Relevant bibliographies by topics / Tumour necrosis factor receptor I

Academic literature on the topic 'Tumour necrosis factor receptor I'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Tumour necrosis factor receptor I"

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Nezu, M., H. Iwagaki, H. Aoki, N. Tanaka, and K. Orita. "Tumour Necrosis Factor-α Upregulates Transferrin Receptors in K 562 Cells." Journal of International Medical Research 22, no. 3 (May 1994): 145–52. http://dx.doi.org/10.1177/030006059402200302.

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The effects of tumour necrosis factor-α on transferrin receptor expression in a human chronic myelocytic leukaemia cell line, K 562 cells, were studied. Cytofluorometry studies showed that the numbers of transferrin receptors in exponentially growing K 562 cells were increased when the cells were incubated with tumour necrosis factor-α for 24 h. The induction of transferrin receptors by tumour necrosis factor-α may be mediated by a mechanism that is independent of growth since cell growth in treated cultures did not differ from that in the controls. The DNA contents of K 562 cells treated with tumour necrosis factor-α showed that after 24 h there were less cells in the G1 and S phases and more cells in the G2/M phase than in the control group. The phase of upregulation of transferrin receptors induced by tumour necrosis factor-α may be dependent on the cell cycle. This new evidence that tumour necrosis factor-α upregulates transferrin receptors suggests a cancer-anaemia cascade in which the cancer burden state activates macrophage release of tumour necrosis factor-α as a result of transferrin receptor expression.
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Süttmann, U., O. Selberg, H. Gallati, J. Ockenga, H. Deicher, and M. J. Müller. "Tumour Necrosis Factor Receptor Levels Are Linked to the Acute-Phase Response and Malnutrition in Human-Immunodeficiency-Virus-Infected Patients." Clinical Science 86, no. 4 (April 1, 1994): 461–67. http://dx.doi.org/10.1042/cs0860461.

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1. Increased release of tumour necrosis factor is thought to contribute to human-immunodeficiency-virus-associated wasting syndrome. Elevated serum concentrations of tumour necrosis factor have, however, mainly been found during acute opportunistic infections and were not correlated with the degree of wasting. This finding may be explained by the paracrine release and the rapid inactivation of tumour necrosis factor. Serum levels of the two recently detected soluble tumour necrosis factor receptor proteins (p55 and p75) are assumed to reflect tumour necrosis factor release. 2. Serum levels of soluble tumour necrosis factor receptors 55 and 75 were measured by an enzyme-linked immunological and biological binding assay in 45 human-immunodeficiency-virus-infected patients and seven healthy control subjects. Patients were followed up for survival. Serum albumin, prealbumin, total iron-binding capacity (transferrin) and C-reactive protein concentrations were measured using standard laboratory methods. Body composition was determined by bioelectrical impedance analysis. 3. Serum concentrations of soluble tumour necrosis factor receptor 55 and 75 were both significantly increased in human-immunodeficiency-virus-infected patients as compared with the healthy control subjects (P < 0.05); soluble tumour necrosis factor receptor concentrations were even more increased in patients with elevated C-reactive protein levels (≥ 5 mg/l) as compared with those with normal C-reactive protein levels (< 5 mg/l; P < 0.0001 and P < 0.01, respectively). An association was observed between serum soluble tumour necrosis factor receptor 55 and 75 concentration and (i) serum albumin concentration (r = −0.46, P < 0.005 and r = −0.63, P < 0.001, respectively), (ii) serum prealbumin concentration (r = −0.42, P < 0.005 and r = −0.57, P < 0.001, respectively), and (iii) serum total iron-binding capacity (transferrin; r = −0.31, P < 0.05 and r = −0.44, P < 0.005, respectively). A correlation was also found between serum soluble tumour necrosis factor receptor 55 level and the extracellular mass-body cell mass quotient (r = 0.63, P < 0.001). 4. The present data provide evidence that the tumour necrosis factor system is involved in the genesis of human-immunodeficiency-virus-associated malnutrition. Serum levels of soluble tumour necrosis factor receptors may be useful for diagnosis and management of the wasting syndrome.
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BARBER, Matthew D., Kenneth C. H. FEARON, and James A. ROSS. "Relationship of serum levels of interleukin-6, soluble interleukin-6 receptor and tumour necrosis factor receptors to the acute-phase protein response in advanced pancreatic cancer." Clinical Science 96, no. 1 (January 1, 1999): 83–87. http://dx.doi.org/10.1042/cs0960083.

