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recombinant mouse tumor necrosis factor α  (R&D Systems)


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    Structured Review

    R&D Systems recombinant mouse tumor necrosis factor α
    Recombinant Mouse Tumor Necrosis Factor α, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 370 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/recombinant+mouse+tumor+necrosis+factor+%CE%B1/Recombinant+Mouse+TNF-alpha+(aa+80-235)+Protein/pm42019888-56-8-26
    Average 96 stars, based on 370 article reviews
    recombinant mouse tumor necrosis factor α - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Incubation:

    Article Title: Expression and function of β-site amyloid precursor protein cleaving enzyme 2 in vascular endothelium
    Article Snippet: Images were acquired using a JEOL1400+ TEM (RRID:SCR_020179, JEOL, Peabody, MA) operating at 80kV with an AMT Nanosprint 12 camera (AMT Imaging, Woburn, MA). .. Ten millimeters long aortas obtained from male wild-type (BACE2 +/+ ) mice were opened longitudinally and were incubated in MEM (composing 0.1% BSA, 100 U/mL penicillin/100 μg/mL streptomycin) with PBS or cocktail of inflammatory cytokines containing 20 ng/mL recombinant mouse tumor necrosis factor-α (TNFα; Cat# 410-MT; R&D Systems, Minneapolis, MN; RRID:SCR_006140), 1 ng/mL recombinant mouse interleukin-1β (IL1β; Cat# 401-ML; R&D Systems), and 50 ng/mL recombinant mouse interferon-γ (INFγ; Cat# 485-MI; R&D Systems) for 24 hours at 37°C in CO 2 incubator. ..

    Article Title: Endothelium-specific deletion of amyloid-β precursor protein exacerbates endothelial dysfunction induced by aging
    Article Snippet: Colorimetric cGMP ELISA immunoassay (Cell Biolabs Inc., San Diego, CA) was used to determine cGMP levels and the results were normalized against aortic protein concentrations. .. Ten millimeters long thoracic aortas were opened longitudinally and were incubated with control solution (PBS) or cytokines cocktail composing 20 ng/mL recombinant mouse tumor necrosis factor α (TNFα; R&D Systems, Minneapolis, MN), 50 ng/mL recombinant mouse interferon γ (INFγ; R&D Systems), and 1 ng/mL recombinant mouse interleukin-1ß (IL-1ß; R&D Systems) in MEM in the presence of bovine serum albumin (0.1%), penicillin (100 U/mL) and streptomycin (100 μg/mL) for 24 hours at 37° C in CO 2 incubator [ ]. ..

    Recombinant:

    Article Title: Expression and function of β-site amyloid precursor protein cleaving enzyme 2 in vascular endothelium
    Article Snippet: Images were acquired using a JEOL1400+ TEM (RRID:SCR_020179, JEOL, Peabody, MA) operating at 80kV with an AMT Nanosprint 12 camera (AMT Imaging, Woburn, MA). .. Ten millimeters long aortas obtained from male wild-type (BACE2 +/+ ) mice were opened longitudinally and were incubated in MEM (composing 0.1% BSA, 100 U/mL penicillin/100 μg/mL streptomycin) with PBS or cocktail of inflammatory cytokines containing 20 ng/mL recombinant mouse tumor necrosis factor-α (TNFα; Cat# 410-MT; R&D Systems, Minneapolis, MN; RRID:SCR_006140), 1 ng/mL recombinant mouse interleukin-1β (IL1β; Cat# 401-ML; R&D Systems), and 50 ng/mL recombinant mouse interferon-γ (INFγ; Cat# 485-MI; R&D Systems) for 24 hours at 37°C in CO 2 incubator. ..

    Article Title: Inducible general knockout of Runx3 profoundly reduces pulmonary cytotoxic CD8 + T cells with minimal effect on outcomes in mice following influenza infection
    Article Snippet: .. Recombinant mouse tumor necrosis factor-α (TNFα, no. 410-MT) was from R & D Systems (Minneapolis, MN, USA). .. Vector MOM immunodetection kit (no. PK-2200), Vector NovaRED substrate (no. SK-4800), Vector hematoxylin (no. H-3401), VectaMount permanent mounting medium (no. H-5000), and Vectashield hardset antifade mounting medium with DAPI (no. H-1500) were from Vector Laboratories (Burlingame, CA, USA).

