Relevant bibliographies by topics / Triggering receptor

Academic literature on the topic 'Triggering receptor'

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Published: 11 March 2023

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Journal articles on the topic "Triggering receptor"

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Weiss, R. "Allergy-Triggering Receptor Made en masse." Science News 135, no. 16 (April 22, 1989): 246. http://dx.doi.org/10.2307/3973558.

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Ma, Zhengyu, and Terri H. Finkel. "T cell receptor triggering by force." Trends in Immunology 31, no. 1 (January 2010): 1–6. http://dx.doi.org/10.1016/j.it.2009.09.008.

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van der Merwe, P. Anton, and Omer Dushek. "Mechanisms for T cell receptor triggering." Nature Reviews Immunology 11, no. 1 (December 3, 2010): 47–55. http://dx.doi.org/10.1038/nri2887.

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Zhai, Qian, Feng Li, Xiyao Chen, Ji Jia, Sisi Sun, Dandan Zhou, Lei Ma, et al. "Triggering Receptor Expressed on Myeloid Cells 2, a Novel Regulator of Immunocyte Phenotypes, Confers Neuroprotection by Relieving Neuroinflammation." Anesthesiology 127, no. 1 (July 1, 2017): 98–110. http://dx.doi.org/10.1097/aln.0000000000001628.

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Abstract Background Microglia can not only detrimentally augment secondary injury but also potentially promote recovery. However, the mechanism underlying the regulation of microglial phenotypes after stroke remains unclear. Methods Mice were subjected to middle cerebral artery occlusion for 60 min. At 3 days after reperfusion, the effects of activation and suppression of triggering receptor expressed on myeloid cells 2 on immunocyte phenotypes (n = 5), neurobehavioral scores (n = 7), infarct volumes (n = 8), and neuronal apoptosis (n = 7) were analyzed. In vitro, cultured microglia were exposed to oxygen–glucose deprivation for 4 h. Inflammatory cytokines, cellular viability (n = 8), neuronal apoptosis (n = 7), and triggering receptor expressed on myeloid cells 2 expression (n = 5) were evaluated in the presence or absence of triggering receptor expressed on myeloid cell-specific small interfering RNA or triggering receptor expressed on myeloid cells 2 overexpression lentivirus. Results Triggering receptor expressed on myeloid cells 2 expression in the ischemic penumbra peaked at 3 days after ischemia–reperfusion injury (4.4 ± 0.1-fold, P = 0.0004) and was enhanced in interleukin-4/interleukin-13–treated microglia in vitro (1.7 ± 0.2-fold, P = 0.0119). After oxygen–glucose deprivation, triggering receptor expressed on myeloid cells 2 conferred neuroprotection by regulating the phenotypic conversion of microglia and inflammatory cytokine release. Intraperitoneal administration of triggering receptor expressed on myeloid cells 2 agonist heat shock protein 60 or unilateral delivery of a recombinant triggering receptor expressed on myeloid cells 2 lentivirus into the cerebral ventricle induced a significant neuroprotective effect in mice (apoptotic neurons decreased to 31.3 ± 7.6%; infarct volume decreased to 44.9 ± 5.3%). All values are presented as the mean ± SD. Conclusions Activation or up-regulation of triggering receptor expressed on myeloid cells 2 promoted the phenotypic conversion of microglia and decreased the number of apoptotic neurons. Our study suggests that triggering receptor expressed on myeloid cells 2 is a novel regulator of microglial phenotypes and may be a potential therapeutic target for stroke.
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Menon, A. K., D. Holowka, W. W. Webb, and B. Baird. "Clustering, mobility, and triggering activity of small oligomers of immunoglobulin E on rat basophilic leukemia cells." Journal of Cell Biology 102, no. 2 (February 1, 1986): 534–40. http://dx.doi.org/10.1083/jcb.102.2.534.