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The level of the acute-phase response is a major predictor of survival in patients with advanced pancreatic cancer. This study examines the association between the acute-phase protein response, as determined by serum C-reactive protein, and serum levels of interleukin-6, soluble interleukin-6 receptor and the soluble tumour necrosis factor receptors in patients with pancreatic cancer. Thirty-four blood samples were collected from 13 patients with advanced pancreatic cancer. Samples were also collected from six healthy subjects. Levels of C-reactive protein, interleukin-6, soluble interleukin-6 receptor and soluble tumour necrosis factor receptors 55 and 75 were measured by indirect ELISA. Serum levels of C-reactive protein, interleukin-6 and soluble tumour necrosis factor receptors 55 and 75 were significantly higher in cancer patients than in controls. Levels of serum soluble interleukin-6 receptor were not significantly different between the two groups. In cancer patients, a significant positive association was found between the level of the acute-phase protein response and serum levels of interleukin-6, soluble tumour necrosis factor receptor 55 and soluble tumour necrosis factor receptor 75. No association was found between levels of soluble interleukin-6 receptor and any other factor. There is no significant relationship between the level of soluble interleukin-6 receptor and the acute-phase protein response in vivo and the biological role of soluble interleukin-6 receptor in the chronic inflammatory component of cachexia remains unclear.
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XU, Duorong, Zhenqi SHI, Jay McDONALD, George PAN, Xuemei CAO, Xueqing YU, and Xu FENG. "Development of a chimaeric receptor approach to study signalling by tumour necrosis factor receptor family members." Biochemical Journal 383, no. 2 (October 8, 2004): 219–25. http://dx.doi.org/10.1042/bj20040961.

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Members of the tumour necrosis factor receptor family play a pivotal role in cell differentiation, function and apoptosis. However, signalling by many members of the family remains to be elucidated. In the present study, we developed a chimaeric receptor approach for studying signalling by receptors belonging to this family. The chimaeric receptor comprises the human Fas external domain linked to the transmembrane and cytoplasmic domains of a tumour necrosis factor receptor family member of interest. When the chimaera is expressed in mouse cells, the clustering of the chimaera induced by a human Fas-activating antibody activates the intracellular domain of the chimaera without affecting its endogenous counterpart. Since the antibody recognizes only human Fas, this approach can be used to dissect signalling by any tumour necrosis factor family member using any type of mouse cell including those endogenously expressing Fas. Moreover, we also showed that the chimaeric receptor approach can be used to study signalling at any stage of cell differentiation or function.
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Westbrook, A. M., B. Wei, K. Hacke, M. Xia, J. Braun, and R. H. Schiestl. "The role of tumour necrosis factor- and tumour necrosis factor receptor signalling in inflammation-associated systemic genotoxicity." Mutagenesis 27, no. 1 (October 6, 2011): 77–86. http://dx.doi.org/10.1093/mutage/ger063.

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Holbrook, Jonathan, Samuel Lara-Reyna, Heledd Jarosz-Griffiths, and Michael F. McDermott. "Tumour necrosis factor signalling in health and disease." F1000Research 8 (January 28, 2019): 111. http://dx.doi.org/10.12688/f1000research.17023.1.

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The master pro-inflammatory cytokine, tumour necrosis factor (TNF), has been shown to modulate multiple signalling pathways, with wide-ranging downstream effects. TNF plays a vital role in the typical immune response through the regulation of a number of pathways encompassing an immediate inflammatory reaction with significant innate immune involvement as well as cellular activation with subsequent proliferation and programmed cell death or necrosis. As might be expected with such a broad spectrum of cellular effects and complex signalling pathways, TNF has also been implicated in a number of disease states, such as rheumatoid arthritis, ankylosing spondylitis, and Crohn’s disease. Since the time of its discovery over 40 years ago, TNF ligand and its receptors, TNF receptor (TNFR) 1 and 2, have been categorised into two complementary superfamilies, namely TNF (TNFSF) and TNFR (TNFRSF), and 19 ligands and 29 receptors have been identified to date. There have been significant advances in our understanding of TNF signalling pathways in the last decade, and this short review aims to elucidate some of the most recent advances involving TNF signalling in health and disease.
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Trentin, L., R. Zambello, P. Bulian, A. Cerutti, C. Enthammer, M. Cassatella, D. Nitti, M. Lise, C. Agostini, and G. Semenzato. "Tumour-infiltrating lymphocytes bear the 75 kDa tumour necrosis factor receptor." British Journal of Cancer 71, no. 2 (February 1995): 240–45. http://dx.doi.org/10.1038/bjc.1995.50.

