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Gotowa bibliografia na temat „TNF Receptor-Associated Factor 4”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 1 lutego 2022

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Artykuły w czasopismach na temat "TNF Receptor-Associated Factor 4"

Niu, Fengfeng, Heng Ru, Wei Ding, Songying Ouyang i Zhi-Jie Liu. "Structural biology study of human TNF receptor associated factor 4 TRAF domain". Protein & Cell 4, nr 9 (27.08.2013): 687–94. http://dx.doi.org/10.1007/s13238-013-3068-z.

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Arch, Robert H., i Craig B. Thompson. "4-1BB and Ox40 Are Members of a Tumor Necrosis Factor (TNF)-Nerve Growth Factor Receptor Subfamily That Bind TNF Receptor-Associated Factors and Activate Nuclear Factor κB". Molecular and Cellular Biology 18, nr 1 (1.01.1998): 558–65. http://dx.doi.org/10.1128/mcb.18.1.558.

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ABSTRACT Members of the tumor necrosis factor (TNF)-nerve growth factor (NGF) receptor family have been shown to be important costimulatory molecules for cellular activation. 4-1BB and Ox40 are two recently described members of this protein family which are expressed primarily on activated T cells. To gain insight into the signaling pathways employed by these factors, yeast two-hybrid library screens were performed with the cytoplasmic domains of 4-1BB and Ox40 as baits. TNF receptor-associated factor 2 (TRAF2) was identified as an interacting protein in both screens. The ability of both 4-1BB and Ox40 to interact with TRAF2 was confirmed in mammalian cells by coimmunoprecipitation studies. When the binding of the receptors to other TRAF proteins was investigated, 4-1BB and Ox40 displayed distinct binding patterns. While 4-1BB bound TRAF2 and TRAF1, Ox40 interacted with TRAF3 and TRAF2. Using deletion and alanine scanning analysis, we defined the elements in the cytoplasmic domains of both receptors that mediate these interactions. The 4-1BB receptor was found to have two independent stretches of acidic residues that can mediate association of the TRAF molecules. In contrast, a single TRAF binding domain was identified in the cytoplasmic tail of Ox40. The cytoplasmic domains of both receptors were shown to activate nuclear factor κB in a TRAF-dependent manner. Taken together, our results indicate that 4-1BB and Ox40 bind TRAF proteins to initiate a signaling cascade leading to activation of nuclear factor κB.

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Glauner, Heike, Daniela Siegmund, Hassan Motejadded, Peter Scheurich, Frank Henkler, Ottmar Janssen i Harald Wajant. "Intracellular localization and transcriptional regulation of tumor necrosis factor (TNF) receptor-associated factor 4 (TRAF4)". European Journal of Biochemistry 269, nr 19 (18.09.2002): 4819–29. http://dx.doi.org/10.1046/j.1432-1033.2002.03180.x.

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Kalkan, Tuzer, Yasuno Iwasaki, Chong Yon Park i Gerald H. Thomsen. "Tumor Necrosis Factor-Receptor–associated Factor-4 Is a Positive Regulator of Transforming Growth Factor-β Signaling That Affects Neural Crest Formation". Molecular Biology of the Cell 20, nr 14 (15.07.2009): 3436–50. http://dx.doi.org/10.1091/mbc.e08-03-0325.

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The transforming growth factor (TGF)-β superfamily regulates cell proliferation, apoptosis, differentiation, migration, and development. Canonical TGFβ signals are transduced to the nucleus via Smads in both major signaling branches, bone morphogenetic protein (BMP) or Activin/Nodal/TGFβ. Smurf ubiquitin (Ub) ligases attenuate these pathways by targeting Smads and other signaling components for degradation by the 26S proteasome. Here, we identify tumor necrosis factor (TNF)-receptor–associated factor-4 (TRAF4) as a new target of Smurf1, which polyubiquitylates TRAF4 to trigger its proteasomal destruction. Unlike other TRAF family members, which mediate signal transduction by TNF, interleukin, or Toll-like receptors, we find that TRAF4 potentiates BMP and Nodal signaling. In the frog Xenopus laevis, TRAF4 mRNA is stored maternally in the egg animal pole, and in the embryo it is expressed in the gastrula marginal zone, neural plate, and cranial and trunk neural crest. Knockdown of embryonic TRAF4 impairs signaling, neural crest development and neural folding, whereas TRAF4 overexpression boosts signaling and expands the neural crest. In human embryonic kidney 293 cells, small interfering RNA knockdown of Smurf1 elevates TRAF4 levels, indicating endogenous regulation of TRAF4 by Smurf1. Our results uncover new functions for TRAF4 as a Smurf1-regulated mediator of BMP and Nodal signaling that are essential for neural crest development and neural plate morphogenesis.

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Meng, Xianzhong, Lihua Ao, Yong Song, Christopher D. Raeburn, David A. Fullerton i Alden H. Harken. "Signaling for myocardial depression in hemorrhagic shock: roles of Toll-like receptor 4 and p55 TNF-α receptor". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, nr 3 (marzec 2005): R600—R606. http://dx.doi.org/10.1152/ajpregu.00182.2004.

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Hemorrhagic shock causes myocardial contractile depression. Although this myocardial disorder is associated with increased expression of tumor necrosis factor-α (TNF-α), the role of TNF-α as a myocardial depressant factor in hemorrhagic shock remains to be determined. Moreover, it is unclear which TNF-α receptor mediates the myocardial depressive effects of TNF-α. Toll-like receptor 4 (TLR4) regulates cellular expression of proinflammatory mediators following lipopolysaccharide stimulation and may be involved in the tissue inflammatory response to injury. The contribution of TLR4 signaling to tissue TNF-α response to hemorrhagic shock and TLR4’s role in myocardial depression during hemorrhagic shock are presently unknown. We examined the relationship of TNF-α production to myocardial depression in a mouse model of nonresuscitated hemorrhagic shock, assessed the influence of TLR4 mutation, resulting in defective signaling, on TNF-α production and myocardial depression, and determined the roles of TNF-α and TNF-α receptors in myocardial depression using a gene knockout (KO) approach. Hemorrhagic shock resulted in increased plasma and myocardial TNF-α (4.9- and 4.5-fold, respectively) at 30 min and induced myocardial contractile depression at 4 h. TLR4 mutation abolished the TNF-α response and attenuated myocardial depression (left ventricular developed pressure of 43.0 ± 6.2 mmHg in TLR4 mutant vs. 30.0 ± 3.6 mmHg in wild type, P < 0.05). TNF-α KO also attenuated myocardial depression in hemorrhagic shock, and the p55 receptor KO, but not the p75 receptor KO, mimicked the effect of TNF-α KO. The results suggest that TLR4 plays a novel role in signaling to the TNF-α response during hemorrhagic shock and that TNF-α through the p55 receptor activates a pathway leading to myocardial depression. Thus TLR4 and the p55 TNF-α receptor represent therapeutic targets for preservation of cardiac mechanical function during hemorrhagic shock.