    Article Title: Arsenic attenuates responsiveness to inflammatory stimuli in the SIM-A9 microglial cell line.
    Article Snippet: Arsenic (As) is a major public health threat, with more than 200 million people at risk of consuming drinking water that exceeds World Health Organization safety guidelines.. Given that inorganic arsenic (iAs) is linked to various neuropsychiatric and neurodegenerative disorders, a better understanding of its mechanisms of toxicity is warranted.. Current evidence suggests that microglia are central to the pathophysiology of As-induced effects in the central nervous system.

    Article Title: Hyperglycemia Induces Trained Immunity in Macrophages and Their Precursors and Promotes Atherosclerosis
    Article Snippet: .. Skin-derived mouse endothelial cells were grown to confluence on glass coverslips in 12-well plates and activated by 10 ng/mL recombinant mouse tumor necrosis factor-α (R&D Systems, UK) for 16 hours. .. Unstimulated or IFN-γ+LPS–stimulated peripheral blood monocytes (or BMDMs from streptozotocin diabetic mice cultured in 5 mmol/L glucose) were fluorescently labeled green with the PKH67 fluorescent cell linker kit (Sigma-Aldrich, UK) according to the manufacturer’s instructions.

    Article Title: Endothelium-specific deletion of amyloid-β precursor protein exacerbates endothelial dysfunction induced by aging
    Article Snippet: Colorimetric cGMP ELISA immunoassay (Cell Biolabs Inc., San Diego, CA) was used to determine cGMP levels and the results were normalized against aortic protein concentrations. .. Ten millimeters long thoracic aortas were opened longitudinally and were incubated with control solution (PBS) or cytokines cocktail composing 20 ng/mL recombinant mouse tumor necrosis factor α (TNFα; R&D Systems, Minneapolis, MN), 50 ng/mL recombinant mouse interferon γ (INFγ; R&D Systems), and 1 ng/mL recombinant mouse interleukin-1ß (IL-1ß; R&D Systems) in MEM in the presence of bovine serum albumin (0.1%), penicillin (100 U/mL) and streptomycin (100 μg/mL) for 24 hours at 37° C in CO 2 incubator [ ]. ..

    Article Title: Mycophenolic acid directly protects podocytes by preserving the actin cytoskeleton and increasing cell survival
    Article Snippet: .. After differentiation, the treatment group was pretreated with MPA for 24 h. Afterwards cells were treated with recombinant mouse Tumor Necrosis Factor-α (TNF-α; Recombinant Mouse TNF-alpha [aa 80–235] Protein, #410-MT, R&D Systems, 20 ng/ml), Cycloheximide (CHX; C4859, Sigma-Aldrich, 5 μg/ml) and MPA for an additional 24 h (TCM). ..

    Article Title: Mycophenolic acid directly protects podocytes by preserving the actin cytoskeleton and increasing cell survival.
    Article Snippet: .. After differentiation, the treatment group was pretreated with MPA for 24 h. Afterwards cells were treated with recombinant mouse Tumor Necrosis Factor-α (TNF-α; Recombinant Mouse TNF-alpha [aa 80–235] Protein, #410-MT, R&D Systems, 20 ng/ml), Cycloheximide (CHX; C4859, Sigma-Aldrich, 5 μg/ml) and MPA for an additional 24 h (TCM). ..

    Control:

    Article Title: Endothelium-specific deletion of amyloid-β precursor protein exacerbates endothelial dysfunction induced by aging
    Article Snippet: Colorimetric cGMP ELISA immunoassay (Cell Biolabs Inc., San Diego, CA) was used to determine cGMP levels and the results were normalized against aortic protein concentrations. .. Ten millimeters long thoracic aortas were opened longitudinally and were incubated with control solution (PBS) or cytokines cocktail composing 20 ng/mL recombinant mouse tumor necrosis factor α (TNFα; R&D Systems, Minneapolis, MN), 50 ng/mL recombinant mouse interferon γ (INFγ; R&D Systems), and 1 ng/mL recombinant mouse interleukin-1ß (IL-1ß; R&D Systems) in MEM in the presence of bovine serum albumin (0.1%), penicillin (100 U/mL) and streptomycin (100 μg/mL) for 24 hours at 37° C in CO 2 incubator [ ]. ..



