human tumour necrosis factor alpha (R&D Systems)
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human tumour necrosis factor alpha
Human Tumour Necrosis Factor Alpha, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 829 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tumour+necrosis+factor+alpha/Human+TNF-alpha+DuoSet+ELISA/pmc12926579-106-0-25
Average 97 stars, based on 829 article reviews
Human Tumour Necrosis Factor Alpha, supplied by R&D Systems, used in various techniques. Bioz Stars score: 97/100, based on 829 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tumour+necrosis+factor+alpha/Human+TNF-alpha+DuoSet+ELISA/pmc12926579-106-0-25
Average 97 stars, based on 829 article reviews
human tumour necrosis factor alpha - by Bioz Stars,
2026-10
97/100 stars
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![( A ) Schematic overview of <t>TNFα/TNFR1</t> signalling. Engagement of TNFR1 promotes formation of membrane-associated complex I, leading to activation of NF-κB and MAPK signalling pathways and induction of pro-survival gene expression. Disruption of this pathway can result in formation of cytosolic complex IIa, leading to caspase activation and apoptosis. Birinapant promotes degradation of cIAP1/2, destabilising complex I and favouring early complex II formation, whereas cycloheximide inhibits protein synthesis and prevents accumulation of pro-survival factors downstream of TNFR1 signalling. ( B ) Quantification of live cells following treatment with TNFα, birinapant, or their combination (BT), assessed by flow cytometry in MDA-MB-231 cells. Cells were stained with Annexin V and propidium iodide (PI), and live cells were defined as Annexin V-negative/PI-negative. Data represent mean ± SD from three independent biological replicates. ( C ) Time-resolved analysis of cell viability following treatment with TNFα in combination with birinapant ( left ) or cycloheximide ( right ). Live-cell percentages were quantified from IncuCyte live-cell imaging using FluoroFate. BT treatment induces rapid and near-complete loss of viability, whereas CT treatment results in delayed but progressive cell death, demonstrating distinct temporal dynamics depending on the mode of TNFα pathway perturbation. ( D ) Representative live-cell imaging of MDA-MB-231 cells over the first 6 hours following treatment with untreated control (UT), BT, or CT. Annexin V-positive cells (green) and PI-positive cells (red) are shown overlaid on brightfield images. BT treatment results in rapid and widespread Annexin V staining, whereas CT treatment shows delayed onset of cell death. Scale bar, 100 μm. [ E ] Flow cytometry analysis of Annexin V staining over the first 6 hours following BT treatment. Representative dot plots show progressive increase in Annexin V-positive cells over time, confirming rapid induction of apoptosis at the single-cell level. Statistical significance was determined using one-way ANOVA with Dunnett’s post-hoc test, with **** indicating P < 0.0001 and ns indicating non-significant differences.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_87/10__64898_slash_2026__08__17__745187/10__64898_slash_2026__08__17__745187___F4.large.jpg)
![Aedes aegypti salivary gland extract (SGE) modulates cytokine production by antigen-presenting cell lines during Zika virus (ZIKV) infection. JAWS II dendritic cells and RAW 264.7 macrophages were cultured for 72 h under the indicated conditions (Only Media, SGE, ZIKV, or ZIKV+SGE at different concentrations). Cytokine concentrations [tumour necrosis <t>factor-alpha</t> <t>(TNF-α),</t> interleukin-1beta (IL-1β), IL-10, IL-12] were quantified in culture supernatants by enzyme-linked immunosorbent assay (ELISA). In JAWS II cells (A-D), significant differences were observed <t>for</t> <t>TNF-α,</t> IL-1β, and IL-12, while IL-10 levels remained stable. In RAW 264.7 cells (E-H), SGE <t>enhanced</t> <t>TNF-α,</t> IL-1β, and IL-10 secretion, whereas IL-12 showed no significant modulation. Data represent individual values from independent experiments with bars indicating mean ± standard error of the mean (SEM). Statistical analysis was performed using Kruskal-Wallis with Dunn’s post-hoc test; p < 0.05 was considered significant.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_3171/pmc13143171/pmc13143171__1678-8060-mioc-121-e250272-gf12.jpg)
![( A ) Schematic overview of TNFα/TNFR1 signalling, illustrating that disruption of complex IIa can promote formation of cytosolic complex IIb, from which signalling through RIPK1/RIPK3/MLKL can drive non-apoptotic cell death. ( B ) Western blot analysis of apoptotic signalling following BT treatment in MDA-MB-231 cells over the indicated time course. Cleavage of PARP, caspase 3, and caspase 8 confirms induction of apoptosis. Autophosphorylation of RIPK1 (p-RIPK1) at Ser166 and reduction of cIAP1 levels demonstrate modulation of TNFα/TNFR1 signalling. Β-actin serves as a loading control. ( C ) FluoroFate analysis of cell death dynamics in MDA-MB-231 cells following treatment with BT ( left ) or CT ( right ). The proportion of cells undergoing apoptosis (Annexin V-positive prior to PI), non-apoptotic cell death (PI-positive prior to or concurrent with Annexin V), and total cell death is shown. BT induces rapid and predominantly apoptotic cell death, whereas CT results in delayed and more heterogeneous cell death dynamics. ( D ) Quantification of live cells in SKOV3 WT and RIPK1 KO cells following BT treatment, assessed by flow cytometry. Cells were stained with Annexin V-FITC and PI, and live cells were defined as Annexin V-negative/PI-negative. RIPK1 KO cells exhibit increased resistance to BT-induced cell death compared to WT cells. [ E ] FluoroFate analysis of cell viability in SKOV3 WT and RIPK1 KO cells following BT treatment. Loss of RIPK1 delays and reduces overall cell death kinetics. ( F ) Single-cell classification of apoptotic and non-apoptotic cell death in SKOV3 WT ( left ) and RIPK1 KO ( right ) cells following BT treatment. Loss of RIPK1 selectively reduces apoptotic cell death, whilst non-apoptotic cell death remains largely unchanged, indicating that distinct modes of cell death are independently regulated at the single-cell level. Data represent mean ± SD from three biological replicates. Statistical significance was determined using two-way ANOVA followed by Fisher’s LSD post-hoc test (***P ≤ 0.0002, ****P < 0.0001, ns, not significant).](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_87/10__64898_slash_2026__08__17__745187/10__64898_slash_2026__08__17__745187___F5.large.jpg)