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Cai, Dongqing, Munira Xaymardan, Jacquelyne M. Holm, Jingang Zheng, Jorge R. Kizer i Jay M. Edelberg. "Age-associated impairment in TNF-α cardioprotection from myocardial infarction". American Journal of Physiology-Heart and Circulatory Physiology 285, nr 2 (sierpień 2003): H463—H469. http://dx.doi.org/10.1152/ajpheart.00144.2003.

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Age-associated dysfunction in cardiac microvascular endothelial cells with impaired induction of cardioprotective platelet-derived growth factor (PDGF)-dependent pathways suggests that alterations in critical vascular receptor(s) may contribute to the increased severity of cardiovascular pathology in older persons. In vivo murine phage-display peptide library biopanning revealed a senescent decrease in cardiac microvascular binding of phage epitopes homologous to tumor necrosis factor-α (TNF-α), suggesting that its receptor(s) may be downregulated in older cardiac endothelial cells. Immunostaining demonstrated that TNF-receptor 1 (TNF-R1) density was significantly lower in the subendocardial endothelium of the aging murine heart. Functional studies confirmed the senescent dysregulation of TNF-α receptor pathways, demonstrating that TNF-α induced PDGF-B expression in cardiac microvascular endothelial cells of 4-mo-old, but not 24-mo-old, rats. Moreover, TNF-α mediated cardioprotective pathways were impaired in the aging heart. In young rat hearts, injection of TNF-α significantly reduced the extent of myocardial injury after coronary ligation: TNF-α, 7.9 ± 1.9% left ventricular injury ( n = 4) versus PBS, 16.2 ± 7.9% ( n = 10; P < 0.05). The addition of PDGF-AB did not augment the cardioprotective action of TNF-α. In myocardial infarctions of older hearts, however, TNF-α induced significant postcoronary occlusion mortality (TNF-α 80% vs. PBS 0%; n = 10 each, P < 0.05) that was reversed by the coadministration of PDGF-AB. Overall, these studies demonstrate that aging-associated alterations in TNF-α receptor cardiac microvascular pathways may contribute to the increased cardiovasular pathology of the aging heart. Strategies targeted at restoring TNF-α receptor-mediated expression of PDGF-B may improve cardiac microvascular function and provide novel approaches for treatment and possible prevention of cardiovascular disease in older individuals.

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Zepp, Jarod A., Caini Liu, Wen Qian, Ling Wu, Muhammet F. Gulen, Zizhen Kang i Xiaoxia Li. "Cutting Edge: TNF Receptor-Associated Factor 4 Restricts IL-17–Mediated Pathology and Signaling Processes". Journal of Immunology 189, nr 1 (30.05.2012): 33–37. http://dx.doi.org/10.4049/jimmunol.1200470.

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Wang, Yue, Brent R. Weil, Jeremy L. Herrmann, Aaron M. Abarbanell, Jiangning Tan, Troy A. Markel, Megan L. Kelly i Daniel R. Meldrum. "MEK, p38, and PI-3K mediate cross talk between EGFR and TNFR in enhancing hepatocyte growth factor production from human mesenchymal stem cells". American Journal of Physiology-Cell Physiology 297, nr 5 (listopad 2009): C1284—C1293. http://dx.doi.org/10.1152/ajpcell.00183.2009.

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Human bone marrow mesenchymal stem cells (MSCs) are a potent source of growth factors, which are partly responsible for their beneficial paracrine effects. We reported previously that transforming growth factor-α (TGF-α), a putative mediator of wound healing and the injury response, increases the release of vascular endothelial growth factor (VEGF), augments tumor necrosis factor-α (TNF-α)-stimulated VEGF production, and activates mitogen-activated protein kinases and phosphatidylinositol 3-kinase (PI-3K) pathway in human MSCs. The experiments described in this report indicate that TGF-α increases MSC-derived hepatocyte growth factor (HGF) production. TGF-α-stimulated HGF production was abolished by inhibition of MEK, p38, PI-3K, or by small interfering RNA (siRNA) targeting TNF receptor 2 (TNFR2), but was not attenuated by siRNA targeting TNF receptor 1 (TNFR1). Ablation of TNFR1 significantly increased basal and stimulated HGF. A potent synergy between TGF-α and TNF-α was noted in MSC HGF production. This synergistic effect was abolished by MEK, P38, PI-3K inhibition, or by ablation of both TNF receptors using siRNA. We conclude that 1) novel cross talk occurs between tumor necrosis factor receptor and TGF-α/epidermal growth factor receptor in stimulating MSC HGF production; 2) this cross talk is mediated, at least partially, via activation of MEK, p38, and PI-3K; 3) TGF-α stimulates MSCs to produce HGF by MEK, p38, PI-3K, and TNFR2-dependent mechanisms; and 4) TNFR1 acts to decrease basal TGF-α and TNF-α-stimulated HGF.

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HAVLA, JOACHIM, PETER LOHSE, LISA ANN GERDES, REINHARD HOHLFELD i TANIA KÜMPFEL. "Symptoms Related to Tumor Necrosis Factor Receptor 1-associated Periodic Syndrome, Multiple Sclerosis, and Severe Rheumatoid Arthritis in Patients Carrying the TNF Receptor Superfamily 1A D12E/p.Asp41Glu Mutation". Journal of Rheumatology 40, nr 3 (15.01.2013): 261–64. http://dx.doi.org/10.3899/jrheum.120729.