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    ( A ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or T5z7 or T5z7+N for 6 hours; subsequently whole cell lysate (WCL) was harvested for immunoblot (IB) analysis. Values on left are in kilodaltons. C-, cleaved. ( B ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s (N) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N or T5z7Z or T5z7Z+N for 4 hours; subsequently WCL was harvested for IB analysis. ( C ) SPOP +/+ and SPOP –/– MEFs were pretreated with GSK872 (G) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+G for 4 hours; subsequently WCL was harvested for IB analysis. ( D ) IB analysis of WCL derived from RIPK3 +/+ and RIPK3 –/– MEFs with SPOP knockout through CRISPR technology. Parental MEFs were used as the control. Cells were treated with TSZ or DMSO for 4 hours; subsequently WCL was harvested for IB analysis. ( E ) A schematic illustration of RIPK1-mediated multimodal signaling events downstream of TNFR1. ( F ) SPOP +/+ and SPOP –/– MEFs were stimulated <t>by</t> <t>TNF-α</t> for the indicated periods of time. WCL was harvested for IB analysis. ( G ) SPOP +/+ and SPOP –/– MEFs were stimulated by FLAG–TNF-α for the indicated periods of time, and TNF-RSC was immunoprecipitated (IP) using anti-Flag resin and analyzed using the indicated antibodies. ( H ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N for 4 hours. Necrosome was immunoprecipitated using RIPK1 antibody and analyzed using the indicated antibodies.
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    ( A ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or T5z7 or T5z7+N for 6 hours; subsequently whole cell lysate (WCL) was harvested for immunoblot (IB) analysis. Values on left are in kilodaltons. C-, cleaved. ( B ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s (N) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N or T5z7Z or T5z7Z+N for 4 hours; subsequently WCL was harvested for IB analysis. ( C ) SPOP +/+ and SPOP –/– MEFs were pretreated with GSK872 (G) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+G for 4 hours; subsequently WCL was harvested for IB analysis. ( D ) IB analysis of WCL derived from RIPK3 +/+ and RIPK3 –/– MEFs with SPOP knockout through CRISPR technology. Parental MEFs were used as the control. Cells were treated with TSZ or DMSO for 4 hours; subsequently WCL was harvested for IB analysis. ( E ) A schematic illustration of RIPK1-mediated multimodal signaling events downstream of TNFR1. ( F ) SPOP +/+ and SPOP –/– MEFs were stimulated <t>by</t> <t>TNF-α</t> for the indicated periods of time. WCL was harvested for IB analysis. ( G ) SPOP +/+ and SPOP –/– MEFs were stimulated by FLAG–TNF-α for the indicated periods of time, and TNF-RSC was immunoprecipitated (IP) using anti-Flag resin and analyzed using the indicated antibodies. ( H ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N for 4 hours. Necrosome was immunoprecipitated using RIPK1 antibody and analyzed using the indicated antibodies.
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    ( A ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or T5z7 or T5z7+N for 6 hours; subsequently whole cell lysate (WCL) was harvested for immunoblot (IB) analysis. Values on left are in kilodaltons. C-, cleaved. ( B ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s (N) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N or T5z7Z or T5z7Z+N for 4 hours; subsequently WCL was harvested for IB analysis. ( C ) SPOP +/+ and SPOP –/– MEFs were pretreated with GSK872 (G) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+G for 4 hours; subsequently WCL was harvested for IB analysis. ( D ) IB analysis of WCL derived from RIPK3 +/+ and RIPK3 –/– MEFs with SPOP knockout through CRISPR technology. Parental MEFs were used as the control. Cells were treated with TSZ or DMSO for 4 hours; subsequently WCL was harvested for IB analysis. ( E ) A schematic illustration of RIPK1-mediated multimodal signaling events downstream of TNFR1. ( F ) SPOP +/+ and SPOP –/– MEFs were stimulated <t>by</t> <t>TNF-α</t> for the indicated periods of time. WCL was harvested for IB analysis. ( G ) SPOP +/+ and SPOP –/– MEFs were stimulated by FLAG–TNF-α for the indicated periods of time, and TNF-RSC was immunoprecipitated (IP) using anti-Flag resin and analyzed using the indicated antibodies. ( H ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N for 4 hours. Necrosome was immunoprecipitated using RIPK1 antibody and analyzed using the indicated antibodies.
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    Image Search Results


