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Human Tumor Necrosis Factor Protein expressed in Escherichia coli (E. coli) - ABIN2003118
Black, Rauch, Kozlosky, Peschon, Slack, Wolfson, Castner, Stocking, Reddy, Srinivasan, Nelson, Boiani, Schooley, Gerhart, Davis, Fitzner, Johnson, Paxton, March, Cerretti: A metalloproteinase disintegrin that releases tumour-necrosis factor-alpha from cells. in Nature 1997
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Human Tumor Necrosis Factor Protein expressed in Escherichia coli (E. coli) - ABIN413820
Bhola, Simon: Determinism and divergence of apoptosis susceptibility in mammalian cells. in Journal of cell science 2009
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Rat (Rattus) Tumor Necrosis Factor Protein expressed in Escherichia coli (E. coli) - ABIN413826
Muehlbauer, Lima, Goldman, Jacobson, Rivera, Goldberg, Palladino, Casadevall, Brojatsch: Proteasome inhibitors prevent caspase-1-mediated disease in rodents challenged with anthrax lethal toxin. in The American journal of pathology 2010
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Human Tumor Necrosis Factor Protein expressed in Escherichia coli (E. coli) - ABIN1305134
Hogan, Vogel: Production of tumor necrosis factor by rIFN-gamma-primed C3H/HeJ (Lpsd) macrophages requires the presence of lipid A-associated proteins. in Journal of immunology (Baltimore, Md. : 1950) 1989
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Human Tumor Necrosis Factor Protein expressed in Wheat germ - ABIN1323120
Ku, Kim, Bae: Piperlonguminine downregulates endothelial protein C receptor shedding in vitro and in vivo. in Inflammation 2014
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Human Tumor Necrosis Factor Protein expressed in HEK-293 Cells - ABIN2870564
Ji, Cao, Zeng, Zhang, Xiao, Guan, Chen, Chen, Wang, Guo: The N-terminal ubiquitin-associated domain of Cezanne is crucial for its function to suppress NF-κB pathway. in Journal of cellular biochemistry 2018
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Mouse (Murine) Tumor Necrosis Factor Protein expressed in Escherichia coli (E. coli) - ABIN1305135
Jäättelä: Biologic activities and mechanisms of action of tumor necrosis factor-alpha/cachectin. in Laboratory investigation; a journal of technical methods and pathology 1991
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Human Tumor Necrosis Factor Protein expressed in Yeast (Pichia pastoris) - ABIN988275
Fritz, Radziwill: CNK1 promotes invasion of cancer cells through NF-kappaB-dependent signaling. in Molecular cancer research : MCR 2010
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Human Tumor Necrosis Factor Protein expressed in HEK-293 Cells - ABIN2181831
Dowlati, Herrmann, Swardfager, Liu, Sham, Reim, Lanctôt: A meta-analysis of cytokines in major depression. in Biological psychiatry 2010
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In conclusion, this study revealed the crucial calcium signaling pathway triggered by HIV-1 gp120 to control the production of these two cytokines: TNF-alpha and IL-10.
Semen litchi drug serum can inhibit proliferation of hepatoma cells in vitro. The anti-hepatoma effect of semen litchi drug serum may be exerted through down-regulating the expression of VEGF and MMP-9 and inhibiting angiogenesis of hepatocellular carcinoma.
The level of TNF-alpha plays a critical role in the evaluation of the severity of patients with drug-resistant tuberculosis.
TNF-alpha polymorphisms play a significant role in its secretion and influence the development of dermatomyositis and systemic lupus erythematosus. -308A allele increases TNF-alpha secretion, while -1031C and -863A alleles decrease it.
These findings provide mechanistic insight into promoting apoptosis in prostate cancer cells by ANO1 inhibition through upregulation of TNF-alpha signaling.
These data indicate that the sAbeta1-42 may play a dual role during inflammatory process, wherein, it may be involved in protecting the cells from inflammatory damage due to TNF-alpha.