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Rasmussen, C. A., J. L. Pace, S. Banerjee, T. A. Phillips, and J. S. Hunt. "Trophoblastic Cell Lines Generated from Tumour Necrosis Factor Receptor-deficient Mice Reveal Specific Functions for the Two Tumour Necrosis Factor Receptors." Placenta 20, no. 2-3 (March 1999): 213–22. http://dx.doi.org/10.1053/plac.1998.0356.

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Deuren, M. "Kinetics of tumour necrosis factor-alpha, soluble tumour necrosis factor receptors, interleukin 1-beta and its receptor antagonist during serious infections." European Journal of Clinical Microbiology & Infectious Diseases 13, S1 (January 1994): S12—S16. http://dx.doi.org/10.1007/bf02390680.

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Hehlgans, Thomas, and Klaus Pfeffer. "The intriguing biology of the tumour necrosis factor/tumour necrosis factor receptor superfamily: players, rules and the games." Immunology 115, no. 1 (May 2005): 1–20. http://dx.doi.org/10.1111/j.1365-2567.2005.02143.x.

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Dissertations / Theses on the topic "Tumour necrosis factor receptor I"

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Albataineh, Eman Mohammad. "Studies of tumour necrosis factor receptor-1 in tumour necrosis factor receptor associated periodic sysndrome (TRAPS)." Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537655.

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Björnberg, Flemming. "Processing of TNF-receptors to soluble receptor forms in myeloid cells." Lund : Dept. of Hematology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39176479.html.

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Vagenas, Panagiotis. "Tumour necrosis factor receptor signalling pathways in chronically activated T lymphocytes." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416631.

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Wood, Katrina Mackay. "Lymphocyte signalling through members of the Tumour Necrosis Factor Receptor family." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320268.

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Reddy, Shalini Kamu. "Tumour necrosis factor receptor superfamily memebers in chicken B cell development." Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500214.

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Kamu, Reddy Shalini. "Tumour necrosis factor receptor superfamily members in chicken B cell development." Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500863.

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Connell, Michelle C. "Role of tumour necrosis factor receptor subtypes in endothelial cell inflammatory responses." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430906.

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The signalling cascade, produced after THF ligand binding, involves the recruitment of many different signalling proteins, and includes the activation of mitogen-activated protein kinase (MAPK) pathways (e.g.  p42/p44 MAPK, p38 MAPK and JNK), as well as the activation of many transcription factors e.g. activating protein-1 (AP-1) and nuclear factor-kB( NF-kB) The aim of this thesis was firstly to investigate the role of TNF-a in the activation of the transcription factor AP-1.  Secondly, to investigate TNFR expression in HUVEC cells and then investigates the cellular consequences of TNF treatment on HUVEC cells.  Thirdly, we investigated the activation of the MAPK family and the activation of the transcription factors AP-1 and NF­KB in HUVEC cells.  Finally, we investigated cell adhesion molecule induction as a result of TNF stimulation in endothelial cells, and then assessed the role of MAPK family members on TNF induced induction of cell surface adhesion molecule expression.  Differential activation of TNFRs was also investigated using TNF receptor specific mutant proteins (‘muteins’), to understand the role of either TNFR1 or TNFR2 in these cellular responses. The key finding of this study were that both TNF receptor subtypes were capable of activating AP-1 and NF-kB transcriptional activity in HeLa, HEK 293 or HUVEC cell systems, but to varying degrees.  Huvec cells express both TNF receptor subtypes and TNF was found to result in neither death nor proliferation of endothelial cells.
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Kimberley, Fiona. "A study of the structure and function of tumour necrosis factor receptor superfamily members." Thesis, University of Oxford, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404169.

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Drewe, Elizabeth. "Molecular and therapeutic aspects of tumour necrosis factor receptor 1 associated periodic syndrome (TRAPS)." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416437.