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Objective.Tumor necrosis factor (TNF) receptor 1–associated periodic syndrome (TRAPS) is an autoinflammatory disorder caused by autosomal dominantly inherited mutations in the TNF receptor superfamily 1A (TNFRSF1A) gene. The D12E substitution has been described only once to date, in a 4-year-old boy with fever.Methods.For DNA sequence analysis of the TNFRSF1A gene, genomic DNA was isolated, amplified by PCR, purified, and sequenced.Results.We describe 3 families (8 subjects) with the TNFRSF1A D12E substitution and TRAPS-related symptoms, in 4 cases associated with the autoimmune diseases multiple sclerosis and rheumatoid arthritis.Conclusion.The clinical phenotype might be associated with the TNFRSF1A D12E mutation. There is a close pathophysiological relationship between TNF signaling and autoimmune disorders.

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Luo, Jiing Chyuan, Vivian Yvonne Shin, Ying Hua Yang, William Ka Kei Wu, Yi Ni Ye, Wallace Hau Leung So, Full Young Chang i Chi Hin Cho. "Tumor necrosis factor-α stimulates gastric epithelial cell proliferation". American Journal of Physiology-Gastrointestinal and Liver Physiology 288, nr 1 (styczeń 2005): G32—G38. http://dx.doi.org/10.1152/ajpgi.00093.2004.

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TNF-α is a cytokine produced during gastric mucosal injury. We examined whether TNF-α could promote mucosal repair by stimulation of epithelial cell proliferation and explored further the underlying mechanisms in a rat gastric mucosal epithelial cell line (RGM-1). TNF-α treatment (1–10 ng/ml) for 12 or 24 h significantly increased cell proliferation but did not induce apoptosis in RGM-1 cells. TNF-α treatment significantly increased cytosolic phospholipase A2 and cyclooxygenase-2 (COX-2) protein expression and PGE2 level but did not affect the protein levels of EGF, basic fibroblast growth factor, and COX-1 in RGM-1 cells. The mRNA of TNF receptor (TNF-R) 2 but not of TNF-R1 was also increased. Dexamethasone dose dependently inhibited the stimulatory effect of TNF-α on cell proliferation, which was associated with a significant decrease in cellular COX-2 expression and PGE2 level. A selective COX-2 inhibitor 3-(3-fluorophenyl)-4-[4-(methylsulfonyl)phenyl]-5,5-dimethyl-5H-furan-2-one (DFU) by itself had no effect on basal cell proliferation but significantly reduced the stimulatory effect of TNF-α on RMG-1 cells. Combination of dexamethasone and DFU did not produce an additive effect. PGE2 significantly reversed the depressive action of dexamethasone on cell proliferation. These results suggest that TNF-α plays a regulatory role in epithelial cell repair in the gastric mucosa via the TNF-α receptor and activation of the arachidonic acid/PG pathway.

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Rozprawy doktorskie na temat "TNF Receptor-Associated Factor 4"

Lu, Tsai-Yi. "Molecular Pathways Mediating Glial Responses during Wallerian Degeneration: A Dissertation". eScholarship@UMMS, 2005. http://escholarship.umassmed.edu/gsbs_diss/779.

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Glia are the understudied brain cells that perform many functions essential to maintain nervous system homeostasis and protect the brain from injury. If brain damage occurs, glia rapidly adopt the reactive state and elicit a series of cellular and molecular events known as reactive gliosis, the hallmark of many neurodegenerative diseases. However, the molecular pathways that trigger and regulate this process remain poorly defined. The fruit fly Drosophila melanogaster has glial cells that are strikingly similar to mammalian glia, and which also exhibit reactive responses after neuronal injury. By exploiting its powerful genetic toolbox, we are uniquely positioned to identify the genes that activate and execute glial responses to neuronal injury in vivo. In this dissertation, I use Wallerian degeneration in Drosophila as a model to characterize molecular pathways responsible for glia to recognize neural injury, become activated, and ultimately engulf and degrade axonal debris. I demonstrate a novel role for the GEF (guanine nucleotide exchange factors) complex DRK/DOS/SOS upstream of small GTPase Rac1 in glial engulfment activity and show that it acts redundantly with previously discovered Crk/Mbc/dCed-12 to execute glial activation after axotomy. In addition, I discovered an exciting new role for the TNF receptor associated factor 4 (TRAF4) in glial response to axon injury. I find that interfering with TRAF4 and the downstream kinase misshapen (msn) function results in impaired glial activation and engulfment of axonal debris. Unexpectedly, I find that TRAF4 physically associates with engulfment receptor Draper – making TRAF4 only second factor to bind directly to Draper – and show it is essential for Draper-dependent activation of downstream engulfment signaling, including transcriptional activation of engulfment genes via the JNK and STAT transcriptional cascades. All of these pathways are highly conserved from Drosophila to mammals and most are known to be expressed in mouse brain glia, suggesting functional conservation. My work should therefore serve as an excellent starting point for future investigations regarding their roles in glial activation/reactive gliosis in various pathological conditions of the mammalian central nervous system.

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Lu, Tsai-Yi. "Molecular Pathways Mediating Glial Responses during Wallerian Degeneration: A Dissertation". eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/779.

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Rousseau, Adrien. "Tumor necrosis factor Receptor-Associated Factor 4 (TRAF4) est une nouvelle protéine interagissant avec les phosphoinositides, impliquée dans la polarité et la migration cellulaire". Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ108/document.

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TRAF4 est un gène fréquemment surexprimé dans les carcinomes suggérant qu’il y joue un rôle. Tandis que la protéine TRAF4 est majoritairement localisée dans les jonctions serrées (JS) des cellules épithéliales mammaires (CEM) normales, elle s’accumule dans le cytoplasme des CEM malignes. Dans cette étude, nous montrons que TRAF4 possède un nouveau domaine liant les phosphoinositides (PIP) et que ce dernier est requis pour son recrutement aux JS. Des analyses moléculaires et structurales ont montré que le domaine TRAF de TRAF4 forme un trimère pouvant lier jusqu’à trois molécules de lipides grâce à des résidus basiques présents à la surface. Des études cellulaires indiquent que TRAF4 régule négativement les JS et augmente la migration cellulaire. Ces deux fonctions sont dépendantes de sa capacité à lier les PIPs. Notre travail suggère que la surexpression de TRAF4 pourrait contribuer à la progression des cancers du sein en déstabilisant les JS et en favorisant la migration cellulaire
TRAF4 (tumor necrosis factor (TNF) receptor-associated factor 4) is frequently overexpressed in carcinomas suggesting a specific role in cancer. While TRAF4 protein is predominantly found at tight junctions (TJ) in normal mammary epithelial cells (MEC), it accumulates in the cytoplasm of malignant MEC. How TRAF4 is recruited and functions at TJ is unclear. Here we show that TRAF4 possesses a novel phosphoinositide (PIP)- binding domain crucial for its recruitment to TJ. Molecular and structural analyses revealed that the TRAF domain of TRAF4 exists as a trimer which binds up to 3 lipids using basic residues exposed at its surface. Cellular studies indicated that TRAF4 acts a negative regulator of TJ and increases cell migration. These functions are dependent from its ability to interact with PIPs. Our results suggest that TRAF4 overexpression might contribute to breast cancer progression by destabilizing TJ and favoring cell migration

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Urbano, Ana Catarina Fernandes. "Clinical relevance of serum cytotoxic t-lymphocyte associated protein 4 (CTLA-4) and correlation with the pro-inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) in feline mammary carcinoma". Master's thesis, Universidade de Lisboa, Faculdade de Medicina Veterinária, 2019. http://hdl.handle.net/10400.5/18970.

