889 EUR
1066 USD
737 GBP
known as: RAT ANTI HUMAN TNF ALPHA Azide Free
Catalog number: genta-ABS0332
Product Quantity: 1 mg
Supplier: AbD

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Gene target: tnf alpha

Related genes to: RAT ANTI HUMAN TNF ALPHA Azide Free

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 Azide Free

Gene about :Tnf
Pathway :Rn Toll-like receptor signaling pathway

Related product to: RAT ANTI HUMAN TNF ALPHA Azide Free

Related Articles about: RAT ANTI HUMAN TNF ALPHA Azide Free

Amlexanox downregulates S100A6 to sensitize KMT2A/AFF1-positive acute lymphoblastic leukemia to TNF-α treatment.

Acute lymphoblastic leukemias (ALL) positive for KMT2A/AFF1 (MLL/AF4) translocation, which constitute 60% of all infant ALL cases, have a poor prognosis even after allogeneic hematopoietic stem cell transplantation (allo-HSCT). This poor prognosis is due to one of two factors, either resistance to TNF-α which mediates a graft-versus-leukemia (GVL) response after allo-HSCT, or immune resistance due to upregulated expression of the immune escape factor S100A6. Here we report an immune stimulatory effect against KMT2A/AFF1-positive ALL cells by treatment with the anti-allergy drug amlexanox, which we found to inhibit S100A6 expression in the presence of TNF-α. In KMT2A/AFF1-positive transgenic (Tg) mice, amlexanox enhanced tumor immunity and lowered the penetrance of leukemia development. Similarly, in a NOD/SCID mouse model of human KMT2A/AFF1-positive ALL, amlexanox broadened GVL responses and extended survival. Our findings show how amlexanox degrades the resistance of KMT2A/AFF1-positive ALL to TNF-α by downregulating S100A6 expression, with immediate potential implications for improving clinical management of KMT2A/AFF1-positive ALL. - Source :PubMed

Orientin Attenuates Cerebral Ischemia/Reperfusion Injury in Rat Model through the AQP-4 and TLR4/NF-κB/TNF-α Signaling Pathway.

Orientin has been reported to have extensive pharmaceutical effects of antioxidant, anti-inflammatory, antithrombosis, antiapoptosis, and so on. In the present study, we tried to investigate the protective effects of orientin on cerebral ischemia-reperfusion (I/R) injury and explored the possible mechanisms. - Source :PubMed

Correction: CCR4 promotes metastasis via ERK/NF-κB/MMP13 pathway and acts downstream of TNF-α in colorectal cancer.

- Source :PubMed

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

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