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Key Documents

T8300

Sigma-Aldrich

Anti-Tumor Necrosis Factor-α antibody produced in rabbit

IgG fraction of antiserum, buffered aqueous solution

同義詞:

Anti-TNF-α

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About This Item

MDL號碼:
分類程式碼代碼:
51111800
NACRES:
NA.41

生物源

rabbit

共軛

unconjugated

抗體表格

IgG fraction of antiserum

抗體產品種類

primary antibodies

無性繁殖

polyclonal

形狀

buffered aqueous solution

物種活性

human

技術

dot blot: 1:2,000
microarray: suitable
neutralization: 1-3 μg/mL

UniProt登錄號

運輸包裝

dry ice

儲存溫度

−20°C

目標翻譯後修改

unmodified

基因資訊

human ... TNF(7124)

一般說明

Tumor necrosis factor- α(TNF-α), also known as cachectin, is an inflammatory cytokine that exists primarily as a 51kDa complex built up of 3 identical, non-covalently-linked polypeptide subunits (17 kDa, 157 amino acid residues, in human). TNF- αoccurs as a secreted, soluble form and as a membrane-anchored form, both of which are biologically active. TNF-α is secreted by neutrophils, activated lymphocytes, macrophages, NK cells, LAK cells, astrocytes, endothelial cells, smooth muscle cells, and some transformed cells.

特異性

The antibody binds to TNF-α. It does not cross-react with recombinant human TNF-β, IL-1a, IL-1β or IL-3, nor with recombinant mouse or human IL-6.

免疫原

recombinant human TNF-α produced in bacteria.

應用

Anti-Tumor Necrosis Factor-α antibody may be used for dot blot at a working antibody dilution of 1:2000. The antibody may be used for neutralization assay; the ND50 is 1-3 μg/ml. Anti-TNF-α antibody was used for neutralization of TNF-α of Jurkat cells.
Anti-Tumor Necrosis Factor-α antibody produced in rabbit has been used in western blotting. It may also be used in enzyme linked immunoassay (ELISA).

生化/生理作用

Tumor Necrosis Factor-α (TNF-α) is a cytokine produced by macrophages in response to stimulus by LPS. It plays a major role in mediating inflammation, tissue injury, pathogenic shock, innate immunity, apoptosis and autoimmunity. The physiological effects of TNF-α are mediated by receptors of TNFR super family. The TNF/TNFR signaling axis plays a critical role in mediating either survival or apoptosis depending on the class of adaptor proteins recruited in the cell. Association of receptors with a death domain causes rapid activation of caspases and results in cell death. TNF/TNFR also results in the activation of downstream pathways involving MAPK, p38, JNK and NF-κB that play a major role in innate immunity, acute inflammatory responses and homeostasis. The TNF/TNFR axis is also important in the pathology of various autoimmune and inflammatory disorders including a variety of malignancies and Alzheimer′s disease.

免責聲明

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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儲存類別代碼

12 - Non Combustible Liquids

水污染物質分類(WGK)

nwg

閃點(°F)

Not applicable

閃點(°C)

Not applicable


分析證明 (COA)

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Hongyan Gong et al.
Experimental and therapeutic medicine, 17(1), 41-50 (2019-01-18)
Colon cancer is one of the most common types of gastrointestinal tumor. Previous studies have demonstrated that tumor necrosis factor-(TNF)-related apoptosis-inducing ligand (TRAIL) reduces the aggressiveness of colon cancer tumors and promotes the apoptosis of colon carcinoma cells. In the
Tumor necrosis factor
Chu WM, et al.
Cancer Letters, 328(2), 222-225 (2013)
Transmembrane TNF-alpha: structure, function and interaction with anti-TNF agents
Horiuchi T, et al.
Rheumatology (Basel), 49(7), 1215-1228 (2010)
Z Han et al.
The Journal of biological chemistry, 276(42), 38748-38754 (2001-08-22)
Non-steroidal anti-inflammatory drugs (NSAIDs) are inhibitors of cyclooxygenase-1 and -2 and are useful for prevention and cure of cancers, especially colon and rectal cancers. The NSAIDs indomethacin and sulindac sulfide have been shown to induce apoptosis of colon epithelial cancer
K A Papadakis et al.
Annual review of medicine, 51, 289-298 (2000-04-25)
Recent advances in the drug treatment of inflammatory bowel disease (IBD) have paralleled our understanding of the pathophysiology of ulcerative colitis and Crohn's disease. Several proinflammatory and immune-regulatory cytokines are upregulated in the mucosa of patients with IBD, and differences

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