Tnf α

Manufactured by Merck Group

Sourced in United States, Germany, United Kingdom, China, Italy, Macao, Sao Tome and Principe, France, Australia, Canada, India, Switzerland, Austria, Morocco, Japan

TNF-α is a recombinant human tumor necrosis factor alpha (TNF-α) product. TNF-α is a cytokine that plays a central role in inflammation and immune system regulation.

Automatically generated - may contain errors

Lab products found in correlation

Fetal bovine serum (fbs), by Thermo Fisher Scientific (66 mentions) Il 1β, by Merck Group (60 mentions) Interleukin 6 (il 6), by Merck Group (57 mentions) Ifn γ, by Merck Group (40 mentions) Lipopolysaccharides (lps), by Merck Group (32 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (23 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (22 mentions) Il 10, by Merck Group (21 mentions) Dimethyl sulfoxide (dmso), by Merck Group (18 mentions) Tnf α, by Thermo Fisher Scientific (18 mentions) Dexamethasone (dex), by Merck Group (15 mentions) Cycloheximide (chx), by Merck Group (15 mentions) Tnf α, by R&D Systems (13 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (12 mentions) Ifn γ, by R&D Systems (11 mentions) Bovine serum albumin (bsa), by Merck Group (11 mentions) Insulin, by Merck Group (10 mentions) Rpmi 1640 medium, by Thermo Fisher Scientific (10 mentions) Phorbol myristate acetate (pma), by Merck Group (10 mentions) Fetal bovine serum (fbs), by Merck Group (10 mentions)

744 protocols using tnf α

Investigating Androgen and TNFα Effects on Prostate Cancer Cells

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The LNCaP cells were divided into four groups. The control group was cultured in the absence of treatment for 24 h; the TNFα induction group was induced by TNFα (100 ng/ml; Sigma, St. Louis, MO, USA) for 24 h. the R1881 group was treated for 24 h with a synthetic androgen, R1881 (1×10⁻⁸ M; Sigma); and the TNF + R1881 group was treated concomitantly with TNFα (100 ng/ml) and R1881 (1×10⁻⁸ M) for 24 h.
DU145 cells transfected with STAMP1 or STAMP2 were induced by TNFα (100 ng/ml) or were not induced for 24 h.
In another series of experiments, following NFκB gene silencing, the LNCaP cells transfected for 1 day were induced by TNFα (100 ng/ml) or were not induced for a further 24 h. The cells transfected for 4 days were induced by TNFα (100 ng/ml) or were not induced at the third day of transfection.

GONEN-KORKMAZ C., SEVIN G., GOKCE G., ARUN M.Z., YILDIRIM G., REEL B., KAYMAK A, & OGUT D. (2014). Analysis of tumor necrosis factor α-induced and nuclear factor κB-silenced LNCaP prostate cancer cells by RT-qPCR. Experimental and Therapeutic Medicine, 8(6), 1695-1700.

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NF-κB Activation in Endometrial Cells

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Ishikawa cells and ESCs were grown in serum-free, phenol redfree media (Sigma-Aldrich) for 18 hours. After this step, the cells were treated either with medium only (for the control and TNF-a groups) or 10 À5 M PDTC (Sigma) (for the TNF-a plus PDTC group) for 1 hour. Next, the cells were treated with medium only (control) or 10-nM TNF-a (Sigma) (for the TNF-a and TNF-a plus PDTC groups) for 30 minutes for the NF-kB p65-DNA (deoxyribonucleic acid) binding immunodetection assay, or for 24 hours for Pak4 western blot analysis. Nuclear protein extraction and the NF-kB p65-DNA binding immunodetection assay were performed as described in our previous study (18) . For experimental control for nuclear and cytosol fractions, we performed western blot analysis on lamin B protein (Santa Cruz Biotechnology). We could see clear lamin-B expression in the nuclear fraction (A: Ishikawa cell; B: endometrial stromal cell), whereas no expression was observed in the cytosol fraction (Supplemental Fig. 1, available online). As an experimental control for the NF-kB p65-DNA binding immunodetection assay, we performed western blot analyses on the NF-kB p65 subunit in the nuclear fraction as described in our previous study (18) .

