akt inhibitor  (MedChemExpress)

Journal: Materials Today Bio

Article Title: Alendronic acid modified PLGA drug delivery system loaded with 17β-Estradiol and vitamin D3 has anti-osteoporotic effect

doi: 10.1016/j.mtbio.2026.102789

Figure Lengend Snippet: E2 and VitD3 improves osteogenesis by PI3K/AKT/mTOR pathway. (A) Q-PCR analysis of mRNA level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (B) The protein level of ERα, ERβ and VDR in Ctrl, E2, VD and E2+VD in MC3T3-E1 cells. (C) The WB analysis of protein level of pan and phsopho-PI3K, pan and phospho-Akt, pan and phospho-mTOR, and pan and phospho-FOXO3 in MC3T3-E1 cells treated with PBS, E2, VitD3, E2 plus VitD3. (D) The MC3T3-E1 cells were pretreated with or without Akti1/2 (5uM), and were induced to osteoblasts with PBS, E2, VitD3, E2+VitD3. The ALP staining was utilized to evaluate the osteogenic differentiation in each group.

Article Snippet: The AKT inhibitor (Akti1/2, MedChemExpress, USA) was dissolved in DMSO and used at a final concentration of 10 μM.

Techniques: Staining

Journal: iScience

Article Title: FAM65A, as a potential predictor of prognosis, promotes colorectal cancer progression via activating Ras/ERK/RSK signaling

doi: 10.1016/j.isci.2026.114662

Figure Lengend Snippet: FAM65A promotes CRC tumor progression is dependent on RSK phosphorylation (A) Results from protein kinase microarray analysis of HCT116-MCS and HCT116-FAM65A cells. (B) Quantitative assessment of the protein kinase microarray data, n = 2. (C) Western blot analysis demonstrating the expression levels of p -RSK and total RSK in HCT116-MCS and HCT116-FAM65A cells. (D) Western blot analysis of p -RSK and RSK expression in HCT116-FAM65A cells treated with 4 and 8 μM BRD7389 or without treatment. (E) Results from the CCK8 cell proliferation assay conducted on HCT116-FAM65A cells with and without the application of BRD7389, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (F) Outcomes of the colony formation assay performed on HCT116-FAM65A cells treated with BRD7389 or without treatment. (G) Quantitative analysis of the colony formation assay results, n = 3, ∗∗∗ p < 0.001. (H) Results from the EdU assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 100 μm. (I) Quantitative analysis of the EdU assay results, n = 3, ∗∗∗ p < 0.001. (J) Western blot analysis of Ki-67 expression in HCT116-FAM65A cells treated with BRD7389 or not. (K) Results from the apoptosis assay conducted on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (L) Quantitative analysis of the apoptosis experiments, n = 3, ∗∗∗ p < 0.001. (M) Western blot analysis of the expression levels of cleaved Caspase 3, Bcl-2, and Bax in HCT116-FAM65A cells treated with BRD7389 or not. (N) Results from the Transwell migration assay conducted on HCT116-FAM65A cells with and without the application of BRD7389. Scale bars, 50 μm. (O) Quantitative analysis of the Transwell migration assay results, n = 3, ∗∗∗ p < 0.001. (P) Results from the wound healing assay performed on HCT116-FAM65A cells treated with BRD7389 or not. Scale bars, 50 μm. (Q) Quantitative analysis of the wound healing assay results, n = 3, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (R) Western blot analysis the expression of EMT markers in HCT116-FAM65A cells treated with BRD7389 or not. Data are presented as mean ± SEM of biologically independent experiments.

Article Snippet: The phosphorylation of RSK was inhibited by the selective RSK family kinase inhibitor BRD7389 (Cat. # HY-12185, MedChemExpress, USA).

Techniques: Phospho-proteomics, Microarray, Western Blot, Expressing, Proliferation Assay, Colony Assay, EdU Assay, Apoptosis Assay, Transwell Migration Assay, Wound Healing Assay