mek inhibitor trametinib  (MedChemExpress)

Journal: The Journal of Clinical Investigation

Article Title: THEMIS attenuates MASH by suppressing disease-associated hepatocyte induction and hepatocyte senescence in mice

doi: 10.1172/JCI199303

Figure Lengend Snippet: ( A ) Immunoblotting of total lysates from WT and Themis -KO livers. ( B ) Immunoblotting of total lysates from Themis Flox and HKO livers. ( C ) Immunoblotting of total lysates from mouse and human primary hepatocytes transduced with Ad-GFP or Ad-Themis. ( D ) Immunoblotting of Themis Flox and HKO mice primary hepatocytes stimulated with 100 ng/mL EGF at indicated time points. ( E ) RAS activity assessment of EGF-treated primary hepatocytes isolated from Flox and HKO mice fed MASH diet for 5 months. ( F and G ) Hepa1 cells overexpressing either GFP or Themis were treated with 50 nM doxorubicin (Dox) for 3 days. ( F ) SA-β-GAL staining of Hepa1 cells. ( G ) Immunoblotting of total lysates from Hepa1 cells. ( H ) Immunoblotting of total lysates. Hepa1 cells overexpressing either GFP or Themis were treated with 1 μM Dox for 2 hours, followed by 10 nM MEK inhibitor trametinib treatment for 3 days. Scale bars: 50 μm ( F ).

Article Snippet: Hepa1 cells (ATCC, CRL-1830) were transduced by adenovirus and then treated with Dox (Cayman, 15007), MEK inhibitor trametinib (MedChemExpress, HY-10999)], or the combination.

Techniques: Western Blot, Transduction, Activity Assay, Isolation, Staining

Journal: Alzheimer's & Dementia

Article Title: Human iPSC‐derived GABAergic interneuron transplantation restores circuit balance and cognitive function in an Alzheimer's disease model

doi: 10.1002/alz.71378

Figure Lengend Snippet: Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and NOTCH inhibitors starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.

Article Snippet: From week 5 to week 7, in addition to the continued treatment with the MEK inhibitor, NOTCH inhibitors (DAPT 10 μM; HY‐13027, MCE) and cyclin‐dependent kinase (CDK) inhibitors (PD0332991 2 μM; MCE, HY‐50767) were introduced to induce cell cycle exit in the cells during this stage.

Techniques: Derivative Assay, Immunocytochemistry, Binding Assay