Yi K.W., Kim S.H., Ihm H.J., Oh Y.S., Chae H.D., Kim C.H, & Kang B.M. (2015). Increased expression of p21-activated kinase 4 in adenomyosis and its regulation of matrix metalloproteinase-2 and -9 in endometrial cells. Fertility and sterility, 103(4).

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Periodontal Ligament Stem Cell Culture

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Periodontal ligament stem cells were cultured under several different conditions as follows:

Control group (G5.6 group): cells were incubated in a medium containing 5.6 mM D-glucose (Sigma-Aldrich, St. Louis, MO, USA)

TNF-α treatment group (G5.6+TNF-α group): cells were incubated in a medium containing 5.6 mM D-glucose and TNF-α (10 ng/ml, Sigma-Aldrich, St. Louis, MO, USA);

High-glucose treatment group (G30 group): cells were incubated in a medium containing 30 mM D-glucose

High-glucose and TNF-α treatment group (G30+TNF-α group): cells were incubated in a medium containing 30 mM D-glucose and TNF-α (10 ng/ml)

The osmotic effect was also evaluated by the addition of mannitol (Sigma-Aldrich, St. Louis, MO, USA). Cells were incubated in a medium containing 5.6 mM D-glucose and 24.4 mM mannitol.

Zhu W., Qiu Q., Luo H., Zhang F., Wu J., Zhu X, & Liang M. (2020). High Glucose Exacerbates TNF-α-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1. Stem Cells International, 2020, 4910767.

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Investigating the Role of NF-κB and p38 MAPK in TNF-α-Mediated Sodium Current Modulation

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Tetrodotoxin (TTX; 300 nM in the bath solution of voltage clamp experiments) was used to verify the TTX sensitivity of the channels. In dose-finding experiments, TNF-α (Sigma) of varying concentration (1, 10, 100, and 1000 pg/ml) was included in the medium for 24 h. For subsequent experiments, cultured neurons were exposed to TNF-α at 100 or 1000 pg/ml in 0.1 % bovine serum albumin (BSA) in saline for 4, 8, 24, or 48 h. Neurons were pretreated with an NF-κB inhibitor (10 μM BAY-11 7082 in 0.1 % dimethylsulfoxide) or a p38 mitogen-activated protein kinases (MAPK) inhibitor (10 μM SB203580 in 0.1 % DMSO) for 0.5 h before and during TNF-α exposure (100 pg/ml 24 h) to determine whether the activation of NF-κB and/or p38 MAPK contributes to the TNF-α-induced enhancement of voltage-gated Na⁺ currents.

Chen W., Sheng J., Guo J., Gao F., Zhao X., Dai J., Wang G, & Li K. (2015). Tumor necrosis factor-α enhances voltage-gated Na+ currents in primary culture of mouse cortical neurons. Journal of Neuroinflammation, 12, 126.

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Melanoma Cell Lines and TNF-α Stimulation

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The human melanoma cell line WM266.4 was kindly provided by the Department of Medical Biochemistry of the Jagiellonian University Medical College (Kraków, Poland) in 2006 and authenticated in 2021 using STR profiling with Identifiler Plus (ABI) and an ABI 3130xl Genetic Analyzer (Applied Biosystems, Waltham, MA, USA). Human melanoma cell line A375 was obtained from the American Type Culture Collection (CRL_1619, ATCC, Manassas, VA, USA) in 2020. Both cell lines were cultured in RPMI1640 containing 10% FBS (Gibco, Thermo Fisher Scientific, Waltham, MA, USA), penicillin 150 U/ml (Sigma-Aldrich, St. Louis, MO, USA), and streptomycin 100 µg/mL (Sigma-Aldrich, St. Louis, MO, USA) at 37 °C at 5% CO₂ and 95% humidity. TNF-α (100 ng/mL, Sigma-Aldrich, St. Louis, MO, USA) was dissolved in 0.1% BSA/ PBS, aliquoted, and stored at − 20 °C. For ELISA analysis, the cell culture medium was replaced with serum-free medium and TNF-α (10 ng/mL) was added 24 h, while for qRT-PCR, TNF-α was added to the complete media for 3 h. The effect of p38 MAPK was studied using a p38 inhibitor SB203580 (10 μM, Sigma Aldrich, St. Louis, MO, USA) which was applied 1 h before TNF-α stimulation and present during the treatment.