S100A8/A9 induced the activation of NF-kappaB and expression of MMP-9 protein through facilitating secretion of TNFalpha from macrophages, which may play a role in triggering extracellular matrix degradation and cardiac rupture.
no significant correlation between TNF-alpha-308G/A polymorphism (rs1800629) and colorectal cancer risk (Meta-Analysis)
TNF takes part in preparation of endometrial lining for implantation of embryo in assisted reproductive treatment procedures.
A significant difference was observed for mean tumour necrosis factor alpha values between normal and osteoporotic groups. Tumour necrosis factor alpha showed negative correlation with bone mineral density in osteopenic and osteoporotic groups.
various forms of DNA bind to TNFalpha with low mum dissociation constants, the interaction stabilizes the trimeric form of TNFalpha and enhances its cytotoxic effect.
current study shows an important role of transmembrane TNFalpha as mediator of interferon alpha-dendritic cell (DC) tumoricidal activity and as molecular target for the restoration of defective DC killer activity in high-grade glioma patients
In this study, we investigated polymorphisms located in the TREM2 gene region and association with TNF-alpha levels and the intima media thickness of the femoral artery.
paradoxical psoriasis is caused by the absence of TNF and represents an ongoing type-I interferon-driven innate inflammation that fails to elicit T-cell autoimmunity and lacks memory T cell-mediated relapses.
TNF-alpha might exert a different effect on the odontoblastic differentiation of Human dental pulp cells depending on their proliferating activity. In addition, the calcification of pulp chamber with age may be related with increased reactivity of pulp cells to TNF-a.
TNF-alpha is a critical host-protective cytokine against mycobacterial diseases. We proved that toll-like receptor (TLR)-2 is responsible for TNF-alpha production by human macrophages infected with mycobacteria. Subsequent analysis showed that HDL downregulates TLR2 expression and suppresses its intracellular signaling pathways.
Serum levels of TNF-alpha was a biomarker for evaluating the disease severity in IgA nephropathy.
the data indicate the methylation levels of CpG sites in the Tumor Necrosis Factor-alpha gene may be related to the difference between Graves' disease and Hashimoto's disease in autoimmune thyroid diseases and may be influenced by the Tumor Necrosis Factor-alpha gene polymorphism.
These findings indicate that the let-7e/EZH2/H3K27me3/NF-kappaB p65 pathway is a novel regulatory axis of TNF-alpha expression.
This fragmentation is DRP1-independent and might be caused by a deficit of mitochondrial fusion. However, mitochondrial fragmentation does not change neither Brucella replication efficiency, nor the susceptibility of infected cells to TNFalpha-induced apoptosis.
These results demonstrate that TNF can act as mediator of metaplasticity, which is of considerable relevance in the context of brain diseases associated with increased TNF levels and alterations in synaptic plasticity. Plasticity effects of TNF are modulated by intracellular calcium stores.
TNF-induced pathology was induced specifically through the TNFR1 receptor, while TNFR2-mediated signaling was distinctly protective in colitis and ankle joint inflammation. Overall, our data show that TNF is a critical modulator of pyrin expression, inflammasome activation, and pyrin-inflammasomopathy.
key roles for TNF and, to a lesser extent, IL-17 as mediators of liver inflammation and fibrosis induced by constitutive NLRP3 inflammasome activation in myeloid-derived cells.
Activation of hematopoiesis and myeloid differentiation in tumor-bearing mice was induced by TNFalpha, which was mainly secreted by activated CD4(+) T cells.
IL1beta and TNFalpha enhance RANKL-dependent expression of adseverin, which contributes to fusion processes in osteoclastogenesis
study reveals that TNF-alpha triggers glutamate release in BG, thereby increasing the intrinsic excitability of cerebellar PCs in a mGluR1-dependent manner.
in vivo, niche-derived TNF is the principal PU.1 inducing signal in HSCs and is both sufficient and required to relay signals from inflammatory challenges to HSCs.
