Academic literature on the topic 'Complement-like pathway'
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Journal articles on the topic "Complement-like pathway"
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Blandin, Stéphanie A., Eric Marois, and Elena A. Levashina. "Antimalarial Responses in Anopheles gambiae: From a Complement-like Protein to a Complement-like Pathway." Cell Host & Microbe 3, no. 6 (June 2008): 364–74. http://dx.doi.org/10.1016/j.chom.2008.05.007.
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Delvaeye, Mieke, Astrid DeVriese, Michael Moons, Naomi Esmon, Charles Esmon, and Edward M. Conway. "Regulation of Complement Activation by Thrombomodulin." Blood 114, no. 22 (November 20, 2009): 5127. http://dx.doi.org/10.1182/blood.v114.22.5127.5127.
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Abstract Abstract 5127 Thrombomodulin (TM) is an integral membrane glycoprotein, ubiquitously expressed by vascular endothelial cells. Its epidermal growth factor (EGF)-like repeats amplify thrombin-mediated generation of activated protein C and activated thrombin activatable fibrinolysis inhibitor, thereby suppressing coagulation, inflammation and fibrinolysis, and inactivating the anaphylatoxins, C3a and C5a. TM also has direct anti-inflammatory properties, interfering with leukocyte adhesion, and preventing complement activation via its lectin-like domain. We recently established that TM is a physiologically important negative regulator of the alternative pathway (AP) of complement activation, defects of which increase the risk of the thrombotic microangiopathy, atypical hemolytic uremic syndrome. In this report, we assessed the role of TM in the other complement activation pathways. In serum, TM interferes with classical pathway (CP) mediated erythrocyte cell lysis, and protects against CP-induced cell death. TM co-precipitates with C4b, and enhances its inactivation and cleavage to C4c and C4d by complement factor I in the presence of the cofactor C4b binding protein. TM also interferes with the coagulation complement pathway by interfering with thrombin cleavage and activation of C5 to C5a. Overall, TM negatively regulates complement via the major recognized pathways. The findings implicate defects in TM in a wide range of diseases in which complement plays a role, and underlines the potential of TM as a therapeutic target. Disclosures No relevant conflicts of interest to declare.
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Zhang, Kang, Jingyan Zhang, Lei Wang, Qiang Liang, Yuhui Niu, Linlin Gu, Yanming We, and Jianxi Li. "Integrative Transcriptomics and Proteomics Analysis Reveals Immune Response Process in Bovine Viral Diarrhea Virus-1-Infected Peripheral Blood Mononuclear Cells." Veterinary Sciences 10, no. 10 (September 28, 2023): 596. http://dx.doi.org/10.3390/vetsci10100596.
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Bovine viral diarrhea virus (BVDV) causes bovine viral diarrhea-mucosal disease, inflicting substantial economic losses upon the global cattle industry. Peripheral blood mononuclear cells (PBMCs) are the central hub for immune responses during host-virus infection and have been recognized as crucial targets for BVDV infection. In order to elucidate the dynamics of host-BVDV-1 interaction, this study harnessed RNA-seq and iTRAQ methods to acquire an extensive dataset of transcriptomics and proteomics data from samples of BVDV-1-infected PBMCs at the 12-h post-infection mark. When compared to mock-infected PBMCs, we identified 344 differentially expressed genes (DEGs: a total of 234 genes with downregulated expression and 110 genes with upregulated expression) and 446 differentially expressed proteins (DEPs: a total of 224 proteins with downregulated expression and 222 proteins with upregulated expression). Selected DEGs and DEPs were validated through quantitative reverse transcriptase-polymerase chain reaction and parallel reaction monitoring. Gene ontology annotation and KEGG enrichment analysis underscored the significant enrichment of DEGs and DEPs in various immunity-related signaling pathways, including antigen processing and presentation, complement and coagulation cascades, cytokine-cytokine receptor interaction, and the NOD-like receptor signaling pathway, among others. Further analysis unveiled that those DEGs and DEPs with downregulated expression were predominantly associated with pathways such as complement and coagulation cascades, the interleukin-17 signaling pathway, cytokine-cytokine receptor interaction, the PI3K-Akt signaling pathway, the tumor necrosis factor signaling pathway, and the NOD-like receptor signaling pathway. Conversely, upregulated DEGs and DEPs were chiefly linked to metabolic pathways, oxidative phosphorylation, complement and coagulation cascades, and the RIG-I-like receptor signaling pathway. These altered genes and proteins shed light on the intense host-virus conflict within the immune realm. Our transcriptomics and proteomics data constitute a significant foundation for delving further into the interaction mechanism between BVDV and its host.