Madej E., Lisek A., Brożyna A.A., Cierniak A., Wronski N., Deptula M., Wardowska A, & Wolnicka-Glubisz A. (2024). The involvement of RIPK4 in TNF-α-stimulated IL-6 and IL-8 production by melanoma cells. Journal of Cancer Research and Clinical Oncology, 150(4), 209.

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Cytokine-Stimulated LPMC Profiling

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LPMCs (1 × 10⁶ cells/ml) from 3 subjects were stimulated with various combinations of TNF-α (Sigma-Aldrich) and IL-10 (Sigma-Aldrich) using a total concentration of 10 ng/mL (i.e. a 9 ng/mL TNF-α and 1 ng/mL IL-10 combination sample was used as 9:1 TNF-α:IL-10 samples). Unstimulated cells were used as a negative control. The incubation and staining method were the same with above.

Yamada E., Martin C.G., Moreno-Huizar N., Fouquier J., Neff C.P., Coleman S.L., Schneider J.M., Huber J., Nusbacher N.M., McCarter M., Campbell T.B., Lozupone C.A, & Palmer B.E. (2021). Intestinal microbial communities and Holdemanella isolated from HIV+/− men who have sex with men increase frequencies of lamina propria CCR5+ CD4+ T cells. Gut Microbes, 13(1), 1997292.

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Modulation of Tau Phosphorylation by TNF-α and Propofol

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Recombinant mouse TNF-α was obtained from Sigma-Aldrich (St. Louis, MO, USA) and was reconstituted with sterile water to a stock concentration of 0.1 mg/mL. To investigate the effect of TNF-α on p-Tau accumulation, neurons were exposed to different concentrations of TNF-α (10, 20, 40, 80, and 160 ng/mL) for different durations (1, 2, 4, and 8 h). By measuring the expression and phosphorylation of Tau protein, we aimed to determine the optimal condition, under which TNF-α exerted significant effect on the accumulation of p-Tau.
To investigate the protective effects of propofol against TNF-α in hippocampal neurons, we incubated neurons with different concentrations (1, 5, 10, 25, 50, and 100 μM) of propofol (Sigma-Aldrich, St Louis, MO, USA) or its solvent 0.1% dimethyl sulfoxide (DMSO, Sigma-Aldrich, St Louis, MO, USA) for 1 h followed by TNF-α treatment (with the presence of propofol or DMSO). By observing the expression and phosphorylation of Tau protein, we intended to identify the optimal concentration, at which propofol exerted protective effects against p-Tau accumulation.

Zhang L., Song H., Ding J., Wang D.J., Zhu S.P., Liu C., Jin X, & Chen J.W. (2022). The Mechanism of TNF-α-Mediated Accumulation of Phosphorylated Tau Protein and Its Modulation by Propofol in Primary Mouse Hippocampal Neurons: Role of Mitophagy, NLRP3, and p62/Keap1/Nrf2 Pathway. Oxidative Medicine and Cellular Longevity, 2022, 8661200.