    ( A ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or T5z7 or T5z7+N for 6 hours; subsequently whole cell lysate (WCL) was harvested for immunoblot (IB) analysis. Values on left are in kilodaltons. C-, cleaved. ( B ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s (N) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N or T5z7Z or T5z7Z+N for 4 hours; subsequently WCL was harvested for IB analysis. ( C ) SPOP +/+ and SPOP –/– MEFs were pretreated with GSK872 (G) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+G for 4 hours; subsequently WCL was harvested for IB analysis. ( D ) IB analysis of WCL derived from RIPK3 +/+ and RIPK3 –/– MEFs with SPOP knockout through CRISPR technology. Parental MEFs were used as the control. Cells were treated with TSZ or DMSO for 4 hours; subsequently WCL was harvested for IB analysis. ( E ) A schematic illustration of RIPK1-mediated multimodal signaling events downstream of TNFR1. ( F ) SPOP +/+ and SPOP –/– MEFs were stimulated by TNF-α for the indicated periods of time. WCL was harvested for IB analysis. ( G ) SPOP +/+ and SPOP –/– MEFs were stimulated by FLAG–TNF-α for the indicated periods of time, and TNF-RSC was immunoprecipitated (IP) using anti-Flag resin and analyzed using the indicated antibodies. ( H ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N for 4 hours. Necrosome was immunoprecipitated using RIPK1 antibody and analyzed using the indicated antibodies.

    Journal: JCI Insight

    Article Title: SPOP mediates apoptosis and protects against necroptosis by regulating ubiquitination of RIPK1 and RIPK3

    doi: 10.1172/jci.insight.180655

    Figure Lengend Snippet: ( A ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or T5z7 or T5z7+N for 6 hours; subsequently whole cell lysate (WCL) was harvested for immunoblot (IB) analysis. Values on left are in kilodaltons. C-, cleaved. ( B ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s (N) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N or T5z7Z or T5z7Z+N for 4 hours; subsequently WCL was harvested for IB analysis. ( C ) SPOP +/+ and SPOP –/– MEFs were pretreated with GSK872 (G) or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+G for 4 hours; subsequently WCL was harvested for IB analysis. ( D ) IB analysis of WCL derived from RIPK3 +/+ and RIPK3 –/– MEFs with SPOP knockout through CRISPR technology. Parental MEFs were used as the control. Cells were treated with TSZ or DMSO for 4 hours; subsequently WCL was harvested for IB analysis. ( E ) A schematic illustration of RIPK1-mediated multimodal signaling events downstream of TNFR1. ( F ) SPOP +/+ and SPOP –/– MEFs were stimulated by TNF-α for the indicated periods of time. WCL was harvested for IB analysis. ( G ) SPOP +/+ and SPOP –/– MEFs were stimulated by FLAG–TNF-α for the indicated periods of time, and TNF-RSC was immunoprecipitated (IP) using anti-Flag resin and analyzed using the indicated antibodies. ( H ) SPOP +/+ and SPOP –/– MEFs were pretreated with Nec-1s or DMSO for 1 hour and then treated with DMSO or TSZ or TSZ+N for 4 hours. Necrosome was immunoprecipitated using RIPK1 antibody and analyzed using the indicated antibodies.

    Article Snippet: The reagent and concentration used in the experiment are as follows: recombinant mouse TNF-α (Cell sciences, CRT192C, 100 ng/mL), SM-164 (MedChemExpress [MCE], HY-15989, 50 nM), Nec-1s (Selleck, S8641, 20 μM), 5z7 (Sigma, 09890, 500 nM), zVAD.fmk (Sigma, V116, 25 μM), cycloheximide (Sigma, C-6255, 1 μM), and GSK872 (MilliporeSigma, 530389, 10 μM).