Tissue-level TLR4 signaling involves interactions between different cell types, which regulate local propagation of TNF-alpha by competitive uptake; the heterogeneous activation of macrophages by TLR4 results in proximal TNF-alpha-dependent NF-kappaB signaling between neighboring tissue-resident cells but prevents out-of-context TNF-alpha signalling at longer ranges.
This study showed that TNF-alpha, either metabolized or applied in vitro, significantly accelerated the aging of cumulus denuded oocytes.
It is shown that TNF-alpha signaling regulates the phosphorylation of serine-5 and -7 in L-plastin which increases the actin bundling capacity of L-plastin and hence the formation of nascent sealing zones in mouse osteoclasts.
TNF overproduction impairs epithelial staphylococcal response in hyper IgE syndrome.
TNF-alpha that is intrinsic to muscle and TNF-alpha secreted by immune cells work together to influence muscle aging.
Glucocorticoid receptor dimers control intestinal STAT1 and TNF-induced inflammation in mice
The present study identifies the critical role of TNF-alpha and mast cells in the host defense against Staphylococcus aureus infection.
the effects of tumor necrosis factor-alpha (TNFalpha) and interleukin-6 (IL6) gene knockout in preserving the bone loss induced by ovariectomy, was examined.
Investigation of 2-AP demonstrated its nociception inhibition and ability to reduce reactive oxygen species. Its interaction with A2a receptors may well be related to proinflammatory cytokines TNF-alpha and IL-1beta reduction activity, corroborating its antinociceptive effect.
Here, we show that TNF-alpha, which is induced by various psychological stresses, induces the p38-dependent phosphorylation of ATF7, a stress-responsive chromatin regulator, in mouse testicular germ cells. This caused a release of ATF7 from the TERRA gene promoter in the subtelomeric region, which disrupted heterochromatin and induced TERRA.
Study results demonstrate that transmembrane Tnf is an important mediator of renal tissue damage in mouse nephrotoxic serum nephritis by induction of glomerular and tubulointerstitial cell death, and loss of glomerular endothelial cells and podocyte integrity. NFkB-mediated expression of pro-inflammatory mediators and recruitment of infiltrating leukocytes into nephritic kidney is dependent on the presence of soluble Tnf.
miR-1225 is significant in multiple malignancies and other pathological reactions; transfection of a miR-1225 mimic or Keap1 silencing inhibits osteoclastogenesis; after miR-1225 inhibition and Keap1 overexpression, TNF was increased; TNFalpha overexpression promoted Keap1 depletion-inhibited BMM osteoclastogenesis; miR-1225 activates Keap1-Nrf2-HO-1 signal to inhibit TNFalpha-induced osteoclastogenesis
TNF-alpha-TNF-Rp55 axis may have essential roles in the resolution of venous thrombus in mice.
Data suggest that luteolytic factors (such as TNFa, interferon gamma, and PGF2a) control expression of MMP1, other matrix metalloproteinases, and tissue inhibitors of metalloproteinase in cultured luteal cells.
These results suggest that polymorphism of the TNFalpha-824 A>G gene and mTNFalpha protein expression play an important role in the pathogenesis of enzootic bovine leukosis.
These results suggest that the endometrium might lower the TNF concentration in the blastocyst by (1) regulating TNF secretion into the uterine fluid and (2) inducing decreased TNF and TNFR2 mRNA transcription in the embryo.
There was a significant association between the proviral load and a low frequency of the G/G genotype of TNF-alpha at position -824.
SNP in the TNF-alpha gene affects immune function and reproductive performance in dairy cows.
Studied genotypic and expression profiling of partial TNF-alpha gene and its association with mastitis susceptibility in 129 crossbred cattle.
Messenger RNA and protein levels of prostaglandin (PG) E synthase (PGES), PGF2alpha receptor (PGFR), tumor necrosis factor-alpha (TNF) and Fas were found to be higher in the corpus luteum of pregnancy than in corpus luteum of the cycle.