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Dissertação de Mestrado Integrado em Medicina Veterinária
The association between CTLA-4 expression and cancer prognosis has been extensively investigated in recent years, pointing to the link with inflammation, and highlighting the role of the tumor microenvironment (TME), of which inflammatory mediators like cytokines are an important non-cellular component. To the best of our knowledge, no studies on immune checkpoint regulators had been conducted on cats with mammary carcinoma before, nor had cytokine profiles been previously assessed. Thus, we investigated the serum profiles of CTLA-4 and pro-inflammatory cytokines IL-6 and TNF-α in 57 female cats with mammary carcinoma and checked for associations between CTLA-4 and cytokine serum levels. Our results clearly demonstrate that serum CTLA-4 levels are increased in cats with mammary carcinoma when compared to healthy animals (P=0.022). Furthermore, we show a strong positive correlation with TNF-α (R=0.88, P<0.001) and IL-6 levels (R=0.72, P<0.001), advancing the concept of an immunomodulatory role for this regulator in breast cancer pathogenesis. We also show a statistically significant association between higher levels of serum CTLA-4 and less aggressive clinicopathological features: smaller tumors (P<0.001), lower stage (P=0.002), absence of necrosis (P<0.001), no lymph node involvement (P=0.007), no lymphatic vessel invasion (P=0.006), positive hormone receptor status (P=0.007), non-TN status (P=0.041), non-basal status (P<0.001) and low Ki67 index (P=0.001). Our findings further expand this concept by indicating an association with specific breast cancer subtypes, namely, HER-2 positive with CTLA-4 (P<0.001) and TNF-α (P=0.004) and luminal A-like with IL-6 (P=0.020). We could not confirm an association between serum CTLA-4 and cytokines levels and survival due to the small sample size. Nevertheless, our findings suggest a potentially concentration-dependent protective role for serum CTLA-4 and IL-6, as evidenced by higher median survival times in the CTLA-4high (28 vs 22 months for the CTLA-4low group) and IL-6high (28 vs 19 months for the IL-6low group) groups. Conversely, TNF-α seems to be a negative prognostic factor, as shown by the lower median survival in the TNF-αhigh group (16.5 vs 23.5 months for the TNF-αlow group). An intriguing question that remains is how serum CTLA-4 influences or is influenced by the pro-inflammatory cytokines. Assessment of CTLA-4 tumor expression, T-lymphocyte subtypes, and tumor associated macrophages and myeloid derived suppressor cell profiles in the microenvironment, are important features to evaluate in future studies.
RESUMO - RELEVÂNCIA CLÍNICA DA PROTEÍNA 4 ASSOCIADA AO LINFÓCITO T CITOTÓXICO 4 (CTLA-4) E SUA CORRELAÇÃO COM AS CITOQUINAS PRÓ-INFLAMATÓRIAS INTERLEUCINA 6 (IL-6) E FACTOR DE NECROSE TUMORAL ALFA (TNF-α) NO CARCINOMA MAMÁRIO FELINO - A associação entre a expressão da CTLA-4 e o prognóstico no cancro tem sido amplamente investigada, valorizando o papel da inflamação e do microambiente tumoral (TME), do qual mediadores inflamatórios como as citoquinas são uma importante componente não celular. Até à data, não existem estudos sobre reguladores de checkpoint imunológico em gatos com carcinoma mamário, nem foram avaliados perfis de citoquinas. Assim, foram investigados pela primeira vez, os perfis séricos da CTLA-4 e das citoquinas pró-inflamatórias IL-6 e TNF-α em 57 gatas com carcinoma mamário e verificada a existência de associações entre os níveis séricos da CTLA-4 e das referidas citoquinas. Os resultados obtidos demonstram que os níveis de CTLA-4 estão aumentados no soro das gatas com carcinoma mamário, quando comparadas com animais saudáveis (P=0.022). Foi também demonstrada uma correlação forte com os níveis séricos do TNF-α (R=0.88, P<0.001) e da IL-6 (R=0.72, P<0.001), reforçando o papel imunomodulatório deste regulador. Adicionalmente foi encontrada uma associação significativa entre os níveis séricos elevados da CTLA-4, e várias características clinicopatológicas menos agressivas: tumores mais pequenos (P<0.001), estadiamento precoce, (P=0.002), ausência de necrose tumoral (P<0.001), sem envolvimento dos linfonodos (P=0.007), sem invasão linfática (P=0.006), com positividade para os receptores hormonais (P=0.007), subtipo não-TN (P=0.041), subtipo não-basal (P<0.001), e baixo índice Ki67 (P=0.001). Os resultados obtidos ainda revelaram uma associação com subtipos específicos de cancro da mama, nomeadamente o HER-2 positivo com sobre-expressão da CTLA-4 (P<0.001) e do TNF-α (P=0.004) e o luminal A com sobre-expressão da IL-6 (P=0.020). Não foi possível confirmar a associação entre os níveis séricos da CTLA-4 e das citoquinas e o tempo de sobrevivência, devido ao tamanho reduzido da amostra. No entanto, os resultados obtidos sugerem um efeito protetor dependente da concentração da CTLA-4 e IL-6 séricos, como evidenciado pelos tempos medianos de sobrevivência mais altos nos grupos CTLA-4high (28 vs 22 meses para o grupo CTLA-4low) e IL-6high (28 vs 19 meses para o grupo IL-6low). Em contraste, o TNF-α parece ser um fator de prognóstico negativo, como sugere o tempo mediano de sobrevivência mais baixo no grupo TNF-αhigh (16.5 vs 23.5 meses para o grupo TNF-αlow). Permanece a questão de como o CTLA-4 influencia ou é influenciado pelas citoquinas pró-inflamatórias. A avaliação da expressão tumoral da CTLA-4, dos subtipos de linfócitos T, e dos perfis de macrófagos associados ao tumor e células supressoras da linha mieloide no microambiente tumoral, são aspetos importantes a avaliar em estudos futuros.
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Gu, Xiaolian. "p63 and epithelial homeostasis studies of p63 under normal, hyper-proliferative and malignant conditions /". Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33894.