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Kim, Sook Young, Sang Eun Lee, Man Sup Kwak, and Jeon-Soo Shin. "Regulatory Role of HMGB1 on complement activation via the classical pathway (169.3)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 169.3. http://dx.doi.org/10.4049/jimmunol.188.supp.169.3.
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Abstract Serum complement proteins play an important role in resistance to infection. The complement system is strongly activated in sepsis and the complement-activated products of anaphylatoxins have biological activities leading to inflammation. The nuclear protein, high mobility group box 1 protein (HMGB1) is released by inflammatory stimuli and plays a key role as a pro-inflammatory cytokine-like molecule. To investigate whether HMGB1 can induce complement activation, we have looked at the relationship between HMGB1 and complement system in this study. We first demonstrated the involvement of HMGB1 in binding to C1q for classical pathway activation. We observed the activation of complement cascade components such as C4b, C3b, C3c, and the membrane attack complex after C1q activation by HMGB1 in a dose-dependent manner. Moreover, complement activation could be observed in serum from mice after the intravenous injection of HMGB1. We then investigated the involvement of the A and B domain of HMGB1 during complement activation. HMGB1 B box, a well-known pro-inflammatory domain, was able to activate the complement system like wild type HMGB1, while HMGB1 A box showed no activation. The possible role of HMGB1 A box as an inhibitory domain in complement activation is now under investigation. In conclusion, the classical pathway of complement activation could be activated by the interaction of HMGB1 and C1q, showing the novel role of HMGB1 in the pathogenesis of HMGB1-induced shock.
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De Marco Verissimo, Carolina, Heather L. Jewhurst, József Dobó, Péter Gál, John P. Dalton, and Krystyna Cwiklinski. "Fasciola hepatica is refractory to complement killing by preventing attachment of mannose binding lectin (MBL) and inhibiting MBL-associated serine proteases (MASPs) with serpins." PLOS Pathogens 18, no. 1 (January 10, 2022): e1010226. http://dx.doi.org/10.1371/journal.ppat.1010226.
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The complement system is a first-line innate host immune defence against invading pathogens. It is activated via three pathways, termed Classical, Lectin and Alternative, which are mediated by antibodies, carbohydrate arrays or microbial liposaccharides, respectively. The three complement pathways converge in the formation of C3-convertase followed by the assembly of a lethal pore-like structure, the membrane attack complex (MAC), on the pathogen surface. We found that the infectious stage of the helminth parasite Fasciola hepatica, the newly excysted juvenile (NEJ), is resistant to the damaging effects of complement. Despite being coated with mannosylated proteins, the main initiator of the Lectin pathway, the mannose binding lectin (MBL), does not bind to the surface of live NEJ. In addition, we found that recombinantly expressed serine protease inhibitors secreted by NEJ (rFhSrp1 and rFhSrp2) selectively prevent activation of the complement via the Lectin pathway. Our experiments demonstrate that rFhSrp1 and rFhSrp2 inhibit native and recombinant MBL-associated serine proteases (MASPs), impairing the primary step that mediates C3b and C4b deposition on the NEJ surface. Indeed, immunofluorescence studies show that MBL, C3b, C4b or MAC are not deposited on the surface of NEJ incubated in normal human serum. Taken together, our findings uncover new means by which a helminth parasite prevents the activation of the Lectin complement pathway to become refractory to killing via this host response, in spite of presenting an assortment of glycans on their surface.