TNF-alpha up-regulates NaV1.7 mRNA in both adrenal chromaffin cells and dorsal root ganglia (DRG) neurons, highlighting the peripheral nociceptive mechanism of TNF-alpha
These results provide evidence for a high prevalence of subclinical endometritis in repeat breeding cows as well as the involvement of TNFalpha and iNOS pathways in the regulation of this pathological condition.
Exposure to follicular fluid transiently increased the transcript levels of IL8 and PTGS2, and decreased the expression of SOD2, GPX3, DAB2, and NR3C1. TNF and IL6 levels were also decreased while those of NAMPT were unaffected.
the effects of lysophopatidic acid on TNFalpha and IFNgamma - induced decrease of progesterone synthesis and on the cytokine - induced apoptosis of the cultured luteal cells.
potential DNA markers in the improvement of immunity to mastitis
A role for TNFalpha in intervertebral disc degeneration: a non-recoverable catabolic shift.
Results indicate that TNF-alpha does not affect autonomous, pulsatile progesterone (P(4)) release, increases P(4) secretion by bovine corpus luteum (CL) with increasing dose & reduces in a dose-dependent manner responsiveness of CL to luteotropic factors.
The differences in genetic polymorphism of TNFalpha between dairy dairy cattle herds infected and not infected with the bovine leukemia virus are reported.
These results suggest that TNF-alpha sources include immune cells, as well as large and small luteal cells, and that TNF-RI and TNF-RII are present in the luteal cells of the bovine corpus luteum.
Role of TGF-beta1 and TNF-alpha in IL-1beta mediated activation of proMMP-9 in pulmonary artery smooth muscle cells: involvement of an aprotinin sensitive protease.
Plasma tumor necrosis factor-alpha response to either of two lipopolysaccharide challenges was lower in progesterone-treated than in 17beta-estradiol-treated steers. Xanthine oxidase response to either challenge was greater for estradiol-treated steers.
The expression and cellular localization of tumor necrosis factor-alpha (TNF) and its receptors (TNFRI and TNFRII) mRNAs and proteins, were determined.
Gene expression changes were observed, but there were no changes in TNFalpha concentrations, which may indicate its local involvement in catabolic adaptation of adipose tissue.
The present study showed that TNF-alpha, which was secreted by the tracheal epithelial cells when they were stimulated with several swine pathogens, damaged tight junction proteins and disrupted the epithelial barrier of a pig tracheal epithelial cell model.
Mechanistically, Porcine productive and respiratory syndrome virus induced an elevated level of tumor necrosis factor (TNF-alpha), through the nuclear factor kappaB (NF-kappaB) signaling pathway to inhibit the replication of classical swine fever virus -C in vitro.
this study shows of TNF-alpha to the form of post-traumatic osteoarthritis induced by "idealized" anterior cruciate ligament reconstruction in a porcine model
these findings provide the direct evidence that ADAM17 cleaves porcine TNFalpha, which represents a new view for identifying potential therapeutic targets in anti-porcine reproductive and respiratory syndrome virus therapy
TMZ pretreatment effectively reduced the myocardial damage caused by CME via inhibiting the PDCD4/NF-kappaB/ TNF-alpha pathway in cardiomyocytes.
TNF-alpha, secreted from activated Monocytes, mediates the downregulation of OTX2 and essential retinal pigment epithelium genes.
TNF-alpha induced MMP-13 expression by condylar cells might be involved in the degradation of the juvenile condyle.
TNF-alpha was able to promote theca interna cell proliferation. Our results suggest that TNF-alpha might play a role in hyperandrogenism, cortex thickness, and the increased ovary volume observed in polycystic ovaries.
This study showed that the -791(C-->T) mutation of the TNF-alpha gene could be considered an important potential genetic marker of enterotoxigenic Escherichia coli F18 resistance.