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Tucker, S. J. "Development of novel technologies used to measure tumour necrosis factor receptor signalling in living cells." Thesis, University of Aberdeen, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590943.

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The aim of this work was firstly to assess novel reporter constructs as potential methods for investigating TNF signalling. The key early findings of this study suggested the GFP-linked reporter construct system as more suitable for studying TNF signalling. Subsequently a series of optimisation experiments maximised this system in HeLa and TF-1 cells. In both cell lines TNF strongly induced p38 MAPK, p42/44 MAPK, JNK and NF-κB reporter constructs. In functional terms p42/44 MAPK activation was shown to be critical for TF-1 cell proliferation, whilst JNK related to TNF-induced cell death in both cell types. Interestingly, p38 MAPK was also related to TNF-induced cell death, but only in TF-1 cells. In contrast, NF-κB were shown to exist in a co-inhibitory relationship, in which inhibition of one resulted in potentiation of the other. This was shown to be an important regulatory controller of cell death following TNF stimulation of HeLa and TF-1 cells. In addition, TNF-induced JNK activation was related to caspases, with suppression of caspases reducing the degree of JNK activity. Finally, receptor constructs were used to assess the signalling prowess of sodium salicylate in TF-1 cells, which activated the same signal pattern as TNF in dying TF-1 cells. Indeed sodium salicylate reciprocated the selective induction of cell death in proliferating TF-1 cells seen with TNF, suggesting potential for this drug in the treatment of leukaemia. Associated with early experiments, polymeric sponge toxin fractions (polyAPS and halitoxin) were shown to mediate successful HEK 293 and HeLa transfection on account of their porative activity.
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Books on the topic "Tumour necrosis factor receptor I"

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

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Tumor necrosis factor. New York: Nova Biomedical Books, 2009.

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Gregory, Bock, Marsh Joan, and Symposium on Tumour Necrosis Factor and Related Cytotoxins (1987 : London, England), eds. Tumour necrosis factor and related cytotoxins. Chichester: Wiley, 1987.

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Zurita, Maria Trinidad. Tumour necrosis factor inhibitory drugs in meningitis. Birmingham: University of Birmingham, 1994.

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S, Grewal Iqbal, ed. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.

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Bock, Gregory, and Joan Marsh, eds. Ciba Foundation Symposium 131 - Tumour Necrosis Factor and Related Cytotoxins. Chichester, UK: John Wiley & Sons, Ltd., 1987. http://dx.doi.org/10.1002/9780470513521.

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Mahony, Susan Maria. Weight loss and metabolic alterations induced by recombinant tumour necrosis FACTOR-ALPHA (TNF). Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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Ennis, Maurice. Tumour necrosis factor alpha and ultraviolet light activation of programmed cell death by apoptosis in D. melanogaster. Ottawa: National Library of Canada, 2001.

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Aerts, Joeri. Progesterone Induces Apoptosis in Eosinophilic Granulocytes & Induces Tumour Necrosis Factor-Alpha / Tumour Necrosis Factor Receptor. Leuven Univ Pr, 2002.

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Book chapters on the topic "Tumour necrosis factor receptor I"

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Aggarwal, Bharat B., Ramani A. Aiyer, Diane Pennica, Patrick W. Gray, and David V. Goeddel. "Human Tumour Necrosis Factors: Structure and Receptor Interactions." In Novartis Foundation Symposia, 39–51. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513521.ch4.

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Mohr, Verena, Catharina Schuetz, and Erkan Demirkaya. "Tumor Necrosis Factor Receptor-Associated Periodic Syndrome (TRAPS)." In Genetic Syndromes, 1–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-66816-1_650-1.

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Papadopoulou, Charalampia, and Helen J. Lachmann. "Tumor Necrosis Factor Receptor-Associated Periodic Syndrome (TRAPS)." In Periodic and Non-Periodic Fevers, 235–45. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19055-2_13.

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Hsu, Hui-Chen, Yalei Wu, and John D. Mountz. "Tumor Necrosis Factor Ligand-Receptor Superfamily and Arthritis." In Current Directions in Autoimmunity, 37–54. Basel: KARGER, 2005. http://dx.doi.org/10.1159/000090770.