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Irmscher, Sarah, Nadia Döring, Luke D. Halder, Emeraldo A. H. Jo, Isabell Kopka, Christine Dunker, Ilse D. Jacobsen, et al. "Kallikrein Cleaves C3 and Activates Complement." Journal of Innate Immunity 10, no. 2 (December 14, 2017): 94–105. http://dx.doi.org/10.1159/000484257.
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The human plasma contact system is an immune surveillance system activated by the negatively charged surfaces of bacteria and fungi and includes the kallikrein-kinin, the coagulation, and the fibrinolytic systems. Previous work shows that the contact system also activates complement, and that plasma enzymes like kallikrein, plasmin, thrombin, and FXII are involved in the activation process. Here, we show for the first time that kallikrein cleaves the central complement component C3 directly to yield active components C3b and C3a. The cleavage site within C3 is identical to that recognized by the C3 convertase. Also, kallikrein-generated C3b forms C3 convertases, which trigger the C3 amplification loop. Since kallikrein also cleaves factor B to yield Bb and Ba, kallikrein alone can trigger complement activation. Kallikrein-generated C3 convertases are inhibited by factor H; thus, the kallikrein activation pathway merges with the amplification loop of the alternative pathway. Taken together, these data suggest that activation of the contact system locally enhances complement activation on cell surfaces. The human pathogenic microbe Candida albicans activates the contact system in normal human serum. However, C. albicans immediately recruits factor H to the surface, thereby evading the alternative and likely kallikrein-mediated complement pathways.
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Koethe, S. M., K. E. Nelson, and C. G. Becker. "Activation of the classical pathway of complement by tobacco glycoprotein (TGP)." Journal of Immunology 155, no. 2 (July 15, 1995): 826–35. http://dx.doi.org/10.4049/jimmunol.155.2.826.
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Abstract Tobacco glycoprotein (TGP), a polyphenol-rich glycoprotein isolated from tobacco leaves, activates the classical complement pathway through a mechanism that appears to involve direct interaction with C1q. A binding site on C1q for TGP can be localized by competitive inhibition with DNA to a region located in the junction between the collagen-like and globular regions of the molecule. A protein with activity similar to TGP has also been isolated from cigarette smoke condensate (TGP-S); it shares a binding site on C1q with TGP and has similar functional activity, with the exception that complement activation does not proceed to formation of a C3 cleaving enzyme. The ability of TGP and TGP-S to activate complement can be partially duplicated using polyphenols associated with tobacco leaf and smoke, i.e., chlorogenic acid and rutin. These polyphenols also compete with TGP for a binding site on immobilized C1q, suggesting that the polyphenol portion of TGP is critical for activation of complement. These results provide an additional mechanism for complement activation by cigarette products that, in vivo, could result in a localized complement depletion, generation of biologically active complement cleavage products, and initiation of an inflammatory response.
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Lee, Garam, Yonghyan Nam, Manu Shivakumar, Apoorva Joshi, Weixuan Fu, Rebecca Anne Simmons, Paul Wang, Dokyoon Kim, and Sara Elizabeth Pinney. "A Novel Graph Based Semi-Supervised Learning Approach to Identify Pathways Contributing to the Development of Diabetes and Obesity." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A656—A657. http://dx.doi.org/10.1210/jendso/bvab048.1339.
