sn 52  (MedChemExpress)

Journal: Journal of Medical Virology

Article Title: Heterogeneous Activation of Signaling Pathways and Therapeutic Vulnerabilities in KSHV‐Associated Primary Effusion Lymphoma Cell Lines

doi: 10.1002/jmv.70534

Figure Lengend Snippet: Effects of noncanonical NF‐κB inhibitor SN52 on PEL cell lines. (A) PEL cell lines were treated with different concentrations of SN52 and live cells were counted for 5 consecutive days. (B, C) PEL cell lines were analyzed for apoptotic and dead cells (B) and cell cycle progression (C) following treatment with 100 µM SN52 for 2 days. Experiments were independently repeated at least three times and representative results were presented.

Article Snippet: Cells were treated with the following inhibitors: PI3K inhibitors GDC0941 (Selleckchem, Cat. No. S1065) and HS173 (Selleckchem, Cat. No. S7356); mTOR inhibitors Torin 2 (Selleckchem, Cat. No. S2817) and Rapamycin (Selleckchem, Cat. No. S1039); FOXO1 inhibitor AS1842856 (Sigma‐Aldrich, Cat. No. 344355); AKT inhibitor MK2206 (Selleckchem, Cat. No. S1078); NF‐κB inhibitors Bay11‐7082 (Bay11) (Selleckchem, Cat. No. S2913) and JSH23 (Selleckchem, Cat. No. S7351); NF‐κB2 inhibitor SN52 (MCE, Cat. No. HY‐P3229); and dual PI3K/mTOR inhibitors BGT226 (Selleckchem, Cat. No. S2749) and Dactolisib (NVP‐BEZ235; Selleckchem, Cat. No. S1009).

Techniques:

Journal: Communications Biology

Article Title: Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection

doi: 10.1038/s42003-024-06365-5

Figure Lengend Snippet: a The expression of p52, RelB and IDO in purified human dMDSCs of uninfected and infected groups were examined by qPCR (data represent the mean ± SD from five independent experiments). b The protein levels of IDO, STAT3, p-STAT3 (Y705), IKKα, p-IKKα, p-p100 in purified human dMDSCs, p52 and RelB in nucleus of dMDSCs of uninfected and infected groups were determined by western blot. c The statistical analysis of IDO, p-STAT3 (Y705), p-IKKα, p-p100, p52 and RelB in protein levels from infected groups and uninfected human dMDSCs by western blot. (data represent the mean ± SD from three independent experiments). d The expression levels of p-STAT3 in mouse dMDSCs were examined by flow cytometry in uninfected ( n = 7) and infected groups ( n = 8) and the results were analyzed by statistical analysis. Data are presented as the mean ± SD, * P < 0.05, ** P < 0.01, human samples in each group assayed individually by the paired t -test and mice samples in each group assayed individually by the unpaired t -test. MFI: mean fluorescence intensity.

Article Snippet: To investigate if IDO expression was regulated by the STAT3/p52-RelB pathway after T. gondii infection, the p-STAT3 inhibitor (stattic; MCE, China) and p52-RelB nuclear translocation inhibitor (SN52; MCE, China) were separately introduced to human dMDSCs.

Techniques: Expressing, Purification, Infection, Western Blot, Flow Cytometry, Fluorescence

Journal: Communications Biology

Article Title: Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection

doi: 10.1038/s42003-024-06365-5

Figure Lengend Snippet: a The mRNA levels of IDO in human dMDSCs of infected group, infected with static treated group and infected with SN52 treated group were detected by qPCR (data represent the mean ± SD from three independent experiments by one-way ANOVA). b The expression changes of STAT3, p-STAT3 (Y705), IKKα, p-IKKα, p-p100, IDO and the expression of p52 and RelB of nucleus in purifed human dMDSCs of the uninfected, infected and infected with static treated groups were determined by western blot (data represent the mean ± SD from three independent experiments by one-way ANOVA). c The expression changes of IDO in human dMDSCs and the expression of p52 and RelB in nucleus of dMDSCs from the infected and infected with SN52 treated groups were determined by western blot (data represent the mean ± SD from three independent experiments by the paired t -test). d The IDO expression in mouse dMDSCs of infected and infected with JSI-124 groups were examined by flow cytometry ( n = 6). Data are presented as the mean ± SD, * P < 0.05, ** P < 0.01, unpaired t -test. MFI mean fluorescence intensity.

Article Snippet: To investigate if IDO expression was regulated by the STAT3/p52-RelB pathway after T. gondii infection, the p-STAT3 inhibitor (stattic; MCE, China) and p52-RelB nuclear translocation inhibitor (SN52; MCE, China) were separately introduced to human dMDSCs.

Techniques: Infection, Expressing, Western Blot, Flow Cytometry, Fluorescence

Journal: Communications Biology

Article Title: Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection

doi: 10.1038/s42003-024-06365-5

Figure Lengend Snippet: T. gondii infection upregulated the transcriptional levels of IDO in dMDSCs through STAT3/p52-RelB pathway. But IDO protein expression was decreased due to the degradation induced by the increase of SOCS3 by infection, which in turn the reduction of IDO metabolite kynurenine further downregulated TGF-β and IL-10 expression in dNK cells through Kyn/AhR/SP1 signaling pathway, ultimately leading to the dysfunction of dNK and the disorders of maternal-fetal tolerance.

Article Snippet: To investigate if IDO expression was regulated by the STAT3/p52-RelB pathway after T. gondii infection, the p-STAT3 inhibitor (stattic; MCE, China) and p52-RelB nuclear translocation inhibitor (SN52; MCE, China) were separately introduced to human dMDSCs.

Techniques: Infection, Expressing