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Savic, Sinisa, and Michael F. McDermott. "Tumor Necrosis Factor (TNF) Receptor-Associated Periodic Syndrome (TRAPS)." In 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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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "E3 Ubiquitin-Protein Ligase, Tumor Necrosis Factor Receptor-Associated Factor 6 (TRAF6)." In Encyclopedia of Signaling Molecules, 539. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100374.

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Benschop, Robert, Tao Wei, and Songqing Na. "Tumor Necrosis Factor Receptor Superfamily Member 21: TNFR-Related Death Receptor-6, DR6." In Advances in Experimental Medicine and Biology, 186–94. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89520-8_13.

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De Valck, Dirk, Rudi Beyaert, Frans Van Roy, and Walter Fiers. "Tumor Necrosis Factor Cytotoxicity is Associated with Activation of Cellular Phospholipases." In New Developments in Lipid-Protein Interactions and Receptor Function, 29–37. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2860-9_4.

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Heilig, B., M. Mapara, T. Kubin, M. Brockhaus, B. Dörken, and W. Hunstein. "Tumor Necrosis Factor Receptor Expression on Human Normal and Malignant B Lymphocytes: Anti-75-kDa Tumor Necrosis Factor Receptor Antibody Inhibits B-Cell Proliferation." In Cytokines in Hemopoiesis, Oncology, and AIDS II, 239–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-48715-6_31.

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Gonçalves, João, Helena Soares, Norman L. Eberhardt, Sarah C. R. Lummis, David R. Soto-Pantoja, David D. Roberts, Umadas Maitra, et al. "TRAIL-R1 (Tumor Necrosis Factor-Related Apoptosis-Inducing ligand Receptor 1)." In Encyclopedia of Signaling Molecules, 1928. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101394.

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Conference papers on the topic "Tumour necrosis factor receptor I"

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Pettersson, T., H. Nevala, L. Karenko, S. Stjernberg, M. Raatikainen, H. Suomalainen, J. Rauta, MF McDermott, P. Peterson, and A. Ranki. "OP0122 Tumour necrosis factor-receptor associated periodic syndrome in a finnish family." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.745.

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Bell, H., S. Lalnunhlimi, M. Green, F. Van Delft, and A. Krippner-Heidenreich. "Tumour Necrosis Factor receptor (TNFR)-signalling dependent killing in T-cell acute lymphoblastic leukaemia (T-ALL)." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687172.

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Kontzias, A., S. Zarabi, C. Calabrese, and Y. W. Cheng. "AB1130 Late onset tumour necrosis factor receptor (TNFR)–associated periodic syndrome (TRAPS) caused by somatic tnfrsf1 mosaicism." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6083.

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Makwana, Raj, Dom Spina, and Clive Page. "Cannabinoid Receptor Activity In The Tumour Necrosis Factor (TNF)-a-Induced Increased Contractility Of The Guinea-Pig Isolated Trachea." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2154.

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Rego, Stephen, Krista Ricci, Muthulekha Swamydas, and Didier Dreau. "Abstract 397: Soluble Tumor Necrosis Factor Receptor shed by breast tumor cells modulates macrophage migration." In 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.am2012-397.

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Atkinson, JE, RV House, PS Cranmer, AE Colucil, H. Davis, CK Edwards, and DM Miller. "THU0096 Effect of anakinra (il-1ra) and soluble tumour necrosis factor receptor i (stnf-ri) on cellular immune function in rats." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.973.

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Niessen, N. M., J. L. Simpson, K. J. Baines, P. G. Gibson, and M. Fricker. "Differential Tumor Necrosis Factor Ligand and Receptor Expression on Monocyte Subsets in Blood and Sputum." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3812.

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Kang, K., SR Lee, X. Piao, HS Byun, SR Lee, M. Won, KA Park, and GM Hur. "PO-063 Triterpenoids isolated from natural product regulates TNF(tumour necrosis factor)-mediated RIP(receptor-interacting serine/threonine-protein kinase)1-dependent apoptosis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.107.

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Bertok, S., MR Wilson, J. Dokpesi, KP O'Dea, N. Marczin, and M. Takata. "Tumour Necrosis Factor-α (TNF) Receptor p75 Plays a Substantial Role in TNF-Mediated Upregulation of Leukocyte Adhesion Molecules in Mouse Lung Microvasculature." In 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.a2495.