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Caco-2 Cell Stimulation with TNF-α

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The human intestinal cell line Caco-2 (American Tissue Type Culture Collection, Rockville, MD, USA) cells were cultivated as monolayers and maintained as previously described.^{23 (link)} For stimulation experiments, 10⁶ cells were seeded in 24-well plates (NUNC Brand, Thermo Fisher, Rochester, NY, USA) and grown to >95% confluence. Cells were then stimulated in medium with or without TNF-α (R&D Systems, Minneapolis, MN, USA) in the presence or absence of tosyl phenylalanyl chloromethyl ketone (TPCK) NF-κB inhibitor; 100 µM; Sigma-Aldrich, St. Louis, MO, USA), FR180204 (ERK inhibitor; 30 µM; Merck Chemicals, Darmstadt, Germany), or vehicle [0.4% dimethyl sulphoxide (DMSO); Sigma-Aldrich] as done previously.^{24 (link)} In experiments involving treatment with inhibitors, cells were exposed to the inhibitors 1 h prior to the addition of TNF-α and subsequently stimulated with TNF-α (10 nM) for 24 h. For CAGE analysis, we used biological triplicates with or without TNF-α (10 nM).

Boyd M., Coskun M., Lilje B., Andersson R., Hoof I., Bornholdt J., Dahlgaard K., Olsen J., Vitezic M., Bjerrum J.T., Seidelin J.B., Nielsen O.H., Troelsen J.T, & Sandelin A. (2014). Identification of TNF-α-Responsive Promoters and Enhancers in the Intestinal Epithelial Cell Model Caco-2. DNA Research: An International Journal for Rapid Publication of Reports on Genes and Genomes, 21(6), 569-583.

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Cytokine-Induced Signaling Pathways in U937 Cells

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U937/PMA (differentiated U937) cells were treated with 5 ng/ml TNFα (Sigma-Aldrich), 10 ng/ml IFNγ (ImmunoTools GmbH, Friesoythe, Germany) or combined IFNγ and TNFα in the presence or absence of 0.1 μg/ml cycloheximide. At various time periods after activation, U937/PMA cells were harvested and analyzed to detect CIC expression levels. Where indicated U937/PMA cells were treated with 20 μM IKK inhibitor VII (IKK VII, Millipore, Billerica, MA, USA), 10 μM nifuroxazide (NIFU, Sigma-Aldrich), 5 mM sodium acetate (Sigma-Aldrich) or 1 μM 4-chloro-3-{[(3-nitrophenyl)amino]sulfonyl}benzoic acid (CNFASB, Millipore), 1 h before stimulation with TNFα, IFNγ, or combined cytokines.

Infantino V., Iacobazzi V., Menga A., Avantaggiati M.L, & Palmieri F. (2014). A key role of the mitochondrial citrate carrier (SLC25A1) in TNFα- and IFNγ-triggered inflammation. Biochimica et biophysica acta, 1839(11), 1217-1225.

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Colon Epithelium Mimicry with Caco2 and T84 Cells

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Caco2 and T84 cell can form monolayers in plates, and are used widely as colon
epithelium models to mimic the epithelium of the human colon mucosa.^{3 (link)} Caco2 and T84 cell lines were obtained from the American Type Culture
Collection (Rockville, MD, USA). For more details of cell culture, see Supplemental Digital Content 1.
Following establishment of monolayer of Caco2 and T84 cells at about 12 days
after seeding, TNF-α (Sigma, St Louis, MO, USA) was added to the medium at three
different concentrations (5 ng/ml, 10 ng/ml, and 20 ng/ml) to mimic different
disease activity in CD. Another group of cells had double distilled water added
as a control. After culturing with TNF-α for 24 h, cells in six-well plates were
harvested to determine the RNA expression of uc.261 by PCR.
Transepithelial electrical resistance assays (TEER) values of Caco2 and T84 cells
in Transwell plates were determined with Millicell ERS-2 (Millipore, Billerica,
MA, USA), in units of Ω·cm². For more details of TEER assays, see
Supplemental Digital Content 1.

Qian X.X., Cai C.W., Li H.Y., Lai L.J., Song D.J., Qiao Y.Q., Shen J, & Ran Z.H. (2019). Transcribed ultraconserved region (T-UCR) uc.261 expression is closely correlated with disease activity and intestinal permeability in Crohn’s disease. Therapeutic Advances in Gastroenterology, 12, 1756284819880733.

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