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Abstract Background: Gestational diabetes (GDM) has profound effects on the intrauterine metabolic milieu, induces marked abnormalities in fetal glucose and insulin secretion and is linked to obesity and diabetes in the offspring, but the mechanisms remain largely unknown. Epigenetic modifications in stems cells may be one mechanism by which an in utero exposure can lead to the development of diabetes and obesity later in life. Objective: To identify novel pathways contributing to the development of diabetes and obesity in offspring exposed to GDM in utero by integrating data generated from transcriptome and methylome analysis from second trimester human amniocytes exposed to GDM in utero. Methods: We analyzed RNAseq and genome wide DNA methylation data (ERRBS) generated from second trimester amniocytes obtained from women with GDM (n=14). Amniocytes have stem cells-like characteristics and are derived from the fetus. Expression data of 22,271 genes were retrieved from RNAseq data. CpGs with significant changes in DNA methylation were mapped into 20,028 genes by collapsing methylation probes into promoter and gene regions. To better understand the associations among diverse gene sets or among gene sets and GDM,we first constructed two weighted co-expression networks from RNAseq and DNA methylation data, respectively. Then, two co-expression networks were integrated using a linear combination. With the integrated co-expression network, graph-based label propagation algorithm was employed to prioritize GDM-associated genes. Results: From the differential expression analysis between GDM and control, the top 20 query genes, including 11 genes and 9 methylated genes, were selected for label propagation. Finally, the top 100 genes were picked up for the pathway enrichment testusing an over-representation analysis approach. Significantly enriched pathways included: Interferon Signaling, N-glycan Antennae Elongation, Sphingolipid Pathway and Metabolism, Classical Complement Pathway, Complement and Coagulation Cascades, Tryptophan Metabolism, Peroxisomal Protein Import, Unsaturated Fatty Acid Metabolism, Complement Activation, Human Innate Immune Response, Ceramide Metabolism, Fertilization Pathway, Keratan Sulfate Biosynthesis Pathway, Transport to the Golgi and Modification Pathway (FDR q<0.05 for all pathways). Conclusion: Using a novel bioinformatic approach to synthesize transcriptome and methylome data derived from human amniocytes exposed to GDM in utero, we identified potential pathways involved in programming of diabetes and obesity in offspring including pathways involving the immune response, complex lipid metabolism, the complement pathway, and protein transport and processing. Further investigation of these pathways may yield new mechanisms contributing to diabetes and obesity.
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Györffy, Balázs A., Judit Kun, György Török, Éva Bulyáki, Zsolt Borhegyi, Péter Gulyássy, Viktor Kis, et al. "Local apoptotic-like mechanisms underlie complement-mediated synaptic pruning." Proceedings of the National Academy of Sciences 115, no. 24 (May 29, 2018): 6303–8. http://dx.doi.org/10.1073/pnas.1722613115.
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C1q, a member of the immune complement cascade, is implicated in the selective pruning of synapses by microglial phagocytosis. C1q-mediated synapse elimination has been shown to occur during brain development, while increased activation and complement-dependent synapse loss is observed in neurodegenerative diseases. However, the molecular mechanisms underlying C1q-controlled synaptic pruning are mostly unknown. This study addresses distortions in the synaptic proteome leading to C1q-tagged synapses. Our data demonstrated the preferential localization of C1q to the presynapse. Proteomic investigation and pathway analysis of C1q-tagged synaptosomes revealed the presence of apoptotic-like processes in C1q-tagged synapses, which was confirmed experimentally with apoptosis markers. Moreover, the induction of synaptic apoptotic-like mechanisms in a model of sensory deprivation-induced synaptic depression led to elevated C1q levels. Our results unveiled that C1q label-based synaptic pruning is triggered by and directly linked to apoptotic-like processes in the synaptic compartment.
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Staels, F., W. Meersseman, P. Stordeur, K. Willekens, S. Van Loo, A. Corveleyn, I. Meyts, G. Meyfroidt, and R. Schrijvers. "Terminal Complement Pathway Deficiency in an Adult Patient with Meningococcal Sepsis." Case Reports in Immunology 2022 (May 23, 2022): 1–6. http://dx.doi.org/10.1155/2022/9057000.
