TNF-alpha Antibody - #BF0170

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产品: TNF-alpha 抗体
货号: BF0170
描述: Mouse monoclonal antibody to TNF-alpha
应用: WB ELISA
文献验证: WB
反应: Human
蛋白号: P01375
RRID: AB_2833613

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 50ul RMB¥ 1800 现货
 100ul RMB¥ 2800 现货

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产品描述

来源:
Mouse
应用:
ELISA 1:10000, WB 1:500-1:2000
*The optimal dilutions should be determined by the end user. For optimal experimental results, antibody reuse is not recommended.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human
克隆:
Monoclonal [AFB1588]
特异性:
TNF-alpha antibody detects endogenous levels of total TNF-alpha.
RRID:
AB_2833613
引用格式: Affinity Biosciences Cat# BF0170, RRID:AB_2833613.
偶联:
Unconjugated.
纯化:
Affinity-chromatography.
保存:
Mouse IgG1 in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

APC1; APC1 protein; Cachectin; DIF; Differentiation inducing factor; Macrophage cytotoxic factor; Tnf; TNF superfamily, member 2; TNF, macrophage derived; TNF, monocyte derived; TNF-a; TNF-alpha; TNFA; TNFA_HUMAN; TNFSF2; Tumor necrosis factor alpha; Tumor necrosis factor; Tumor necrosis factor ligand superfamily member 2; Tumor Necrosis Factor, Membrane Form; Tumor necrosis factor, soluble form;

抗原和靶标

免疫原:

Purified recombinant fragment of human TNF-alpha expressed in E. Coli.

基因/基因ID:
TNF(7124)
描述:
TNF-alpha (tumor necrosis factor alpha) is an important cytokine produced by numerous cell types including neutrophils, activated lymphocytes, macrophages and NK cells. It plays a critical role in inflammatory responses and in apoptosis. TNF-alpha is believed to mediate pathogenic shock and tissue injury associated with endotoxemia. TNF-alpha exists as a multimer of two, three, or five non covalently linked units, but shows a single 17 kDa band following SDS PAGE under non reducing conditions. Although it has little effect on many cultured normal human cells, TNF-alpha appears to be directly toxic to vascular endothelial cells. Other actions of TNF-alpha include stimulating growth of human fibroblasts and other cell lines, activating polymorphonuclear neutrophils and osteoclasts, and induction of interleukin 1, prostaglandin E2 and collagenase production. TNF-alpha is currently being evaluated in treatment of certain cancers and AIDS Related Complex.

研究领域

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TGF-beta signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > Antifolate resistance.

· Human Diseases > Endocrine and metabolic diseases > Type II diabetes mellitus.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Endocrine and metabolic diseases > Type I diabetes mellitus.

· Human Diseases > Neurodegenerative diseases > Alzheimer's disease.

· Human Diseases > Neurodegenerative diseases > Amyotrophic lateral sclerosis (ALS).

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Immune diseases > Asthma.

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Systemic lupus erythematosus.

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Human Diseases > Immune diseases > Allograft rejection.

· Human Diseases > Immune diseases > Graft-versus-host disease.

· Human Diseases > Cardiovascular diseases > Hypertrophic cardiomyopathy (HCM).

· Human Diseases > Cardiovascular diseases > Dilated cardiomyopathy (DCM).

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Antigen processing and presentation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > RIG-I-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Hematopoietic cell lineage.   (View pathway)

· Organismal Systems > Immune system > Natural killer cell mediated cytotoxicity.   (View pathway)

· Organismal Systems > Immune system > IL-17 signaling pathway.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Fc epsilon RI signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

文献引用

1). The novel hyaluronic acid granular hydrogel attenuates osteoarthritis progression by inhibiting the TLR-2/NF-κB signaling pathway through suppressing cellular senescence. Bioengineering & Translational Medicine, 2023 (PubMed: 37206234) [IF=7.4]

Application: IF/ICC    Species: Human    Sample:

FIGURE 3 (a) Cell viability of chondrocytes after incubation with different concentrations of ARTZ® and novel HA (n‐HA) using the CCK‐8 assay. (b) Cell proliferation measurement of chondrocytes after incubation with 1 mg/ml ARTZ® and n‐HA for 1, 2, and 3 days using CCK‐8 assay. (c) Live/Dead staining of chondrocytes after incubation with 1 mg/ml ARTZ® and n‐HA for 1, 2, and 3 days, the live cells were stained green, whereas the dead cells were stained red. Scale bar = 200 μm. (d) Representative confocal images of phalloidin stained chondrocytes with or without TNF‐α, ARTZ®, and n‐HA treatment. Scale bar = 100 μm. (e) The quantification of apoptotic rates of chondrocytes with various treatment by flow cytometry. (n = 3, *p 
2). Salidroside ameliorates endothelial inflammation and oxidative stress by regulating the AMPK/NF-κB/NLRP3 signaling pathway in AGEs-induced HUVECs. European Journal of Pharmacology, 2020 (PubMed: 31747547) [IF=4.2]

Application: WB    Species: Human    Sample: HUVECs

Fig. S1. Effect of a RAGE receptor inhibitor (FPS-ZM1) on cell viability, pro-inflammatory gene expression, cell apoptosis and reactive oxygen species production. The HUVECs in the experiment were divided into four groups: control, AGEs (200 µg/mL), AGEs+Sal (50 µM), and AGEs+FPS-ZM1 (1 µg/ml, 1 h). (A) Cell viability of HUVECs. (B-D) Expression of pro-inflammatory genes (B: TNF-a; C: IL-1β; D: IL-6). (E) Representative cell apoptosis images were after Hoechst 33342 staining. (F) Representative images of reactive oxygen species induced fluorescence signals. The data are representative of one experiment performed in triplicate and are expressed as the mean ± S.D. **P<0.01 vs. control group; ##P<0.01 vs. AGEs group.
3). Inflammation Is More Sensitive than Cell Proliferation in Response to Rapamycin Treatment in Polycystic Kidney Disease. Kidney & blood pressure research, 2024 (PubMed: 38167222) [IF=2.8]

Application: WB    Species: Rat    Sample:

Fig. 3. mTOR cell signaling pathways and pro-inflammatory factors in rapamycin (Rap) or vehicle-treated cystic kidneys. a The inhibition of the mTOR pathway (p-p70S6K) and the feedback activation of Akt (p-Akt) were analyzed by Western blot in 12-week-old +/+ and Cy/+ kidneys (6 rats in each group). b The expression of CFB, TNF-α, and MCP-1 was analyzed by Western blot in 12-week-old +/+ and Cy/+ kidneys. Blots are representative of three independent experiments. c Western blot expression quantified by densitometry, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

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