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Colbert, Jeff D. "Compartmentalization of the TNF-Receptor 1-mediated signal transduction /". Connect to full text at ProQuest Digital Dissertations. IP filtered, 2005.

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Thesis (Ph.D. in Immunology) -- University of Colorado at Denver and Health Sciences Center, 2005.
Typescript. Includes bibliographical references (leaves 144-178). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;

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Yin, Qian. "Signal transduction by oligomerization structural : and biochemical studies of TRAF6 and Caspase-9 activation /". Access full-text from WCMC, 2008. http://proquest.umi.com/pqdweb?did=1528857091&sid=18&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Brittain, George C. IV. "A Novel Role for the TRAFs as Co-Activators and Co-Repressors of Transcriptional Activity". Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/451.

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The tumor necrosis factor (TNF) receptor-associated factors (TRAFs) were initially discovered as proteins that inducibly interact with the intracellular region of TNF receptors (TNFRs). Because the TNFRs lack intrinsic catalytic activity, the TRAFs are hypothesized to orchestrate signaling activation downstream of the TNFR superfamily, however their mechanism of activation remains unclear (Inoue et al., 2000; Bishop, 2004). Originally, the TRAFs were compared to the signal transducers and activators of transcription (STAT) protein family, due to their sequence homology, and the presence of multiple RING- and zinc-finger domains, suggesting that their function may be to regulate transcriptional activity (Rothe et al., 1994; Hu et al., 1994; Sato et al. 1995; Cheng et al., 1995). However, subsequent research focused predominantly on their cytoplasmic functions, and more recently on their function as E3 ubiquitin ligases (Pineda et al., 2007). In my research, I analyzed the subcellular localizations of the TRAFs following CD40 ligand (CD40L)-stimulation, and found that TRAF2 and 3 rapidly translocate into the nucleus of primary neurons and Neuro2a cells. Interestingly, similar analysis conducted in pre-B lymphocytes (Daudi cells) revealed a different response to CD40L-stimulation, with TRAF2 and 3 being rapidly degraded within 5-minutes of stimulation. These findings are significant because they demonstrate for the first time that the TRAFs translocate into the nucleus and suggest that they may function within the nucleus in a cell-specific manner. I next analyzed the ability of TRAF2 and 3 to bind to DNA, and found that they both bind to chromatin and the NF-kappaB consensus element in Neuro2a cells, following CD40L-stimulation. Similar analyses of the chromatin binding of TRAF2 and 3 in Daudi cells revealed that they were rapidly degraded, similar to the results from my analysis of their subcellular localization. These findings show for the first time that the TRAFs interact with DNA, and therefore support the hypothesis that the TRAFs may function within the nucleus as transcriptional regulators. Finally, I analyzed the ability of the TRAFs to regulate transcriptional activity by luciferase assay. Previous studies showed that overexpression of TRAF2 and 6 could induce NF-kappaB transcriptional activity; however researchers have not been able to determine the mechanism by which they do so. In my studies, I found that every TRAF can directly regulate transcriptional activity either as co-activators or co-repressors of transcription, in a cell- and target protein-specific manner. Additionally, I found that TRAF2 can act as a transcriptional activator, and that its ability to regulate transcription is largely dependent upon the presence of its RING-finger domain. In conclusion, these studies have revealed an entirely novel function for the TRAFs as immediate-early transcriptional regulators. Future research into the genes that are regulated by the specific TRAF complexes will further elucidate how the TRAFs regulate TNFR signaling, as well as whether dysfunctions in TRAF signaling may be associated with known disorders. If specific TRAF complexes are found to regulate specific genes, then pharmacological targeting of the individual TRAF complexes may allow for the highly specific inhibition of signaling events downstream of the TNFRs, without compromising overall receptor signaling, transcription factor pathways, or cellular systems.

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Santana, Sepúlveda Roxana Carolina. "LPS a través de TLR4 previene la diferenciación de fibroblasto a miofibroblasto cardiaco inducida por TGF-[beta]1". Tesis, Universidad de Chile, 2014. http://www.repositorio.uchile.cl/handle/2250/117231.

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Memoria para optar al título de Químico Farmacéutico
Autorizada por el autor, pero con restricción para ser publicada a texto completo hasta diciembre de 2015, en el Portal de Tesis Electrónicas.
La diferenciación de fibroblastos cardiacos (FC) a miofibroblastos cardiacos (MFC) es gatillada por TGF-β1, la cual señaliza principalmente a través de las proteínas Smad. Los MFC muestran como principal característica la presencia de microfilamentos citoplásmicos de α-SMA, estructuradas como fibras de estrés, lo que les permite la contracción. Por otro lado, LPS es un ligando del receptor TLR4, que señaliza de manera dependiente e independiente de MyD88 teniendo como principal efector el NF-κB, induciendo así la expresión de genes de citoquinas proinflamatorias. Sin embargo, aunque se ha descrito un efecto antagónico entre la señalización inducida por LPS y la señalización canónica de TGF- β, a la fecha no se ha estudiado si en FC y en MFC la expresión de α-SMA inducida por TGF-β1 es antagonizada por LPS. Para responder estas interrogantes se utilizaron FC y MFC de ratas adultas, y se determinó in vitro la capacidad de LPS de inhibir la expresión de α-SMA. Además, utilizando TAK- 242, un inhibidor de las vías intracelulares dependientes de TLR4, se determinó que los efectos gatillados por LPS ocurrían a través de este receptor. La utilización de los inhibidores PD98059, LY29002 y BAY 11-7082 permitió determinar que en FC LPS a través de la vía de señalización PI3K/Akt, disminuye la expresión de α-SMA. Por lo que nuestros resultados demuestran que LPS inhibe la expresión de α-SMA en FC, a través del receptor TLR4 mediante la activación de vía de señalización PI3K/Akt y que LPS es capaz de disminuir la expresión de α-SMA en MFC a través de TLR4 inhibiendo la mantención del fenotipo miofibroblasto
The difference between cardiac fibroblasts (CF) and cardiac myofibroblast (CMF) is triggered by TGF-β1, which mainly signals via Smad proteins. The main characteristic of CMF is cytoplasmic microfilaments of α-SMA; this are structured as stress fibers, which allow the contraction of CMF. Also, LPS is a ligand of the TLR4 receptor that signals via a dependant and independent pathway of MyD88 whose main factor is NF-κB; this induces the expression of inflammatory cytokine genes. However, despite an opposite effect has been described between the signaling induced by LPS and the canonical signaling of TGF-β, the opposite effect that LPS may have on the expression of α-SMA on CF and CMF induced by TGF-β1 has not been studied so far. In order to answer these questions, CF and CMF of adult rats were used; this showed in vitro evidence that LPS is capable of inhibiting the expression of α-SMA. Also, with the use of TAK-242, which is an inhibitor of the dependant intracellular domain of TLR4, we determined that the effects triggered by LPS occurred through said receptor. Using PD98059, LY29002 and BAY11-7082 inhibitors allowed us to determine that, via the PI3K/Akt signaling pathway, LPS decreases the expression of α-SMA in CF. Therefore, our results show that LPS inhibit the expression of α-SMA in CF through the TLR4 receptor via the activation of the PI3K/Akt signaling pathway, and that LPS is capable of decreasing the expression of α-SMA in CMF through TLR4 receptor, which inhibits the maintenance of the myofibroblast phenotype

