430 EUR
516 USD
356 GBP
known as: MOUSE ANTI PIG TNF ALPHA Azide Free
Catalog number: genta-ABS0420
Product Quantity: 0.5 mg
Supplier: AbD

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Gene target: tnf alpha

Related genes to: MOUSE ANTI PIG 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: MOUSE ANTI PIG TNF ALPHA Azide Free

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

Related product to: MOUSE ANTI PIG TNF ALPHA Azide Free

Related Articles about: MOUSE ANTI PIG TNF ALPHA Azide Free

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

TNF-α exerts cytotoxic effects on multidrug resistant breast cancer MCF-7/MX cells via a non-apoptotic death pathway.

Tumor necrosis factor-α (TNF-α) is a cytokine involved in the various physiopathological processes such as autoimmune disorders and inflammation related diseases. Some multidrug resistant (MDR) cancer cell lines including MCF-7/MX are more vulnerable to cytotoxic effects of TNF-α than their parental lines. In this study, breast cancer cell line MCF-7 and its MDR derivative MCF-7/MX were exposed to TNF-α afterward various downstream signaling mediators of TNF-α were analyzed. Although, treatment of MCF-7 cells with TNF-α activated NF-kB and caused RIP1 ubiquitination, TNF-α exposure led to JNK and RIP1 phosphorylation in MCF-7/MX cells. In both cell lines TNF-α did not activate the caspase cascade. Moreover, AnexinV/PI analysis showed that cytotoxic effects of TNF-α on MCF-7/MX is mediated via apoptosis independent mechanisms and inhibition of RIP1 kinase activity using necrostatin-1 revealed that kinase activity of RIP1 plays role in the production of ROS, activation of JNK and cellular death following exposure of MCF-7/MX cells to TNF-α. Overall, it seems that RIP1 ubiquitination and NF-kB activation are prosurvival signaling mediators protecting MCF-7 cells against cytotoxic effects of TNF-α while TNF-α drives MCF-7/MX cells to non-apoptotic cellular death via kinase activity of RIP1, activation of JNK and ROS production. - Source :PubMed

Mediators go together: High production of CXCL9, CXCL10, IFN-γ and TNF-α in HAM/TSP.

HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic demyelinating and disabling syndrome caused by HTLV-1. Although the pathogenic mechanisms that lead to HAM/TSP outcome have not been elucidated, genetic and immunological factors may be involved in the myelopathy occurrence. The present study aimed to compare cytokines, chemokines and nitric oxide levels in asymptomatic and HAM/TSP HTLV-1 infected patients. The study group consisted of 21 HAM/TSP and 48 asymptomatic HTLV-1 patients. Chemokines (CCL5, CCL2, CXCL8, CXCL9 and CXCL10) and cytokines (IL-2, IFN-γ, TNF-α, IL-4, IL-6 and IL-10) were measured using CBA while nitric oxide (NO) production was measured after reaction of supernatants with nitrate reduction solution. CXCL9 and CXCL10 chemokines levels were found to be higher in HAM/TSP group. CXCL9 was also strongly correlated with CXCL10 and both CXCL9 as well as CXCL10 were moderately correlated with CCL2 and CCL5 levels, in both HAM/TSP and asymptomatic groups. There was no significant difference related to NO, IL-4, IL-6 and IL-10 levels between the clinical groups but TNF-α and IFN-γ levels were increased in HAM/TSP patients. Thus, factors such as CXCL9, CXCL10, TNF-α and IFN-γ could be good prognostic biomarkers candidates, and further studies may help to clarify their association with HAM/TSP immunopathogenesis. - Source :PubMed

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