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The complement system is an essential part of our innate immune system. Three enzymatic activation pathways are described, all converging into a common terminal pathway which causes lysis of the target cell. Late complement deficiencies (LCDs) are typically diagnosed in children or adolescents with invasive meningococcal disease (IMD). However, IMD can also be a first manifestation in adulthood and should prompt for the evaluation of the LCD. We report the case of a young adult with IMD who was found to have a LCD, caused by a compound heterozygous mutation in C6. His vaccination status was optimized and prophylactic antibiotic treatment was initiated. By means of this case, we would like to raise awareness of underlying LCD in (young) adults presenting with IMD by N. meningitidis. Screening for complement deficiencies after IMD, followed by genetic testing, can be lifesaving and allows for genetic counselling. In addition, we discuss the diagnosis and treatment of LCD.
Dissertations / Theses on the topic "Complement-like pathway"
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Zmarlak, Natalia Marta. "Regulation of immune signalling in the malaria mosquito vector, Anopheles : the secreted mosquito leucine-rich repeat protein APL1C is a pathogen binding factor essential for immunity to Plasmodium ookinetes and sporozoites." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS053.
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L’anophèle est le moustique vecteur du parasite Plasmodium, responsable du paludisme. Chez ce moustique, des protéines de type LRR (à motifs riches en leucine) ont été décrites comme antagonistes cruciaux du développement de Plasmodium. L’une d’entre elles, APL1C (Anopheles Plasmodium-responsive factor) protège spécifiquement le moustique contre les parasites Plasmodium de rongeurs en collaboration avec la protéine TEP1 du complément. En combinant des approches de biologie cellulaire et de génomique fonctionnelle, mon travail de thèse montre que le repas sanguin des moustiques induit le recrutement d’APL1C au niveau du pôle basal de l’épithélium digestif. Ce positionnement d’APL1C lui permet de se lier aux stades ookinètes du parasite émergeant du côté basal de l’épithélium, et ce, indépendamment de la fonction de TEP1. Néanmoins, cette action d’APL1C requiert la contribution des phagocytes et de la Nitration. Par ailleurs, mon travail montre que l’action d’APL1C ne se restreint pas à l'ookinète car elle agit aussi contre le dernier stade de développement de Plasmodium, les sporozoïtes. Avec la capacité de se lier aux sporozoites, APL1C contrôle la prévalence d’infection des glandes salivaires du moustique, mais avec des partenaires différents de ceux agissant sur les ookinètes. Finalement, une étude transcriptomique m’a permis d’identifier des facteurs agissant en aval d’APL1C. L’ensemble de ces résultats génère de nouvelles connaissances relatives à la fonction de cette famille de protéines LRR en tant que récepteurs de reconnaissance d'agents pathogènes capable de déclencher une réponse immunitaire dans différents compartiments tissulaires du moustiqueAnopheles mosquito is a vector of Plasmodium parasite, the causative agent of malaria. The Anopheles leucine-rich repeat (LRR) proteins were described as key antagonists of Plasmodium parasites in Anopheles mosquito midgut. APL1C (Anopheles Plasmodium-responsive factor) is a representative of LRR members which specifically protects against rodent malaria parasites by stabilizing the complement-like protein TEP1. By combining cell biology with functional genomic approaches, this study shows that mosquito bloodmeal induce the presence of an extracellular layer of APL1C protein surrounding the midgut beneath of the basal lamina. Consistently with the formation of this layer, APL1C binds to the ookinetes that emerged on the basal side of the midgut. This presence occurs independently from TEP1 function, requires the contribution of the phagocytic cells and nitration pathway. In addition, APL1C defence function is not restricted to the ookinete in the midgut but it also acts against the latest Plasmodium stage, the sporozoites. APL1C inhibits salivary glands infection prevalence, and consistently, it also binds to the surface of the sporozoites in the hemocoel. However, unlike to the midgut stages, anti-sporozoites APL1C-dependent mechanism involves different partners. Moreover, RNAseq study revealed APL1C gene targets, including genes with immune-like function. These results generate novel biological insight for the function of APL1C, and probably other LRR family members, as a pathogen recognition receptor inducing immune response against pathogens that come in contact with mosquito hemolymph compartment
Books on the topic "Complement-like pathway"
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Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.