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Beildeck, Marcy Ellen. "The role of vitamin D and the vitamin D receptor in TCF-4 regulation and silencing of CYP24A1". Connect to Electronic Thesis (CONTENTdm), 2009. http://worldcat.org/oclc/454140383/viewonline.

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Książki na temat "TNF Receptor-Associated Factor 4"

D, Wu Hao Ph, red. TNF receptor associated factors (TRAFs). New York: Springer Science+Business Media, 2007.

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Wu, Hao. TNF Receptor Associated Factors (Advances in Experimental Medicine and Biology,). Springer, 2007.

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Isaacs, John D., i Philip M. Brown. Rituximab and abatacept. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept's licence permits it use as a first-line biologic. In the United Kingdom, however, the National Institute for Health and Clinical Excellence (NICE) restricts the use of abatacept to patients who develop adverse effects with rituximab or in whom rituximab is contraindicated. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.

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Alharbi, Yousef, Manish S. Patankar i Rebecca J. Whelan. Antibody-Based Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0006.

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With their role in connecting disease-associated antigens to the cellular immune response, antibodies hold considerable promise as therapeutic agents. This chapter discusses three classes of therapeutic antibodies that have been developed for use in ovarian cancer therapy. The first includes antibodies selected against tumor-associated antigens such as MUC16/CA125, mesothelin, epithelial cell adhesion molecule, and folate receptor α‎. Antibodies in the second class target proteins such as CTLA-4 and PD1 that act as immune response checkpoint receptors. The third class of antibodies target secreted factors that promote tumor growth: targets in this class include vascular endothelial growth factor, cytokines, and chemokines. The development of each of these is described. The chapter also discusses the complications presented by soluble antigens, which serve to limit the applicability of antigens (such as MUC16/CA125) that are both cell-surface associated and circulating and the prospects for the combination of antibody-based immunotherapy and chemotherapy.

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Części książek na temat "TNF Receptor-Associated Factor 4"

Yamaoka, Toshimitsu, D. Brent Polk, Tohru Ohmori, Sojiro Kusumoto, Tomohide Sugiyama, Takao Shirai, Masanao Nakashima i in. "Epidermal Growth Factor (EGF) Receptor Kinase Activity is Required for Tumor Necrosis Factor (TNF)-α Mediated Intestinal Epithelial Survival". W New Trends in the Molecular and Biological Basis for Clinical Oncology, 37–54. Tokyo: Springer Japan, 2009. http://dx.doi.org/10.1007/978-4-431-88663-1_3.

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Savic, Sinisa, i Michael F. McDermott. "Tumor Necrosis Factor (TNF) Receptor-Associated Periodic Syndrome (TRAPS)". W Textbook of Autoinflammation, 329–45. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98605-0_18.

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Malejczyk, Jacek, Magdalena Malejczyk, Slawomir Majewski, Anna Hyc, Françoise Breitburd, Gerard Orth i Stefania Jablonska. "Release of Soluble Tumor Necrosis Factor-α (TNF-α) Receptor by HPV-Associated Neoplastic Cells". W Immunology of Human Papillomaviruses, 315–20. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2449-6_49.

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Lachmann, Helen J., i Philip N. Hawkins. "Hereditary periodic fever syndromes". W Oxford Textbook of Medicine, 1760–66. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.121202_update_001.

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The hereditary periodic fever syndromes are autoinflammatory diseases that mostly present in childhood and are characterized by recurrent, self-limiting, seemingly unprovoked episodes of fever and systemic inflammation that occur in the absence of autoantibody production or identifiable infection. Disorders include (1) familial Mediterranean fever (FMF), due to mutation in the gene encoding pyrin; (2) tumour necrosis factor (TNF) receptor associated periodic syndrome (TRAPS), due to mutation in a gene for a TNF receptor; (3) Mevalonate kinase deficiency and period fever (MKD), caused by mutations in the mevalonate kinase gene; and (4) the cryopyrin associated periodic syndromes (CAPS), which include (a) familial cold urticarial syndrome, (b) Muckle–Wells syndrome, and (c) chronic infantile neurological, cutaneous and articular syndrome. Understanding of the molecular pathogenesis of these disorders provides unique insights into the regulation of innate immunity and inflammation....

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Lachmann, Helen J., Stefan Berg i Philip N. Hawkins. "Hereditary periodic fever syndromes". W Oxford Textbook of Medicine, redaktor Timothy M. Cox, 2207–18. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0240.