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We have recently shown that small oligomers of IgE bound to univalent receptors for IgE on the surface of rat basophilic leukemia cells induce extensive aggregation of the receptors at 4 degrees C into patches resolvable by fluorescence microscopy and that this does not occur with monomeric IgE (Menon, A. K., D. Holowka, and B. Baird, 1984, J. Cell Biol. 98:577-583). Here we use fluorescence photobleaching recovery measurements to show that receptor oligomerization by this means is accompanied by a dramatic reduction of receptor lateral mobility, and that this immobilization occurs even when the clustering is not microscopically detectable. Furthermore, the degree of immobility induced by a particular oligomer fraction from a gel filtration column correlates positively with its ability to trigger cellular degranulation, whereas receptors labeled with monomeric IgE have no triggering activity and exhibit typical membrane protein mobility. The slow, large-scale oligomer-induced clustering appears to be a long term consequence of earlier selective interactions that result in receptor immobilization, and this highly clustered state provides a competent, noninhibitory triggering signal resulting in cellular degranulation upon warming to 37 degrees C. We conclude that even limited clustering of IgE receptors on rat basophilic leukemia cells induces interactions with other cellular components that constrain receptor mobility and eventually cause massive coalescence of the clusters. These primary selective interactions occurring at the level of receptor oligomers or small clusters of oligomers that result in immobilization may play a role in triggering cellular degranulation.
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Dalpke, Alexander, and Klaus Heeg. "Signal Integration Following Toll-like Receptor Triggering." Critical Reviews™ in Immunology 22, no. 3 (2002): 34. http://dx.doi.org/10.1615/critrevimmunol.v22.i3.40.

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Xu, Xinyi, Hua Li, and Chenqi Xu. "Structural understanding of T cell receptor triggering." Cellular & Molecular Immunology 17, no. 3 (February 11, 2020): 193–202. http://dx.doi.org/10.1038/s41423-020-0367-1.

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Davis, Simon J., and P. Anton van der Merwe. "TCR triggering: co-receptor-dependent or -independent?" Trends in Immunology 24, no. 12 (December 2003): 624–26. http://dx.doi.org/10.1016/j.it.2003.10.009.

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Pazin, Michael J., and Lewis T. Williams. "Triggering signaling cascades by receptor tyrosine kinases." Trends in Biochemical Sciences 17, no. 10 (October 1992): 374–78. http://dx.doi.org/10.1016/0968-0004(92)90003-r.

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Ma, Zhengyu, Paul A. Janmey, and Terri H. Finkel. "The receptor deformation model of TCR triggering." FASEB Journal 22, no. 4 (November 5, 2007): 1002–8. http://dx.doi.org/10.1096/fj.07-9331hyp.

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Dissertations / Theses on the topic "Triggering receptor"

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Fernandes, Ricardo A. "Controls on T-cell receptor phosphorylation and triggering." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:f0933a44-e1d6-4941-a541-c0cf903532ca.

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An effective immune response in mammalian cells relies on a network of molecular interactions to detect and respond to pathogens. The T-cell receptor (TCR) is one of the most important components of this system responsible for the outcome of the immunological response. Paramount to its role is its ability to efficiently signal a productive interaction with a peptide embedded in an MHC molecule. Important aspects of TCR structure and organization are unknown, limiting the current understanding of this process and rendering it highly controversial. The work described in this thesis seeks to define the valency, structural organization and signalling properties of the TCR in order to provide a better framework for thinking about the receptor-triggering problem. The results suggest that a largely monovalent complex diffuses at the surface of T cells, which is able to trigger intracellular signalling in the absence of large structural rearrangements of the extracellular subunits of the TCR. Moreover, a recently proposed mechanism involving conformational rearrangements of the cytoplasmic domains of the complex is shown to fail to explain the regulation of TCR phosphorylation. Steps are also taken toward investigating the role of more subtle conformational rearrangements at atomic resolution. Finally, an investigation of what controls tyrosine phosphorylation of the receptor in resting T lymphocytes led to the development of new approaches to address the role of specific phosphatases. The outcome of this analysis suggested how a finely-tuned balance between kinase and phosphatase activity, at both global and local levels, regulates TCR phosphorylation and T-cell activation.
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Mackus, Wendelina Johanna Maria. "Antigen receptor triggering and apoptotic pathways in neoplastic B cells." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/67206.

