499 EUR
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Catalog number: genta-ABS0501
Product Quantity: 50 µg
Supplier: AbD

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Gene target: tnf alpha

Related genes to: RABBIT ANTI RAT TNF ALPHA Biotin

Symbol : biotin NIH gene
LocusTag : Bathy11g00270
chromosome : 11
description : biotin synthase
type of gene : protein-coding
Modification date : 2015-06-26
Symbol : tnf NIH gene
description : tumor necrosis factor
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: RABBIT ANTI RAT TNF ALPHA Biotin

Gene about :Tnf
Pathway :Rn Toll-like receptor signaling pathway
Gene about :biotin
Pathway :Sc Protein Modifications

Related product to: RABBIT ANTI RAT TNF ALPHA Biotin

Related Articles about: RABBIT ANTI RAT TNF ALPHA Biotin

Sustained secretion of anti-TNF alpha monoclonal antibody from ex-vivo genetically engineered dermal tissue demonstrates therapeutic activity in mouse model of rheumatoid arthritis.

Rheumatoid arthritis is a symmetric inflammatory polyarthritis associated with high concentrations of pro-inflammatory cytokines including TNF-α. Adalimumab is a monoclonal antibody (mAb) that binds TNF-α, and is widely used to treat rheumatoid arthritis. Despite its proven clinical efficacy, adalimumab and other therapeutic mAbs have disadvantages including the requirement for repeated bolus injections and the appearance of treatment limiting anti-drug antibodies. To address these issues, we have developed an innovative ex-vivo gene therapy approach, Transduced Autologous Restorative Gene Therapy (TARGT), to produce and secrete adalimumab for the treatment of RA. - Source :PubMed

IL-22 Enhances TNF-α- and IL-1-Induced CXCL8 Responses by Intestinal Epithelial Cell Lines.

IL-22 is known to induce intestinal epithelial cells (IECs) to produce the chemokine CXCL8. However, IECs exist in a cytokine network during mucosal inflammation, such that IL-22 must act in concert with potent pro-inflammatory cytokines like TNF-α and IL-1. Our studies show that IL-22 alone increased CXCL8 secretion from HT-29 cells, but the levels were minimal compared to that of the cells treated with TNF-α or IL-1 only. More significantly, co-stimulation with IL-22 and TNF-α enhanced both CXCL8 secretion and mRNA levels well over that of TNF-α stimulation alone. A similar enhancing effect was seen with IL-22- and IL-1-stimulated CXCL8 secretion. The enhancing effect of IL-22 on TNF-α-induced CXCL8 secretion was then determined to require the p38 MAPK, but not STAT1/3, PI3K, Akt, c-Jun N-terminal kinase, ERK, or IκBα. These experiments indicate that more significant effect of IL-22 on IECs responses may not be in inducing CXCL8 by itself, but in enhancing TNF-α- and IL-1-induced CXCL8 secretion to augment the contribution of IECs to local inflammatory responses. - Source :PubMed

Correction: TRAF2 regulates TNF and NF-κB signalling to suppress apoptosis and skin inflammation independently of Sphingosine kinase 1.

- Source :PubMed

TNF-α and Beyond: Rapid Mitochondrial Dysfunction Mediates TNF-α-Induced Neurotoxicity.

This short communication describes our research which demonstrates that TNF-α causes a rapid decline in mitochondrial function, leading to neuronal cell death. As such, this neurotoxic proinflammatory cytokine may play a role in brain damage from stroke and neurodegeneration in chronic conditions such as Alzheimer's disease (AD) and Parkinson's disease. We have extended this initial observation by demonstrating that TNF-α stimulates a microRNA (miR-34a) which we have shown reduces five key proteins in the mitochondrial electron transport chain through base-pair complementarity. miR-34a is increased in affected brain regions of Alzheimer's patients and transgenic AD mouse models. We have further shown that oligomeric amyloid beta 42 (oAβ42) stimulates miR-34a. Collectively, these data suggest that TNF-α, oAβ42, and miR-34a participate in a vicious cycle, resulting in mitochondrial dysfunction, which is critical to the neuropathology of AD. - Source :PubMed

Hidradenitis suppurativa is characterised by dysregulation of the Th17:Treg cell axis, which is corrected by anti-TNF therapy.

Hidradenitis suppurativa (HS) is a chronic, inflammatory and debilitating disease of hair follicles with 1-4% prevalence and high morbidity. There is a dearth of information on the pathogenesis and immune dysregulation underlying HS therefore we carried out a detailed analysis of skin infiltrating T cells. Cells isolated from skin biopsies and blood from HS patients and healthy controls were analysed by 16-parameter flow cytometry to provide detailed profiles of CD4 T cell subsets. We observed substantial infiltration of inflammatory T cells with a striking Th17-skewed cytokine profile in HS skin, these cells expressed the Th17 lineage marker CD161 and IL-17, as well as other pro-inflammatory cytokines GM-CSF, IL-22, IFN-γ, and TNF. Regulatory T (Treg) cells were also enriched in HS lesional skin, however the ratio of Th17:Treg cells was nonetheless highly dysregulated in favour of Th17 cells. In contrast, lesional skin from anti-TNF treated HS patients who showed substantial clinical improvement, exhibited a significant reduction in the frequency of Th17 cells and normalisation of the Th17:Treg cell ratio. These data suggest that inhibition of pathogenic IL-17 via TNF blockade is associated with improvement in the immune dysregulation in HS and may provide a rationale for targeting IL-17 in the disease. - Source :PubMed

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