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The hereditary periodic fever syndromes or hereditary autoinflammatory diseases are disorders of innate immunity that mostly present in childhood and are characterized by recurrent, self-limiting, seemingly unprovoked episodes of fever and systemic inflammation that occur in the absence of autoantibody production or identifiable infection. Disorders include (1) familial Mediterranean fever (FMF), due to mutations in the gene encoding pyrin; (2) tumour necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS), due to mutations in a gene for a TNF receptor; (3) mevalonate kinase deficiency and period fever (MKD), caused by mutations in the mevalonate kinase gene; and (4) the cryopyrin-associated periodic syndromes (CAPS), which include (a) familial cold urticarial syndrome, (b) Muckle–Wells syndrome, and (c) chronic infantile neurological, cutaneous, and articular syndrome. With advances in genetics, further syndromes are continually being recognized. These are all extremely rare and in the majority are only known to affect a handful of kindred or individuals. Diagnosis relies on recognition of suggestive clinical features that are almost always accompanied by a substantial acute phase response, and is supported by genetic testing. With the exception of FMF, which is a common disease in certain geographic areas, hereditary periodic fever syndromes are rare and easily overlooked in the differential diagnosis of recurrent fevers. Clinical features and management—attacks can be mild to debilitating and short to prolonged, while their most feared complication is AA amyloidosis. Effective therapies are available for some syndromes, for example: (1) FMF—daily prophylactic colchicine prevents clinical attacks and susceptibility to AA amyloidosis, (2) CAPS—treatment with anti-IL-1 agents produces rapid and often complete clinical and serological remission, and (3) TRAPS—anti-IL therapies are extremely effective.

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Singh Chauhan, Vikram. "Vitamin D and the Immune System". W Vitamin D. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97300.

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In the past few decades, various novel actions of vitamin D have been discovered. The mechanism of action of calcitriol or vitamin D is mediated by the Vitamin D receptor (VDR), a subfamily of nuclear receptors, which acts as a transcription factor in the target cells after formation of a heterodimer with the retinoid X receptor (RXR). As the VDR has been found in virtually all cell types, vitamin D exerts multiple actions on different tissues. Vitamin D has important immunomodulatory actions, which includes enhancement of the innate immune system and inhibition of the adaptative immune responses. These actions are associated with an increase in production of interleukin (IL)-4 by T helper (Th)-2 lymphocytes and the up-regulation of regulatory T lymphocytes. Vitamin D can regulate the immune responses in secondary lymphoid organs as well as in target organs through a number of mechanisms. Vitamin D inhibits the expression of APC cytokines, such as interleukin-1 (IL-1), IL-6, IL-12, and tissue necrosis factor- α (TNF-α) and decreases the expression of a set of major histocompatibility complex (MCH) class II cell surface proteins in macrophages. Vitamin D also inhibits B cell differentiation and antibody production. These actions reflect an important role of Vitamin D in balancing the immune system.

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"TNF receptor-associated factor 6". W Dictionary of Rheumatology, 215. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-79280-3_1117.

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"TRAF6 — TNF receptor-associated factor 6". W Dictionary of Rheumatology, 216. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-79280-3_1128.

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Isaacs, John D., i Philip M. Brown. "Rituximab and abatacept". W Oxford Textbook of Rheumatology, 642–49. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0083_update_002.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept’s licence permits use as a first-line biologic. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.

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Two biologics that target cells have been licensed to treat rheumatoid arthritis (RA). Rituximab is a chimeric monoclonal antibody (mAb) against CD20 that depletes B cells; abatacept is a soluble form of CTLA-4 that blocks costimulation and interferes with T-cell function. Both drugs alleviate signs and symptoms of RA and have been shown to retard radiographic progression. Rituximab is licensed for use following failure of tumour necrosis factor (TNF) blockade whereas abatacept’s licence permits use as a first-line biologic. As with other biologics, the use of either drug is associated with an enhanced risk of serious infections; additionally, rituximab in particular can cause infusion reactions, requiring prophylaxis. By targeting cells that are central to RA pathogenesis, these drugs provide important additional therapeutic options for patients with RA.

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Streszczenia konferencji na temat "TNF Receptor-Associated Factor 4"

Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli i C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α. TNF-α is known to bind its receptor (TNFR1) to cause a cascade that ends with degradation of an inhibitor, IκBα, and release of the transcription factor NF-κB [3]. The actions of TNF-α are also known to be affected by at least three NF-κB independent pathways including the p38, ERK, and JNK pathways [4]. The objective of this study was to determine whether cyclic compression could affect TNF-α induced cartilage degradation and to determine the roles of p38, ERK, and JNK pathways in TNF-induced cartilage degradation. We hypothesized that cyclic loading would inhibit the degradative effects caused by TNF-α.

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BRINK, K., F. DERKX, E. BROMMER, J. STIBBE, H. KOLSTEE i M. SCHALEKAMP. "THE FIBRINOLYTIC, FACTOR VIII:C, VON WILLEBRAND FACTOR AND HEMODYNAMIC RESPONSES TO DDAVP IN PATIENTS WITH HEREDITARY NEPHROGENIC DIABETES INSIPIDUS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644709.

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The pressor response of vasopressin (AVP) is mediated by a calcium-dependent mechanism (VI-receptor), whereas its antidiuretic effect depends on c-ANP (V2-receptor). DDAVP (1-desamino-8-D-arginine vasopressin) is a synthetic V2 analog of AVP. AVP and DDAVP also increase FVIII:C vWF:Ag and tissue-type plasminogen activator (t-PA) in plasma. The mechanism by which AVP and DDAVP elevate these factors is unclear. Patients with X-linked nephrogenic diabetes insipidus (NDI) are resistant to the V2-mediated antidiuretic action of AVP and DDAVP. We therefore have studied the effect of DDAVP (0.4 ug/kg iv infusion in 10 min) in 2 brothers with NDI, their mother and an unrelated patient.In control subjects (n=12) FVIII:C rose 122 (6) % ,mean (SEM), vWF:Ag 104 (4) % and t-PA 115 (7) % over basal levels. This rise was associated with a fall in diascolic blood pressure -11 (3) mmHg and an increase in heart rate from 62 (4) to 91 (5) bpm. Plasma noradrenaline rose from 262 (34) to 590 (84) pg/ml and renin from 16 (3) to 42 (6) uU/ml. Ten out of 12 controls showed facial flusning. The patients with NDI had normal basal FVIII:C, vWF:Ag and t-PA levels. Plasma noradrenaline and renin were within the nor mam range. Tne patients with NDI were also resistant to the stimulatory effect of DDAVP on the release of FVIII:C, vWF:Ag and t-PA. They also showed no change in blood pressure, nearc rate, plasma noradrenaline and renin and had no facial flushing. The carrier had normal responses to DDAVP.Tne increase in FVII:C, vWF:Ag and t-PA and the hemodynamic responses after DDAVP infusion probably appear to depend on extrarenal V2-receptor activation. DDAVP cannot be used in identifying carriers in families at risk.