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Zhao, Mengzhu, Yi Luo, Min Shen, DI Wu, Wen Zhang, and Xiaofeng Zeng. "THU0593 CLINICAL AND GENETIC FEATURES OF CHINESE ADULT PATIENTS WITH TUMOR NECROSIS FACTOR RECEPTOR-ASSOCIATED PERIODIC SYNDROME." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5204.

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Reports on the topic "Tumour necrosis factor receptor I"

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Meidan, Rina, and Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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2

Belenska-Todorova, Lyudmila Filipova, Valeriya Gyurkovska, and Nina Dimitrova Ivanovska. Neutralization of Tumour Necrosis Factor-related Apoptosis-inducing Ligand Ameliorates the Symptoms of Zymosan-induced Septic Shock. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, November 2021. http://dx.doi.org/10.7546/crabs.2021.11.15.

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3

Evans, Donald L., Avigdor Eldar, Liliana Jaso-Friedmann, and Herve Bercovier. Streptococcus Iniae Infection in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Towards the Pathogen and Vaccine Formulation. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7586538.bard.

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The objectives of the BARD proposal were to determine the mechanisms of nonspecific cytotoxic cells (NCC) that are necessary to provide heightened innate resistance to infection and to identify the antigenic determinants in Streptococcus iniae that are best suited for vaccine development. Our central hypothesis was that anti-bacterial immunity in trout and tilapia can only be acquired by combining "innate" NCC responses with antibody responses to polysaccharide antigens. These Objectives were accomplished by experiments delineated by the following Specific Aims: Specific aim (SA) #1 (USA) "Clone and Identify the Apoptosis Regulatory Genes in NCC"; Specific aim #2 (USA)"Identify Regulatory Factors that Control NCC Responses to S. iniae"; Specific aim #3 (Israel) "Characterize the Biological Properties of the S. iniae Capsular Polysaccharide"; and Specific aim #4 (Israel) "Development of an Acellular Vaccine". Our model of S. iniae pathogenesis encompassed two approaches, identify apoptosis regulatory genes and proteins in tilapia that affected NCC activities (USA group) and determine the participation of S.iniae capsular polysaccharides as potential immunogens for the development of an acellular vaccine (Israel group). We previously established that it was possible to immunize tilapia and trout against experimental S. difficile/iniaeinfections. However these studies indicated that antibody responses in protected fish were short lived (3-4 months). Thus available vaccines were useful for short-term protection only. To address the issues of regulation of pathogenesis and immunogens of S. iniae, we have emphasized the role of the innate immune response regarding activation of NCC and mechanisms of invasiveness. Considerable progress was made toward accomplishing SA #1. We have cloned the cDNA of the following tilapia genes: cellular apoptosis susceptibility (CAS/AF547173»; tumor necrosis factor alpha (TNF / A Y 428948); and nascent polypeptide-associated complex alpha polypeptide (NACA/ A Y168640). Similar attempts were made to sequence the tilapia FasLgene/cDNA, however these experiments were not successful. Aim #2 was to "Identify Regulatory Factors that Control NCC Responses to S. iniae." To accomplish this, a new membrane receptor has been identified that may control innate responses (including apoptosis) of NCC to S. iniae. The receptor is a membrane protein on teleost NCC. This protein (NCC cationic antimicrobial protein-1/ncamp-1/AAQ99138) has been sequenced and the cDNA cloned (A Y324398). In recombinant form, ncamp-l kills S. iniae in vitro. Specific aim 3 ("Characterize the Biological Properties of the S.iniae Capsular Polysaccharide") utilized an in- vitro model using rainbow trout primary skin epithelial cell mono layers. These experiments demonstrated colonization into epithelial cells followed by a rapid decline of viable intracellular bacteria and translocation out of the cell. This pathogenesis model suggested that the bacterium escapes the endosome and translocates through the rainbow trout skin barrier to further invade and infect the host. Specific aim #4 ("Development of an Acellular Vaccine") was not specifically addressed. These studies demonstrated that several different apoptotic regulatory genes/proteins are expressed by tilapia NCC. These are the first studies demonstrating that such factors exist in tilapia. Because tilapia NCC bind to and are activated by S. iniae bacterial DNA, we predict that the apoptotic regulatory activity of S. iniae previously demonstrated by our group may be associated with innate antibacterial responses in tilapia.
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