RAT ANTI HUMAN TNF ALPHA APC

Price:
374 EUR
448 USD
310 GBP
known as: RAT ANTI HUMAN TNF ALPHA APC
Catalog number: genta-ABS0160
Product Quantity: 100 TESTS
Category:
Supplier: AbD

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Gene target: tnf alpha apc

Related genes to: RAT ANTI HUMAN TNF ALPHA APC

Symbol : Apc NIH gene
chromosome : Un
description : adenomatous polyposis coli
type of gene : protein-coding
Other designations : Adenomatous polyposis coli protein
Modification date : 2016-02-20
Symbol : tnf NIH gene
description : tumor necrosis factor
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: RAT ANTI HUMAN TNF ALPHA APC

Gene about :Tnf
Pathway :Rn Toll-like receptor signaling pathway
Tnf
Gene about :APC
Pathway :Sc Cell Cycle and Cell Division
APC

Related product to: RAT ANTI HUMAN TNF ALPHA APC

Related Articles about: RAT ANTI HUMAN TNF ALPHA APC

Long-term risk of infection in patients with Crohn's disease on anti-TNF treatment: A prospective single center cohort study in China.

Anti-TNF agents have demonstrated to greatly improve management strategies for inflammatory bowel disease (IBD). Clinical trials and registry studies in Western countries have shown that infections and malignancy are the most concerned complications of anti-TNF treatment. However, data derived from clinical practice in China are limited. The aim of this study is to explore the long-term infection risk of infliximab (IFX) in treating patients with Crohn's disease (CD) from a tertiary IBD center in China. - Source :PubMed

Critical role of TNF inhibition in combination therapy for elderly mice with atherosclerosis.

We have previously shown that the combination of pravastatin and sarpogrelate is synergistically beneficial for atherosclerosis. In this study, we investigated whether the pravastatin-sarpogrelate combination was sufficient for treatment in an old mouse model of atherosclerosis or if additional intervention would be needed to address the newly included aging factor and its complex pathophysiological impact on the atherosclerogenic state. We added an anti-TNF biologic to the combination treatment cocktail because of the known pathologic roles of TNF in the aging process. Sixty-week-old low-density lipoprotein receptor knockout mice were fed a high-fat, high-cholesterol diet and treated with the sarpogrelate and pravastatin combination, etanercept alone, or the triple combination. Although, etanercept alone did not significantly reduce aortic root and atherosclerotic plaque areas, the pravastatin-sarpogrelate combination and pravastatin-sarpogrelate-etanercept triple therapy significantly reduced the plaque areas. Surprisingly, TNF-inhibition was critically required to reduce the plaque areas of aortic roots and the expression of ICAM-1, MOMA-2, and TNF. More importantly, a lipid-lowering effect by pravastatin was observed only in the triple therapy group and not in the pravastatin and sarpogrelate combination group. These results suggest that TNF-inhibitory intervention should be added to the conventional therapy as a novel strategy for treating the elderly patients with atherosclerosis. This article is protected by copyright. All rights reserved. - Source :PubMed

Ankylosing spondylitis patients at risk of poor radiographic outcome show diminishing spinal radiographic progression during long-term treatment with TNF-α inhibitors.

To investigate the influence of patient characteristics on the course of spinal radiographic progression in a large prospective longitudinal cohort study of ankylosing spondylitis (AS) patients treated long-term with TNF-α inhibitors. - Source :PubMed

C1q/TNF-Related Protein 3 (CTRP3) Function and Regulation.

As the largest endocrine organ, adipose tissue secretes many bioactive molecules that circulate in blood, collectively termed adipokines. Efforts to identify such metabolic regulators have led to the discovery of a family of secreted proteins, designated as C1q tumor necrosis factor (TNF)-related proteins (CTRPs). The CTRP proteins, adiponectin, TNF-alpha, as well as other proteins with the distinct C1q domain are collectively grouped together as the C1q/TNF superfamily. Reflecting profound biological potency, the initial characterization of these adipose tissue-derived CTRP factors finds wide-ranging effects upon metabolism, inflammation, and survival-signaling in multiple tissue types. CTRP3 (also known as CORS26, cartducin, or cartonectin) is a unique member of this adipokine family. In this review we provide a comprehensive overview of the research concerning the expression, regulation, and physiological function of CTRP3. © 2017 American Physiological Society. Compr Physiol 7:863-878, 2017. - Source :PubMed

Voluntary distance running prevents TNF-mediated liver injury in mice through alterations of the intrahepatic immune milieu.

Physical activity confers a broad spectrum of health benefits. Beyond the obvious role in metabolically driven diseases, the role of physical activity in acute liver injury is poorly explored. To study the role of physical activity in acute liver injury, a novel model of voluntary distance running in mice was developed and mice were subjected to acute liver injury induced by N-galactosamine (GalN) and lipopolysaccharide (LPS). Analyses included histological stains, immunoblotting, qRT-PCR and FACS analysis. Voluntary distance running increased to an average of 10.3 km/day after a learning curve. Running lead to a decrease in the absolute numbers of intrahepatic CD4+ T and B lymphocytes and macrophages after 7 weeks. In parallel, hepatic mRNA expression of inflammatory cytokines including IL-6 and IL-1beta, TGF-beta and monocyte chemoattractant protein-1 (MCP-1/CCL2) were suppressed, while TNF-α was not affected by exercise. Likewise, expression of the macrophage-specific antigen F4/80 was downregulated 1.6-fold from exercise. Notably, acute liver injury from GaIN/LPS was significantly blunted following 7 weeks of voluntary exercise as determined by liver histology, a 84.6% reduction of alanine aminotransferase (P<0.01) and a 54.6% reduction of aspartate aminotransferase (P<0.05) compared with sedentary mice. Additionally, proinflammatory cytokines, activation of caspase 3 and JNK were significantly lower, while antiapoptotic protein A20 increased. Voluntary distance running alters the intrahepatic immune phenotype producing an environment that is less susceptible to acute liver injury. - Source :PubMed

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