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Holst, Rutger van der. "TRAPC : a novel triggering receptor expressed on antigen presenting cells /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-427-3/.

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Denham, Eleanor Mary. "Investigating the mechanism of non-catalytic tyrosine-phosphorylated receptor triggering." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:8cbd8043-d02d-4294-ace9-a2e92670aa63.

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Non-catalytic tyrosine-phosphorylated receptors (NTRs) are a large group of leukocyte receptors that bind to surface-associated ligands and include both activating and inhibitory members. They contain, or associate with adaptor molecules which contain, tyrosine residues within conserved cytoplasmic motifs that are phosphorylated and dephosphorylated by extrinsic kinases and phosphatases respectively. The mechanism by which NTR-ligand engagement leads to sustained phosphorylation of receptor tyrosinebased motifs and initiation of downstream signalling (termed "receptor triggering"), is as yet unknown. Our hypothesis is that the NTRs signal using the kinetic-segregation (KS) model. The model proposes that large inhibitory phosphatases, but not inner leaflet-bound activating kinases, are segregated in a size-dependent manner from engaged receptors upon ligand binding. This favours kinase activity and drives sustained receptor phosphorylation. To systematically test whether predictions of the KS model hold for all NTRs, we have developed an artificial generic ligand system in which biophysical and biochemical properties of NTR-ligand interactions can be manipulated. These include NTR-ligand dimensions, ligand densities and valency. Our system exploits the interaction between a Strep-Tag II, which is attached to the ectodomain of the NTR, and StrepTactin protein. We first demonstrate that representative NTRs, both activating and inhibitory, can be triggered through ligation of this Strep-Tag II. In agreement with a key KS model prediction, we next show that only ligation by surface-associated ligand leads to triggering, whilst ligation by soluble ligand does not. Additionally, by altering ligand valency and mobility, we provide evidence that receptor clustering can enhance activation. Also in agreement with the KS model, we show that elongation of the artificial ligand dramatically affects activation of a representative NTR. Finally, we provide evidence to suggest that increased receptor clustering may be able to compensate for ligand elongation-mediated defects in NTR signalling. The flexibility of this system will allow us to analyse other NTRs, test further predictions of the model, and investigate the role of other properties of NTR signalling.
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Gibot, Sébastien. "Triggering receptor expressed on myeloid cells-1 : implications diagnostiques et thérapeutiques au cours du sepsis." Nancy 1, 2004. http://www.theses.fr/2004NAN11307.

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Au cours du sepsis, l'expression membranaire du Triggering Receptor Expressed on myeloid cells (TREM)-1 ainsi que la production de sa forme soluble (sTREM-1) sont fortement majorées tant chez la souris que chez l'homme. Ces phénomènes dépendent de la présence de ligands bactériens, ne sont pas reliés à la production de TNF-alpha et découlent d'un mécanisme impliquant P13K. STREM atténue la production de cytokines chez la souris. La modulation de la voie de TREM-1 réduit mais sans totalement l'inhiber la production de cytokines et protège l'animal du décès. L'utilisation d'un peptide modulateur pourrait constituer une thérapeutique intéressante.
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Dräger, Sören [Verfasser]. "Die Funktion des Triggering receptor expressed on myeloid cells-1 bei entzündlichen Hauterkrankungen / Sören Dräger." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2019. http://d-nb.info/1191803813/34.

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Lee, Jinju. "IL-23 generates pathogenic Th17 cells by triggering T cell-intrinsic prostaglandin E2-EP2/4 signaling." Kyoto University, 2018. http://hdl.handle.net/2433/235123.