Both Nsp1beta and Nsp11 of porcine reproductive and respiratory syndrome virus were demonstrated to be responsible for the inhibitory effect on TNF-alpha production in pulmonary alveolar macrophages.
Study presents evidence demonstrating a single species of exotoxin ApxI, derived from A. pleuropneumoniae serotype 10, induces the expression and production of proinflammatory cytokines IL-1beta, IL-8 and TNF-alpha in porcine alveolar macrophages.
the role of miR-181a in adipocyte differentiation by regulation of TNF-alpha
The NOS inhibitor, L-NMMA, significantly suppressed the combined effects of HT and CORM-2 on TNFalpha-triggered NFkappaBp65 phosphorylation as well as decreased cell viability.
High-volume hemofiltration improves hemodynamics and heart dysfunction in septic shock pigs, which may be attributed to reduction of TNF-alpha in myocardium but not in circulation.
Basal lipogenesis was not affected by tumor necrosis factor alpha (TNFalpha) treatment; however, insulin stimulated lipogenesis was reduced by TNFalpha. Interleukin 6 and TNFalpha gene expression were acutely (2-4 h) stimulated by exogenous TNFalpha treatment.
In swine, IL-8, TNF-ALPHA, INOS AND MIP-1BETA were increased during mechanical ventilation in a time-related fashion.
These data demonstrate that CRF triggers increases in intestinal paracellular permeability via mast cell dependent release of TNF-alpha and proteases.
We identified critical amino acid residues in PRRSV Nsp1alpha and Nsp1beta that are important for TNF-alpha down-regulation and attenuation in vivo.
Porcine reproductive and respiratory syndrome virus infection impaired TNF-alpha production by inhibiting ERK signaling. pathway.
Data show that all five molecules, BNP, ICAM-1, TNF-alpha, VCAM-1 and IL-6, quickly and reliably signaled adverse interactions.
Macrophage-less irf8 mutants show prolonged inflammation with elevated levels of Tnf-alpha and Il-1beta.
Mecp2 is required for tnfa expression during zebrafish development and inflammation.
Using in vivo, time-lapse imaging we show that as centrally-projecting pioneer axons from dorsal root ganglia (DRG) enter the spinal cord, they initiate expression of the cytokine TNFalpha. This induction coincides with ensheathment of these axons by associated glia via a TNF receptor 2 (TNFR2)-mediated process.
The results reveal a crucial role for TNFalpha/TNFR2 axis in the protection of the skin against DUOX1-mediated oxidative stress.
proinflammatory cytokines IL-1/TNFalpha trigger a novel antiviral mechanism involving AID to regulate host cell permissiveness to HBV infection.
TNF alpha is the first molecule identified that is produced by dying retinal neurons and is necessary to induce Muller glia to proliferate in the zebrafish retinal regeneration response.
The data suggest that Mycobacterium marinum SecA2 modulates adaptive immunity to promote granuloma stability, perhaps through induction of tumor necrosis factor alpha.
The data suggest that during infectious pancreatic necrosis virus infection, the expression of cytokines and metalloproteinases might be initiated through the TNFalpha/NF-kappaB-mediated pathway.
Infectious pancreatic necrosis virus triggers two death pathways via up-stream induction of the pro-inflammatory cytokine TNFalpha.
Antisense knockdown of tnfa rescued hepatic steatosis and liver degeneration in dtp larvae, whereas the overexpression of tnfa and the hepatic phenotype were unchanged in dtp larvae.
TNF is not required for tuberculous granuloma formation, but maintains granuloma integrity indirectly by restricting mycobacterial growth within macrophages and preventing their necrosis.
The main proinflammatory effects of fish TNF-alpha are mediated through the activation of endothelial cells and point to the complexity of the evolution that has taken place in the regulation of innate immunity by cytokines.
These interactions result in the induction of the TNF signaling pathway, activation of apoptosis, and DNA-damage stress response.
Findings showed that both mucosal compartments harbor similar percentages of memory CD4(+) T cells and displayed comparable cytokine TNF-alpha responses to mitogenic stimulations prior to infection.
