TNF alpha Antibody - #DF6080

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产品: TNF alpha 抗体
货号: DF6080
描述: Rabbit polyclonal antibody to TNF alpha
应用: WB IHC
文献验证: WB
反应: Human, Mouse, Rat
预测: Pig, Dog
蛋白号: P01375
RRID: AB_2838048

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产品描述

来源:
Rabbit
应用:
WB 1:1000-1:2000, IHC 1:50-1:100
*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, Mouse, Rat
克隆:
Polyclonal
特异性:
TNF alpha Antibody detects endogenous levels of total TNF alpha.
RRID:
AB_2838048
引用格式: Affinity Biosciences Cat# DF6080, RRID:AB_2838048.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , 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:

A synthesized peptide derived from human TNF alpha, corresponding to a region within the internal amino acids.

基因/基因ID:
TNF(7124)
描述:
TNF-α, the prototypical member of the TNF protein superfamily, is a homotrimeric type-II membrane protein (1,2). Membrane-bound TNF-α is cleaved by the metalloprotease TACE/ADAM17 to generate a soluble homotrimer (2). Both membrane and soluble forms of TNF-α are biologically active. TNF-α is produced by a variety of immune cells including T cells, B cells, NK cells, and macrophages (1). Cellular response to TNF-α is mediated through interaction with receptors TNF-R1 and TNF-R2 and results in activation of pathways that favor both cell survival and apoptosis depending on the cell type and biological context. Activation of kinase pathways (including JNK, Erk (p44/42), p38 MAPK, and NF-κB) promotes the survival of cells, while TNF-α-mediated activation of caspase-8 leads to programmed cell death (1,2). TNF-α plays a key regulatory role in inflammation and host defense against bacterial infection, notably Mycobacterium tuberculosis (3). The role of TNF-α in autoimmunity is underscored by blocking TNF-α action to treat rheumatoid arthritis and Crohn’s disease (1,2,4).

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). S100A9 as a promising therapeutic target for diabetic foot ulcers. Chinese medical journal, 2025 (PubMed: 40143429) [IF=7.5]
2). Stress-induced phosphoprotein 1 restrains spinal cord ischaemia-reperfusion injury by modulating NF-κB signalling. Journal of Cellular and Molecular Medicine, 2021 (PubMed: 34734476) [IF=5.3]

Application: WB    Species: Mouse    Sample: BV2 cells

FIGURE 4 STIP1 restrains OGD-induced inflammation in microglial cells. A, BV2 cell treatments; B, Western blotting determines STIP1 expression in BV2 cells after OGD treatment, C, Immunoprecipitation detects the binding between STIP1 and HSPA8 in BV2 cells; D, Western blotting determines STIP1 expression after STIP1 overexpression; E, Immunoprecipitation detects the interaction between HSPA8 and IκBβ in BV2 cells; F, Western blotting detects IκBβ expression in BV2 cells; G, Western blotting detects cytoplasmic and nuclear NF-κB p65 levels in BV2 cells; H, Immunofluorescent staining detects the location of NF-κB p65. Scale bar =50 μm; I, Immunofluorescent staining detects the expression of the microglia marker Iba-1. Scale bar =50 μm; J, ELISA detects the secretion of inflammatory factors TNF-α and IL-6 in the cell culture supernatant; K, Western blotting determines TNF-α and IL-6 expression in BV2 cells after OGD treatment and STIP1 overexpression. NF-κB, nuclear factor kappa B; OGD, oxygen and glucose deprivation; SCII, spinal cord ischaemia-reperfusion injury; STIP1, stress-induced phosphoprotein 1; TNF, tumour necrosis factor. **p < 0.01, ***p < 0.001 versus the Sham group, #p < 0.05, ##p < 0.01, ###p < 0.001 versus the SCII + LV group
3). SLC15A3 is transcriptionally regulated by HIF1α and p65 to worsen neuroinflammation in experimental ischemic stroke. Molecular neurobiology, 2024 (PubMed: 38717559) [IF=4.6]

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