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Sandalova, Elena. "Regulation of the pro-apoptotic protein bim by T cell receptor triggering in human T cells /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-041-1/.

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Wunderlich, Patrick [Verfasser]. "gamma-Secretase mediated proteolytic processing of the triggering receptor expressed on myeloid cells-2 : functional implications for intracellular signaling / Patrick Wunderlich." Bonn : Universitäts- und Landesbibliothek Bonn, 2011. http://d-nb.info/1043910999/34.

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Bremen, Tobias van [Verfasser]. "Die Rolle von Trem-1 (Triggering receptor expressed on myeloid cells-1) als Mustererkennungsrezeptor bei der humanen Escherichia coli Sepsis / Tobias van Bremen." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2012. http://d-nb.info/102756755X/34.

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Books on the topic "Triggering receptor"

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Garratt, Alistair Neil. Integrin adhesion receptor triggering by the extracellular matrix and anti-integrin antibodies. Manchester: University of Manchester, 1995.

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Zanzinger, Kai Uwe. Expression and signalling of triggering receptor expressed on myeloid cells (TREM)-1. 2008.

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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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Book chapters on the topic "Triggering receptor"

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Shabani, Samaneh H., and Azam Bolhassani. "Role of ROS in Triggering Death Receptor-Mediated Apoptosis." In Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, 1–18. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-4501-6_43-1.

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Shabani, Samaneh H., and Azam Bolhassani. "Role of ROS in Triggering Death Receptor-Mediated Apoptosis." In Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, 517–34. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-15-9411-3_43.

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Coombs, Daniel, Omer Dushek, and P. Anton van der Merwe. "A Review of Mathematical Models for T Cell Receptor Triggering and Antigen Discrimination." In Mathematical Models and Immune Cell Biology, 25–45. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-7725-0_2.

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DeFranco, Anthony L., Paul R. Mittelstadt, Jonathan H. Blum, Tracy L. Stevens, Debbie A. Law, Vivien W. F. Chan, Shaun P. Foy, Sandip K. Datta, and Linda Matsuuchi. "Mechanism of B Cell Antigen Receptor Function: Transmembrane Signaling and Triggering of Apoptosis." In Advances in Experimental Medicine and Biology, 9–22. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-0987-9_2.

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Neagu, Monica, and Carolina Constantin. "Signal Transduction in Immune Cells and Protein Kinases." In Advances in Experimental Medicine and Biology, 133–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49844-3_5.

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AbstractImmune response relies upon several intracellular signaling events. Among the protein kinases involved in these pathways, members of the protein kinase C (PKC) family are prominent molecules because they have the capacity to acutely and reversibly modulate effector protein functions, controlling both spatial distribution and dynamic properties of the signals. Different PKC isoforms are involved in distinct signaling pathways, with selective functions in a cell-specific manner.In innate system, Toll-like receptor signaling is the main molecular event triggering effector functions. Various isoforms of PKC can be common to different TLRs, while some of them are specific for a certain type of TLR. Protein kinases involvement in innate immune cells are presented within the chapter emphasizing their coordination in many aspects of immune cell function and, as important players in immune regulation.In adaptive immunity T-cell receptor and B-cell receptor signaling are the main intracellular pathways involved in seminal immune specific cellular events. Activation through TCR and BCR can have common intracellular pathways while others can be specific for the type of receptor involved or for the specific function triggered. Various PKC isoforms involvement in TCR and BCR Intracellular signaling will be presented as positive and negative regulators of the immune response events triggered in adaptive immunity.
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Schiechl, G., H. J. Schlitt, E. K. Geissler, and S. Fichtner-Feigl. "Triggering receptor expressed on myeloid cells 1 (Trem-1) als Zielstruktur zur Verlängerung des Transplantatüberlebens bei murinen Herztransplantationen." In Chirurgisches Forum und DGAV Forum 2010, 157–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12192-0_61.

