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Merck

T3198

Sigma-Aldrich

Monoclonal Anti-Tumor Necrosis Factor-α antibody produced in mouse

clone 45418.111, purified immunoglobulin, lyophilized powder

Sinónimos:

Anti-TNF-α

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

45418.111, monoclonal

form

lyophilized powder

species reactivity

rat

technique(s)

capture ELISA: suitable
neutralization: suitable
western blot: 1-2 μg/mL

isotype

IgG1

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

rat ... Tnf(24835)

General description

The antibody has the ability to neutralize the biological activity of rat TNF-α.and may also be used as a capture antibody in ELISAs.

Immunogen

purified recombinant rat TNF-α expressed in E. coli.

Application

Monoclonal Anti-Tumor necrosis factor-α antibody produced in mouse has been used in immunoneutralization study and western blot analysis.

Biochem/physiol Actions

Tumor Necrosis Factor-alpha (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 Tumor necrosis factor receptor (TNFR) super family. TNF/TNFR also results in the activation of downstream pathways involving mitogen-activated protein kinase (MAPK), p38(a class of MAPK), c-Jun N-terminal kinase (JNK) and NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) that play a major role in innate immunity, acute inflammatory responses and homeostasis.
Tumor necrosis factor-α (TNFα) affects various cellular processes such as blood-brain barrier, inflammatory, thrombogenic and vascular changes following brain damage. TNFα expression is upregulated in various central nervous system disorders, including Alzheimer′s disease, multiple sclerosis, Parkinson′s disease, meningococcal meningitis and human immunodeficiency virus (HIV) infection. Elevated expression of TNFα in the brain and blood in response to lipopolysaccharide might increase brain stem thrombosis, hemorrhage and stroke sensitivity/risk in hypertensive rats. Tumor necrosis factor-α activates polymorphonuclear leukocyte NADPH oxidase, thereby facilitates development of systemic oxidative stress (OS), inflammation and hypertension in rats.

Physical form

Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline containing carbohydrates.

Disclaimer

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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Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


Certificados de análisis (COA)

Busque Certificados de análisis (COA) introduciendo el número de lote del producto. Los números de lote se encuentran en la etiqueta del producto después de las palabras «Lot» o «Batch»

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Tumor necrosis factor-alpha: a possible priming agent for the polymorphonuclear leukocyte-reduced nicotinamide-adenine dinucleotide phosphate oxidase in hypertension.
Mazor R, et al
Hypertension, ;55(2), 353-362 (2010)
Effects of IFN-β1a and IFN-β1b treatment on the expression of cytokines, inducible NOS (NOS type II), and myelin proteins in animal model of multiple sclerosis.
Lubina-Dabrowska N, et al.
Arch. Immunol. Ther. Exp., 65(4), 325-338 (2017)
Ilona Obara et al.
Pain, 152(11), 2582-2595 (2011-09-16)
The management of neuropathic pain is unsatisfactory, and new treatments are required. Because the sensitivity of a subset of fast-conducting primary afferent nociceptors is thought to be regulated by the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway, selectively
Tumor necrosis factor-alpha. A mediator of focal ischemic brain injury.
Barone F C, et al.
Stroke, 28(6), 1233-1244 (1997)
Mu-opioid receptor and delta-opioid receptor differentially regulate microglial inflammatory response to control proopiomelanocortin neuronal apoptosis in the hypothalamus: effects of neonatal alcohol.
Shrivastava P, et al.
Journal of Neuroinflammation, 14(1, 83-83 (2017)

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