    Techniques: Western Blot, Derivative Assay, Knock-Out, CRISPR, Control, Immunoprecipitation

    ( A ) After knockdown of RIPK1 in 786-O, HepG2, and MDA-MB-231 cells, the protein levels of apoptotic markers mediated by TNF-α+SM164 (TS) stimulation were detected. ( B ) WT and RIPK3-overexpressing 786-O, HepG2, and MDA-MB-231 cells were treated with DMSO or TSZ for 6 hours; subsequently WCL was harvested for IB analysis. ( C ) Cell viability assay to assess the sensitivity of 786-O, HepG2, and MDA-MB-231 cells to SM164 treatment. ( D ) Cell viability assay for the effect of RIPK1 knockdown on the sensitivity of 786-O, HepG2, and MDA-MB-231 cells to sunitinib treatment. ( E ) Cell viability assay to assess the effect of combined use of SM164 on sunitinib sensitivity in 786-O, HepG2, and MDA-MB-231 cells. ( F ) Cell viability assay for the effect of RIPK1 knockdown on the sensitivity of 786-O, HepG2, and MDA-MB-231 cells to sunitinib alone, and sunitinib combined with SM164 treatment. ( G ) WT and RIPK1-knockdown 786-O, HepG2, and MDA-MB-231 cells were treated with DMSO, sunitinib alone, SM164 alone, or sunitinib combined with SM164 for 24 hours; subsequently WCL was harvested for IB analysis. Cell Counting Kit-8 (CCK-8) experiments were performed in triplicate and repeated 3 times independently. Data are presented as mean ± SD. The significance of differences was revealed based on paired Student’s t test.

    Journal: JCI Insight

    Article Title: SPOP mediates apoptosis and protects against necroptosis by regulating ubiquitination of RIPK1 and RIPK3

    doi: 10.1172/jci.insight.180655

    Figure Lengend Snippet: ( A ) After knockdown of RIPK1 in 786-O, HepG2, and MDA-MB-231 cells, the protein levels of apoptotic markers mediated by TNF-α+SM164 (TS) stimulation were detected. ( B ) WT and RIPK3-overexpressing 786-O, HepG2, and MDA-MB-231 cells were treated with DMSO or TSZ for 6 hours; subsequently WCL was harvested for IB analysis. ( C ) Cell viability assay to assess the sensitivity of 786-O, HepG2, and MDA-MB-231 cells to SM164 treatment. ( D ) Cell viability assay for the effect of RIPK1 knockdown on the sensitivity of 786-O, HepG2, and MDA-MB-231 cells to sunitinib treatment. ( E ) Cell viability assay to assess the effect of combined use of SM164 on sunitinib sensitivity in 786-O, HepG2, and MDA-MB-231 cells. ( F ) Cell viability assay for the effect of RIPK1 knockdown on the sensitivity of 786-O, HepG2, and MDA-MB-231 cells to sunitinib alone, and sunitinib combined with SM164 treatment. ( G ) WT and RIPK1-knockdown 786-O, HepG2, and MDA-MB-231 cells were treated with DMSO, sunitinib alone, SM164 alone, or sunitinib combined with SM164 for 24 hours; subsequently WCL was harvested for IB analysis. Cell Counting Kit-8 (CCK-8) experiments were performed in triplicate and repeated 3 times independently. Data are presented as mean ± SD. The significance of differences was revealed based on paired Student’s t test.

    Article Snippet: The reagent and concentration used in the experiment are as follows: recombinant mouse TNF-α (Cell sciences, CRT192C, 100 ng/mL), SM-164 (MedChemExpress [MCE], HY-15989, 50 nM), Nec-1s (Selleck, S8641, 20 μM), 5z7 (Sigma, 09890, 500 nM), zVAD.fmk (Sigma, V116, 25 μM), cycloheximide (Sigma, C-6255, 1 μM), and GSK872 (MilliporeSigma, 530389, 10 μM).

    Techniques: Knockdown, Viability Assay, Cell Counting, CCK-8 Assay