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Tamir, Idan, and Israel Pecht. "Antigen Receptors Clustering; Mobility, Size and Configurational Requirements for Effective Cellular Triggering." In Progress in Immunology Vol. VIII, 221–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_29.

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Bockaert, J., J. P. Pin, K. Oomagari, M. Sebben, and A. Dumuis. "Triggering of Arachidonic Acid Release from Mature Striatal Neurons by Associative Stimulation of Ionotropic (AMPA) and Quisqualate Receptors Coupled to Phospholipase C (Qp)." In Research and Perspectives in Neurosciences, 30–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-84526-0_3.

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Alarcón, B., and H. M. van Santen. "T Cell Receptor Triggering." In Encyclopedia of Cell Biology, 650–59. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-394447-4.30097-9.

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Alarcón, Balbino, and Wolfgang W. Schamel. "T Cell Receptor Triggering." In Reference Module in Life Sciences. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-12-821618-7.00202-9.

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Conference papers on the topic "Triggering receptor"

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Shafazand, S., S. Alazemi, E. Vadia, E. Manning, D. Fertel, and S. Pham. "Soluble Triggering Receptor Expressed on Myeloid Cells and the Diagnosis of Pneumonia in Lung Transplant Patients." 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.a4620.

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Lin, V., D. D. Xing, Y. Wu, S. Hardy, P. R. Cochran, E. S. Helton, S. V. Pamboukian, et al. "Elucidating the Role of Triggering Receptor Expressed on Myeloid Cells-1 (TREM-1) in Pulmonary Hypertension." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1176.

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Pullikuth, Ashok K., Julia Chifman, Eric D. Routh, Jeff Chou, Guangxu Jin, Michael A. Black, and Lance D. Miller. "Abstract 3791: Triggering receptor expressed in myeloid cells 1 (TREM1) is a predictive marker for breast cancer therapeutics." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3791.

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Proklou, Athanasia, Giorgos Pitsidianakis, Eliza Tsitoura, Chara Koutoulaki, Argyro Hatziantoniou, Despoina Moraitaki, Dimitrios Georgopoulos, Katerina Antoniou, and Nikos Tzanakis. "Triggering receptor expressed on myeloid cells (TREM1): A novel biomarker in the investigation of non-CF bronchiectasis? Preliminary results." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa910.

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Lin, C., C. Ho, M. Yao, S. Hsu, and C. Yu. "sTREM-1 (Soluble Triggering Receptor Expressed on Myeloid Cells-1) as Marker Indicating Infection in Patients with Neutropenic Fever." 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.a4704.

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Molad, Y., Y. Edel, E. Pokroy-Shapira, S. Oren, A. Dortort, Y. Pri-Paz Basson, T. Shochat, and V. Kliminski. "S3D:5 Plasma soluble triggering receptor expressed on myeloid cells-1 is elevated in patients with thrombotic primary antiphospholipid syndrome." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.16.

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Jeremic, I., N. Stojanovic, Z. Stanojevic, B. Jovanovic, J. Tosic, S. Vidicevic, and A. Isakovic. "AB0582 Soluble triggering receptor expressed on myeloid cells-1 (STREM-1) and adrenomedulin are elevated in patients with systemic lupus erythematosus." 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.6570.

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Rowland, Leah K., Lancelot S. McLean, Petreena Campbell, Cheri N. Watkins, Dain Zylstra, Louisa H. Amis, Maheswari Senthil, and Eileen Brantley. "Abstract 2565: Aryl hydrocarbon receptor agonist 5F 203 induces oxidative stress triggering DNA damage and cytoglobin up-regulation in human breast cancer cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2565.

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Luckett, PM, R. Anand, A. Mejias, C. Tagliabue, C. Techasaensiri, and RD Hardy. "Soluble Triggering Receptor Expressed in Myeloid Cells-1 (sTREM-1) in Bronchoalveolar Lavage Fluid (BALF) of Mice FollowingRespiratory Syncytial Virus(RSV),Mycoplasma pneumoniae, andStreptococcus pneumoniaeInfection." 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.a2593.