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Kratz, Annekatrine, Chuanbing Zang, Jan Eucker i Hongyu Liu. "Abstract 943: Retinoid sensitizes Tumor Necrosis Factor (TNF) -related apoptosis inducing ligand -induced cytotoxic effect in breast cancer by upregulating cell surface receptor Death Receptor-4 expression". W Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-943.

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Schleef, R. R., M. P. Bevilacqua, M. Sawdey, M. A. Gimbrone i D. J. Loskutoff. "INTERLEUKIN 1 (IL-1) AND TUMOR NECROSIS FACTOR (TNF) ACTIVATION OF VASCULAR ENDOTHELIUM: EFFECTS ON PLASMINOGEN ACTIVATOR INHIBITOR (PAI-1) AND TISSUE-TYPE PLASMINOGEN ACTIVATOR (tPA)". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642864.

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The regulation of the fibrinolytic system of cultured human umbilical vein endothelial cells (ECs) by two distinct monokines (IL-1 and TNF) was investigated. Conditioned media (CM) was collected from ECs cultured for 24 h in the presence of the monokines and analyzed in quantitative immunological assays for PAI-1 activity and tPA antigen. Both monokines induced a dose-dependent increase in extracellular PAI-1 activity, with a concomitant decrease in tPA antigen. Maximal effects were achieved with either 10 U/ml IL-1 or 200 U/ml of TNF, and resulted in a 4 fold increase in PAI-1 and a 50% decrease in tPA. The kinetics of the effects of both monokines on EC PAI-1 and tPA were similar, with maximal response detected at 24 h. Cell-associated PAI-1 also increased in response to these monokines. For example, a 24 h exposure of EC to TNF (250 U/ml) or IL-1 (5 U/ml) caused a 5-fold increase in cell-associated PAI-1. Northern blot analysis using a PAI-1 cDNA probe indicated that the monokines increased the levels of two RNA species, corresponding to PAI mRNAs of approximately 3.0 and 2.2 kb in length. To determine if the increase in cel 1-associated PAI-1 reflects a storage pool of rapidly releasable PAI-1, ECs were pretreated with IL-1 for 24 h, washed and the PAI-1 activity in CM measured after 5, 15 and 60 min treatment with known secretagogues (i.e., phorbol myristate acetate, calcium ionophore A23187). Although IL-1 treated ECs released PAI-1 at a rate which was 5-fold higher than controls, this rate was not increased further by treatment with phorbol myristate acetate or ionophore. The fact that both monokines act in a similar manner strengthens the hypothesis that the local development of immune and inflammatory processes could reduce endothelial fibrinolytic activity, thus leading to the pathologic formation of intravascular thrombi.

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Bevill, Scott L., i Thomas P. Andriacchi. "Dynamic Compression in the Presence of TNF-Alpha Differentially Effects Gene Expression in Tibial Plateau Cartilage Covered and Uncovered by the Meniscus". W ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192575.

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It has been suggested that altered joint loading may be a cause of the cartilage degeneration commonly observed following joint destabilizing events such as anterior cruciate ligament (ACL) injury [1]. Changes in the biochemical environment of the joint accompany these changes in joint loading, though, with acute and chronic increases in synovial concentrations of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFα) [2, 3]. TNFα is a potent catabolic factor associated with increased expression [4] and synthesis [5] of matrix proteases in articular cartilage, and therefore may play in important role in the degenerative events following joint injury.

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Shimp, Samuel K., Christopher M. Reilly i Marissa Nichole Rylander. "Empirical Modeling the Effect of Hsp90 Inhibition on Cytokines Associated With Impaired Biotransport of Apoptotic Debris". W ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19572.

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Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder that can affect nearly every organ in the body. A link has been established between abnormal biotransport of apoptotic cell debris and pathogenesis of SLE [1]. Lupus mice are hyper-responsive to immune stimulation and overproduce inflammatory mediators including IL-6, IL-12, and nitric oxide (NO) [2]. Extracellular expression and transport of inflammatory cytokines are thought to be involved with the inhibited clearance of cellular debris [1]. Hsp90 has a prominent role in folding and conformational regulation of several client proteins, including proteins involved with production of inflammatory mediators [3]. Hsp90 readily binds ATP at the amino (N-) terminal domain. This binding event causes a conformational change in Hsp90 making it “clamp down” on its client protein [3]. Geldanamycin (Geld) is a known inhibitor of Hsp90 that out competes ATP binding at the N-terminal. This prevents chaperone capability and ultimately leads to client protein deactivation, destabilization, and degradation [3]. Hsp90 inhibitors have been shown to suppress immune stimulated release of interleukin 6 (IL-6), IL-12, tumor necrosis factor alpha (TNF-α), and nitric oxide (NO) [4].

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Stenson, E., E. Killeen, JC Cohen i SI Shah. "100% Hyperoxia at Birth Results in Increased Levels of Heat Shock Protein 27 (HSP27) and Decreased Levels of Tumor Necrosis Factor Alpha (TNF-alpha), Toll-Like Receptor 4 (TLR-4), Thyroid Transcription Factor (TTF-1), and Interleukins 6 and 10 (IL-6,10) in the Lungs of Adult Sprague-Dawley Rats." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4112.

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Pryhuber, GS, i HL Huyck. "TNF Receptor Associated Factor 1 (TRAF1) Enhances Silica Induced Macrophage Retension Potentiating TNF-α Dependent Fibrosis." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1320.

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MATOS, ERICA NAOMI NAKA, MILENA FOIZER LEITE, CAROLINA YUME ARAZAWA, QUEROLAI GOMES GADELHA, RENATO FURTADO TAVARES i LEONARDO PEREIRA WON MUHLEN. "THE EFFICACY OF CANAKINUMAB IN THE TREATMENT OF TUMOR NECROSIS FACTOR (TNF) ALPHA RECEPTOR-ASSOCIATED PERIODIC SYNDROME (TRAPS)". W 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-280.

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Bowers, Laura W., Rebecca De Angel, Rajeshwar Tekmal, Andrew Brenner, Stephen Hursting i Linda deGraffenried. "Abstract 3071: Obesity-associated growth factor signaling upregulates aromatase expression and estrogen receptor activity in breast cancer cells". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3071.

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