Journal: Cell reports

Article Title: KSHV episome tethering sites on host chromosomes and regulation of latency-lytic switch by CHD4

doi: 10.1016/j.celrep.2022.110788

Figure Lengend Snippet:

Article Snippet: Human: BC3 , ATCC , CRL-2277.

Techniques: Produced, Virus, Recombinant, Protease Inhibitor, Magnetic Beads, Luciferase, Sequencing, In Vitro, Software

Journal: Journal of ethnopharmacology

Article Title: Dehydrocorydaline attenuates myocardial ischemia-reperfusion injury via the FoXO signalling pathway: A multimodal study based on network pharmacology, molecular docking, and experimental study.

doi: 10.1016/j.jep.2024.118738

Figure Lengend Snippet: Fig. 5. Prediction and validation of DHC and its potential targets by molecular docking and IHC analysis. (A) Molecular docking of STAT3 and DHC. (B) Molecular docking of MDM2 and DHC. (C) Molecular docking of CDK2 and DHC. (D) Molecular docking of PLK1 and DHC. (E) Molecular docking of CCND1 and DHC. (F) Binding of DHC to CCND1 as determined through microscale thermophoresis (MST). (G) Binding of DHC to MDM2 as determined through MST. (H) Binding of DHC to CDK2 as determined through MST. (I) Relative protein levels of p-FOXO1A (n = 3). (J) Representative IHC images of p-FOXO1A, CCND1, and p-MDM2. (K) Relative protein levels of CCND1 (n = 3). (L) Relative protein levels of p-MDM2 (n = 3). *indicates a significant difference compared with the sham group, # indicates a significant difference compared with the MIRI group: *p < 0.05, **p < 0.01, #p < 0.05, ##p < 0.01. DHC: dehydrocorydaline, IHC: immunohistochemical, MIRI: myocardial ischemia-reperfusion injury.

Article Snippet: The microscale thermophoresis (MST) technique was performed to validate the interaction between CCND1 (#HY-P72119, MedChemExpress, Shanghai, China), CDK2 (#HY-P70014, MedChemExpress, Shanghai, China), MDM2 (#HY-P701593, MedChemExpress, Shanghai, China) and DHC(#HY-N0674, MedChemExpress, Shanghai, China).

Techniques: Biomarker Discovery, Binding Assay, Microscale Thermophoresis, Immunohistochemical staining

Journal: Journal of ethnopharmacology

Article Title: Dehydrocorydaline attenuates myocardial ischemia-reperfusion injury via the FoXO signalling pathway: A multimodal study based on network pharmacology, molecular docking, and experimental study.

doi: 10.1016/j.jep.2024.118738

Figure Lengend Snippet: Fig. 7. Effects of DHC on the expression of predicted targets in the in vitro model of H/R injury. (A) Representative fluorescence images of the TUNEL assay. Photographs were taken at × 400 magnification. (B) Percentage of TUNEL-positive cells in each group. (C) Western blot showing the protein expression of cleaved- caspase 3 and cleaved-caspase 8 in each group. (D) Western blot showing the protein expression of p-FOXO1A, FOXO1A, CCND1, p-MDM2, and MDM2 in each group. (E) Relative protein levels of cleaved-caspase 3 and cleaved-caspase 8 measured in western blots (n = 3). (F) Relative protein levels of p-FOXO1A, FOXO1A, and p- FOXO1A/FOXO1A measured in western blots (n = 3). (G) Relative protein levels of p-MDM2, MDM2, and p-MDM2/MDM2 measured in western blots (n = 3). (H) Relative protein levels of CCND1 measured in western blots (n = 3). * indicates a significant difference compared to the control group; # indicates a significant difference compared to the H/R model group: *p < 0.05, **p < 0.01, #p < 0.05, ##p < 0.01. DHC: dehydrocorydaline, H/R: hypoxia/reoxygenation, TUNEL: TdT- mediated dUTP-biotin nick end labelling.

Article Snippet: The microscale thermophoresis (MST) technique was performed to validate the interaction between CCND1 (#HY-P72119, MedChemExpress, Shanghai, China), CDK2 (#HY-P70014, MedChemExpress, Shanghai, China), MDM2 (#HY-P701593, MedChemExpress, Shanghai, China) and DHC(#HY-N0674, MedChemExpress, Shanghai, China).

Techniques: Expressing, In Vitro, Fluorescence, TUNEL Assay, Western Blot, Control

Journal: The Journal of biological chemistry

Article Title: Anti-IgM-mediated regulation of c-myc and its possible relationship to apoptosis.

doi: 10.1074/jbc.271.31.18875

Figure Lengend Snippet: FIG. 8. Cell growth in various Burkitt’s lymphoma cell lines treated with anti-IgM. Daudi and Ramos cells were seeded at a density of 1 3 105 cells/ml in 200 ml in a 96-well microtiter plate and treated (10 mg/ml anti-IgM). Cell numbers were determined at indi- cated times using a Thomas hemacytometer. (E) untreated cells; (G) anti-IgM-treated. Raji, CA46, Namalwa, and ST486 cells were seeded at a density of 5 3 104 cells/ml in 200 ml in 96-well microtiter plates and treated (10 mg/ml anti-IgM). Cell numbers at the indicated times were determined by an ELISA method. (E) untreated cells; (G) anti- IgM-treated.

Article Snippet: Daudi (ATCC CCL 213), Ramos (ATCC CRL 1596), Raji (ATCC CCL 86), Namalwa (ATCC CRL 1432), ST486 (ATCC CRL 1647), CA46 (ATCC CRL 1648) cell lines and GAPDH plasmid (ATCC 57090) were obtained from American Type Culture Collection (Rockville, MD).

Techniques: Enzyme-linked Immunosorbent Assay

Journal: The Journal of biological chemistry

Article Title: Anti-IgM-mediated regulation of c-myc and its possible relationship to apoptosis.

doi: 10.1074/jbc.271.31.18875

Figure Lengend Snippet: FIG. 11. The role of c-myc in regulating cell growth, and the effect of EBV proteins in preventing apoptosis. Burkitt’s lym- phoma cells which are p53 mutant (103) and express high level of c-myc (10, 17, 105) can grow rapidly in vitro. Cross-linking of B cell antigen receptor by anti-IgM in these cells induces down-regulation of c-myc mRNA as well as Myc protein. Reduction of the c-myc level in these cells will propel the cells to exit the cell cycle. In the absence of EBV proteins (EBNAs, LMPs, and BHRF-1 (bcl-2 homologue)), the cells will result in apoptosis (e.g. Ramos and ST486 cells). However, in the presence of EBV proteins, apoptosis is blocked resulting in growth arrest (e.g. Daudi, Raji, and Namalwa cells). Addition of antisense c-myc oligonu- cleotides to these cells demonstrated a similar result to that seen with anti-IgM.

Article Snippet: Daudi (ATCC CCL 213), Ramos (ATCC CRL 1596), Raji (ATCC CCL 86), Namalwa (ATCC CRL 1432), ST486 (ATCC CRL 1647), CA46 (ATCC CRL 1648) cell lines and GAPDH plasmid (ATCC 57090) were obtained from American Type Culture Collection (Rockville, MD).

Techniques: Mutagenesis, In Vitro