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Lai, Chao-Yang, Hsin-Hung Lin, Alice L. Yu, Huan-Chieh Cho, Shu-Hwa Chen, Kuo-I. Lin, Wen-Bin Yang, Yi-Kai Chiu, and John Yu. "Abstract 316: Triggering receptor expressed on myeloid cell-like transcript 2 (TLT-2) and TLR-4 contribute to activation of human dendritic cells via ERK signaling pathway." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-316.

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Reports on the topic "Triggering receptor"

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Boisclair, Yves R., and Arieh Gertler. Development and Use of Leptin Receptor Antagonists to Increase Appetite and Adaptive Metabolism in Ruminants. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7697120.bard.

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Abstract:
Objectives The original project had 2 major objectives: (1) To determine the effects of centrally administered leptin antagonist on appetite and adaptive metabolism in the sheep; (2) To develop and prepare second-generation leptin antagonists combining high binding affinity and prolonged in vivo half-life. Background Periods of suboptimal nutrition or exaggerated metabolic activity demands lead to a state of chronic energy insufficiency. Ruminants remain productive for a surprisingly long period of time under these circumstances by evoking adaptations sparing available energy and nutrients. The mechanism driving these adaptations in ruminant remains unknown, but could involve a reduction in plasma leptin, a hormone acting predominantly in the brain. In laboratory animals, reduced leptin signaling promotes survival during nutritional insufficiency by triggering energy sparing adaptations such as reduced thyroid hormone production and insulin resistance. Our overall hypothesis is that similar adaptations are triggered by reduced leptin signaling in the brain of ruminants. Testing of this hypothesis in ruminants has not been possible due to inability to block the actions of endogenous leptin and access to ruminant models where leptin antagonistic therapy is feasible and effective. Major achievements and conclusions The Israeli team had previously mutated 3 residues in ovine leptin, with no effect on receptor binding. This mutant was renamed ovine leptin antagonist (OLA) because it cannot activate signaling and therefore antagonizes the ability of wild type leptin to activate its receptor. To transform OLA into an effective in vivo antagonist, the Israeli made 2 important technical advances. First, it incorporated an additional mutation into OLA, increasing its binding affinity and thus transforming it into a super ovine leptin antagonist (SOLA). Second, the Israeli team developed a method whereby polyethylene glycol is covalently attached to SOLA (PEG-SOLA) with the goal of extending its half-life in vivo. The US team used OLA and PEG-SOLA in 2 separate animal models. First, OLA was chronically administered directly into the brain of mature sheep via a cannula implanted into the 3rdcerebroventricule. Unexpectedly, OLA had no effect of voluntary feed intake or various indicators of peripheral insulin action but reduced the plasma concentration of thyroid hormones. Second, the US team tested the effect of peripheral PEG-SOLA administration in an energy sensitive, rapidly growing lamb model. PEG-SOLA was administered for 14 consecutive days after birth or for 5 consecutive days before sacrifice on day 40 of life. Plasma PEG-SOLA had a half-life of over 16 h and circulated in 225- to 288-fold excess over endogenous leptin. PEG-SOLA administration reduced plasma thyroid hormones and resulted in a higher fat content in the carcass at slaughter, but had no effects on feed intake, body weight, plasma glucose or insulin. These results show that the team succeeded in developing a leptin antagonist with a long in vivo half-life. Moreover, in vivo results show that reduced leptin signaling promotes energy sparing in ruminants by repressing thyroid hormone production. Scientific and agricultural implications The physiological role of leptin in ruminants has been difficult to resolve because peripheral administration of wild type leptin causes little effects. Our work with leptin antagonists show for the first time in ruminants that reduced leptin signaling induces energy sparing mechanisms involving thyroid hormone production with little effect on peripheral insulin action. Additional work is needed to develop even more potent leptin antagonists, to establish optimal administration protocols and to narrow down phases of the ruminant life cycle when their use will improve productivity.
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