Signaling Technology, USA), Bcl-2 (Cell Signaling Technology, USA), Bax (Cell Signaling Technology, USA), GAPDH (Proteintech, IL, USA).

Techniques: In Vitro, Staining, Fluorescence, Western Blot, Expressing, Control

Journal: Pharmaceutical Biology

Article Title: Wubie Fanchun Formula-inducible metabolites in primary ovarian insufficiency model mice that facilitate ovarian renovation

doi: 10.1080/13880209.2026.2668132

Figure Lengend Snippet: WBFC regulates ovarian function and activates PI3K/AKT/FOXO3a signaling in POI mice. Immunofluorescence and quantification of (A) p-PI3K, (B) p-AKT, and (C) p-FOXO3a in ovaries. (D) Western blot analysis of protein expression levels and semi-quantitative results of p-PI3K/PI3K, p-AKT/AKT, and p-FOXO3a/FOXO3a in ovarian tissues of POI mice treated with WBFC ( n = 3). Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bar represents 50 μm.

Article Snippet: Subsequently, they were incubated overnight at 4 °C with the following specific primary antibodies: PI3K (1:200, 20584-1-AP, proteintech), p-PI3K (1:200, T40116 , Abmart), AKT (1:200, 4691, Cell Signaling Technology), p-AKT (1:200, 4060, Cell Signaling Technology), and p-FOXO3a (1:200, 28755-1-AP, proteintech).

Techniques: Immunofluorescence, Western Blot, Expressing

Journal: Pharmaceutical Biology

Article Title: Wubie Fanchun Formula-inducible metabolites in primary ovarian insufficiency model mice that facilitate ovarian renovation

doi: 10.1080/13880209.2026.2668132

Figure Lengend Snippet: PI and GLN improve ovarian tissue morphology and ovarian function in 4-VCD induced POI mice. (A) HE-stained histopathological sections of ovarian tissue (400×) with a scale bar of 50 μm. (B) Statistics on the number of primordial follicles, primary follicles, secondary follicles, and sinus follicles of mice in each group. Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001. (C) PAS staining results of mouse liver tissue in each group. (D) Immunofluorescence analysis of the effect of on protein expression in ovarian tissue of POI mice: P-PI3K, P-AKT. Mean values are presented with ± SEM, n = 3. Compared with the model group, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Subsequently, they were incubated overnight at 4 °C with the following specific primary antibodies: PI3K (1:200, 20584-1-AP, proteintech), p-PI3K (1:200, T40116 , Abmart), AKT (1:200, 4691, Cell Signaling Technology), p-AKT (1:200, 4060, Cell Signaling Technology), and p-FOXO3a (1:200, 28755-1-AP, proteintech).

Techniques: Staining, Immunofluorescence, Expressing

Journal: Renal Failure

Article Title: Ubiquitin-specific protease 11 facilitates the activation and proliferation of renal interstitial fibroblasts through epidermal growth factor receptor signaling pathways

doi: 10.1080/0886022X.2026.2666452

Figure Lengend Snippet: USP11 regulates EGFR downstream signaling pathways, PI3K/AKT and MEK/ERK. Western blot analysis of p-PI3K, PI3K, p-Akt and Akt protein expressions in each group were conducted, with normalization to GAPDH (A, E). Quantitative analysis of p-PI3K, PI3K, p-Akt and Akt protein levels in each group (B, F). Western blot analysis of p-MEK1/2, MEK1/2, p-ERK1/2 and ERK1/2 protein expressions in each group were conducted, with normalization to GAPDH (C, G). Quantitative analysis of p-MEK1/2, MEK1/2, p-ERK1/2 and ERK1/2 protein levels in each group (D, H). Data were expressed as mean± SD ( n = 4 for each group). N.S.: no significant difference. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Antibodies to p-PI3K (AF3241) and PI3K (AF6241) were purchased from Affinity (Affinity Biosciences, United States).

Techniques: Protein-Protein interactions, Western Blot

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Article Snippet: Cytochrome c (CYT-C) (#AF0146), cleaved-PARP (#AF7023), Bcl-2 (#AF6139), cleaved-caspase 9 (#AF5240), cleaved-caspase 3 (#AF7022), matrix metalloproteinase 2 (MMP2) (#AF5330), MMP7 (#AF0218), peroxisome proliferator-activated receptor-γ-coactivator 1α (PGC-1α) (#AF5395), nuclear respiratory factor 1 (NRF1) (#AF5298), NRF2 (#AF0639), mitochondrial transcription factor A (TFAM) (#AF0531), PI3K (#AF6241), p-PI3K (#AF3242), AKT (#AF6261), p-AKT (#AF0016), extracellular signal-related kinase (ERK) (#AF0155), Jun N-terminal kinase (JNK) (#AF6318), p-ERK (#AF1015), p-JNK (#AF3318), and Snail (#AF6032) antibodies were purchased from Affinity Biosciences (USA).

Techniques: Protein-Protein interactions, Gene Expression, Control, Western Blot, Migration, Staining, Membrane, Standard Deviation