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LakePharma
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Informa UK Limited
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TC ASK 10(Cat No.:R061891)is a selective inhibitor of apoptosis signal-regulating kinase 1 (ASK1), a key component of the MAPK signaling pathway involved in cellular responses to stress, inflammation, and apoptosis. By inhibiting ASK1, TC ASK
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Image Search Results
Journal: Nature Communications
Article Title: BRCA2 deficiency instigates cGAS-mediated inflammatory signaling and confers sensitivity to tumor necrosis factor-alpha-mediated cytotoxicity
doi: 10.1038/s41467-018-07927-y
Figure Lengend Snippet: BRCA2 inactivation causes sensitivity to TNFα in cancer cells. a KBM-7 harboring shRNAs targeting BRCA2 were treated with doxycycline for 48 h and subsequently plated and treated with indicated TNFα concentrations for 5 days. b KBM-7-shBRCA2 #1 cells with shRNAs targeting SAM68, TNFR1 or SCR were treated with or without doxycycline and treated with indicated TNFα concentrations for 5 days. c Breast cancer cell lines MDA-MB-231, HCC38 and BT-549 harboring shLUC, shBRCA2 #1 or shBRCA2 #2 were pre-treated for 48 h with doxycycline and subsequently treated with indicated TNFα concentrations for 5 days. d DLD-1 wt or BRCA2 −/− cells were plated and treated for 5 days with indicated TNFα concentrations. e , f BT-549 cells harboring shLUC or shBRCA2 #2 were treated with doxycycline for 48 h and subsequently treated with indicated concentrations of TNFα, in the presence or absence of JNK inhibitor ( e ) or ASK1 inhibitor ( f ) for 5 days. g BT-549 cell lines harboring indicated shRNAs were transfected with indicated siRNAs for 24 h, and were subsequently treated with doxycycline for 48 h. Cells were re-plated and treated with indicated TNFα concentrations for 5 days. Error bars represent s.e.m. of three independent experiments, with three technical replicates each. P values were calculated using two-tailed Student’s t -test. * P < 0.05, *** P < 0.001. h BT-549 cells harboring shRNAs targeting BRCA1 or FANCD2 were treated with doxycycline for 48 h, and subsequently plated and treated with indicated TNFα concentrations for 5 days. i MDA-MB-231, HCC38 or BT-549 cells were plated and treated with or without 100 μM HU and indicated TNFα concentrations for 5 days. Throughout the figure, cell viability was assessed by MTT conversion, and error bars indicate s.e.m. of at least three independent experiments with three technical replicates each. Measurements were normalized to untreated cells. P values were calculated using two-tailed Student’s t -test. For P values, see Supplementary Data
Article Snippet: Cells were treated with indicated concentrations of the following agents: Infliximab (Merck, Sharp and Dome), HU (Sigma),
Techniques: Transfection, Two Tailed Test
Journal: Nature Communications
Article Title: BRCA2 deficiency instigates cGAS-mediated inflammatory signaling and confers sensitivity to tumor necrosis factor-alpha-mediated cytotoxicity
doi: 10.1038/s41467-018-07927-y
Figure Lengend Snippet: Schematic model of inflammatory signaling upon BRCA2 inactivation. BRCA2 inactivation (1) leads to micronuclei formation (2) and cGAS/STING-dependent activation of an interferon response (3). This leads to pro-inflammatory cytokines production, and sensitivity to TNFα, in a TNFR/SAM68 (4) and ASK1/JNK-dependent fashion (5)
Article Snippet: Cells were treated with indicated concentrations of the following agents: Infliximab (Merck, Sharp and Dome), HU (Sigma),
Techniques: Activation Assay