akt activator sc79  (MedChemExpress)

Journal: Oncology Reports

Article Title: HMBOX1 inhibits hepatocellular carcinoma progression via PTPN1 mediated AKT1 phosphorylation

doi: 10.3892/or.2026.9052

Figure Lengend Snippet: Inhibitory effect of HMBOX1 on HCC is dependent on the blocking of AKT1 phosphorylation. (A and B) The difference in protein expression between HMBOX1-overexpressing cells and control cells was analyzed through proteomics, and the results are shown in the form of volcano map (A) and heat map (B) respectively. (C and D) HCC cells were transfected with lentiviral vector to overexpress HMBOX1 and then treated with 4 µM SC79 for different times. The expression levels of AKT1 and p-AKT1 (Ser473) were determined through western blotting in Hepa1-6 and Huh-7 cells from different groups. (E-H) The proliferation and cell migration ability of Hepa1-6 and Huh-7 cells from each group were analyzed using a Cell Counting Kit-8 assay (E and F) and wound healing assay (G and H) (I) The proliferation ability of Huh-7 cells from different groups was assessed through the colony formation assay. *P<0.05 and **P<0.01. HMBOX1, homeobox containing 1; HCC, hepatocellular carcinoma.

Article Snippet: In some experiments, the Akt activator SC79 (cat. no. HY-18749; MedChemExpress) at a concentration of 4 μΜ was used to treat Hepa1-6 cells for different times.

Techniques: Blocking Assay, Phospho-proteomics, Expressing, Control, Transfection, Plasmid Preparation, Western Blot, Migration, Cell Counting, Wound Healing Assay, Colony Assay

Journal: The American Journal of Pathology

Article Title: Hepatocyte-Specific MET Deletion Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice

doi: 10.1016/j.ajpath.2025.09.010

Figure Lengend Snippet: MET deletion inhibits AKT signaling enhancing c-Jun N-terminal kinase (JNK) activation and acetaminophen (APAP)-induced liver injury. A and B: Enrichment analysis using DAVID analysis software showing modulation of phosphatidylinositol 3-kinase (PI3K)/AKT signaling, among other altered Reactome ( A ) and Kyoto Encyclopedia of Genes and Genomes (KEGG) ( B ) pathways in MET knockout (KO) versus wild-type (WT) mice at 6 hours after APAP administration. The number of differentially expressed genes associated with each pathway is indicated on the right side of the corresponding bar. C: Immunoblot images and densitometric analysis showing expressions of phospho-AKT (p-AKT) (T308) and AKT at 6 hours. D and E: Representative photomicrographs of hematoxylin and eosin–stained liver sections displaying necrotic areas at 24 hours ( D ) and corresponding serum alanine aminotransferase (ALT) levels ( E ) in MET KO mice treated with APAP alone and in combination with SC79 (AKT activator). F: Immunoblot images and densitometric analysis representing the expressions of phospho-JNK (p-JNK) (T183/Y185) and JNK in total liver lysates at 6 hours in MET KO mice treated with APAP alone and in combination with SC79 (AKT activator). AKT activator (SC79: 10 mg/kg) or its vehicle (4% dimethyl sulfoxide) was administered 2 hours’ post-APAP overdose in MET KO mice, and liver tissue samples were collected at 6 and 24 hours. Data are expressed as means ± SEM. n = 3 to 4 ( C ); n = 5 to 7 ( E and F ). ∗ P < 0.05 versus WT mice. ∗∗ P < 0.01 versus vehicle (Veh)-control MET KO mice. Scale bar: 100 μm ( D ). ECM, extracellular matrix; MAPK, mitogen-activated protein kinase; PDGF, platelet-derived growth factor.

Article Snippet: To investigate if AKT repression is involved in aggravated JNK activation and liver injury in MET KO mice, an AKT activator (SC79: 10 mg/kg, i.p.) (#HY-18749; MedChemExpress, Monmouth Junction, NJ) was used in the MET KO mice.

Techniques: Activation Assay, Software, Knock-Out, Western Blot, Staining, Control, Derivative Assay