Primary role for IL-1beta and TNF-alpha in the triggering of preterm labor associated with inflammation or infection.
The results obtained showed that IL-6 expression in adipose tissue biopsies derived from animals with equine metabolic syndrome was enhanced while TNF-alpha levels of both groups were comparable.
Data indicate that tumor necrosis factor-alpha production is closely related to ovarian steroid actions.
These results indicate that in equine corpus luteum, cytokines TNF, IFNG and FASL regulate nitric oxide activity, via eNOS expression modulation.
These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine corpus luteum and indicate their potential involvement in regulation of luteal function.
These results suggest that basal oxidative stress markers, circulating cytokines and anti-inflammatory neuroendocrine hormones appear to correlate with endurance performance in horses.
The contribution of bronchial epithelium to airway inflammation, with focus on mRNA and protein expression of IL-6, IL-10 and TNF-alpha, in horses with recurrent airway obstruction during exacerbation and in remission is reported.
The effects of semen extender and seminal plasma on the expression of inflammatory modulators in the endometrium of mares are reported.
TUNEL staining was positively correlated with TNF-a protein expression. Our findings suggest that apoptosis can be induced in the vocal fold epithelium after 120min of modal intensity phonation. In contrast, shorter durations of vibration exposure do not result in apoptosis signaling.
Inflammatory factors such as TNF-alpha can stimulate MMP-2/9 activity in corneal epithelium cells. This may be a potential manipulating mechanism of MMP expression in the pathogenesis of corneal diseases.
The JNK pathway plays an important role in mechanical ventilation-stimulated TNF-alpha expression in alveolar macrophages, but the injury-stimulated IL-8 expression may be regulated by other signaling pathways.
The TNFalpha-evoked Cl- current.
IL-1beta and TNF-alpha expression increases significantly during acute lung injury. Ambroxol combined with low-dose heparin inhibits teh release of IL-1beta and TNF-alpha.
Hypercapnia increased expression of TNFa and decreased expression of NFKB in acute lung injury models.
In the early stages of myocardial ischemia, bone marrow stem cells are mobilized and home to ischemic myocardium with a concomitant increase in expression of cytokines VEGF and TNFalpha.
Ammonium perchlorate can increase gene expressions of types I, III collagens, TGF-beta(1) and TNF-alpha in lung of rabbits.
TNFalpha may either be directly or indirectly involved in vascular damage following an embolic stroke. Moreover, TNFalpha may mediate some of the detrimental effects of tPA on the vascular compartment
Data indicate that three single-nucleotide polymorphisms were identified in tumor necrosis factor-alpha (TNF-alpha) gene.
The reduction of CD58 expression in T cells was correlated with the reduced expression of T-cell-mediated IL-2 and TNFalpha production. Together, these results indicate that reduction in the CD2/CD58 interaction pathway in mucosal lymphocytes might play a crucial role in mucosal T-cell dysfunction during acute SIV/HIV infection.
Macrophage- and neutrophil-derived TNF-alpha instructs skin langerhans cells to prime antiviral immune responses.
This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. This cytokine is mainly secreted by macrophages. It can bind to, and thus functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. This cytokine is involved in the regulation of a wide spectrum of biological processes including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. This cytokine has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Knockout studies in mice also suggested the neuroprotective function of this cytokine.
, TNF, macrophage-derived
, TNF, monocyte-derived
, tumor necrosis factor ligand superfamily member 2
, tumor necrosis factor-alpha
, tumor necrosis factor (TNF superfamily, member 2)
, tumor necrosis factor alpha
, tumor necrosis factor
, tumor-necrosis factor
, tumour necrosis factor
, TNF alpha
, ATP-binding cassette, sub-family F (GCN20), member 1
, tumour necrosis factor alpha
, tumor necrosis factor, alpha
, Tumor necrosis factor ligand superfamily member 2
, TNF-alpha 1