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The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.
Book chapters on the topic "Complement-like pathway"
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Kojouharova, Mihaela. "Classical Complement Pathway Component C1q: Purification of Human C1q, Isolation of C1q Collagen-Like and Globular Head Fragments and Production of Recombinant C1q—Derivatives. Functional Characterization." In The Complement System, 25–42. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-724-2_3.
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Kumar Chatterjee, Swapan, and Snigdha Saha. "Glycan and Its Role in Combating COVID-19." In Biotechnology to Combat COVID-19 [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97240.
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Newly identified beta-coronavirus i.e. the 2019 novel coronavirus is associated with a contagious transmittable respiratory disease called COVID-19. This disease has been declared as a “pandemic” by the World Health Organization (WHO). The entry of coronavirus in the human respiratory epithelial cells depends upon the interaction between host cell receptor ACE2 and viral S-glycoprotein. However, this type of molecular recognition in between cell surface receptors and envelope glycoproteins are mediated by specific glycan epitopes and attribute to viral entry through membrane fusion. Glycans are essential biomolecules made by all living organisms, have roles in serving structure, energy storage, and system regulatory purposes. The glycan shield plays a crucial role in concealing the surface S protein from molecular recognition. The immunomodulatory properties of Glycan-binding proteins (GBPs) like Lectins, build them as an attractive candidates for vaccine adjuvant. Investigations involving the complement system activation by the lectin pathway in COVID-19 and diseases are in need of the hour. The innate immune response involving complement system could have varied biological effects against an array of microbial infections. The advances in glycoprotein style methods especially immunomodulatory action of some lectins are necessary to boost the effectiveness of treatment of COVID-19 and other pandemics.
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Michael, A., Newton Hyuna Yang, Patricia A. Gorman Ian Tomlinson, and Rebecca R. Roylance. "A Statistical Approach to Modeling Genomic Aberrations in Cancer Cells." In Bayesian Statistics 7, 293–305. Oxford University PressOxford, 2003. http://dx.doi.org/10.1093/oso/9780198526155.003.0016.
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Abstract Whereas most cells in the body carry the normal complement of 23 chromosome pairs, the cells within a cancerous tumor very often present highly abnormal genomic structure. Deletions, amplifications, rearrangements and mutations are common at various scales and are highly variable amongst tumors, as indicated by molecular technologies which enable ever better measurement. It is an important statistical problem to separate sporadic abnormalities from those that may not be sporadic and that may have some biological significance. We discuss a modelling strategy for genomic aberration data, which allows us to to infer combinations of aberrations that together increase the chance that a precancerous cell will have a descendant tumor lineage. The likelihood component involves a network of pathway structures. Markov chain Monte Carlo is used to sample from the space of these oncogenic networks. We illustrate the methodology with comparative genomic hybridizations from a recent breast cancer study, and we derive a likelihood formula for the larger class of tree-like networks.
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Araújo, Kathleen. "French Nuclear Energy: Concentrated Power." In Low Carbon Energy Transitions. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199362554.003.0008.
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Nuclear energy is one of the most significant sources of low carbon energy in use in the power sector today. In 2013, nuclear energy represented roughly 11% of the global electricity supply, with growth projected to occur in China, India, and Russia (International Atomic Energy Agency [IAEA], n.d.a; NEA, n.d.). As a stable source of electricity, nuclear energy can be a stand-alone, base-load form of electricity or complement more variable forms of low carbon energy, like wind and solar power. Among the energy technologies considered here, nuclear energy is complex not only for the science behind it, but also for its societal, environmental, and economic dimensions.This chapter explores the rapid rise of French nuclear energy in the civilian power sector. It considers what a national energy strategy looks like under conditions of high concern about energy supply security when limited domestic energy resources appear to exist. The case reveals that centralized planning with complex and equally centralized technology can be quite conducive to rapid change. However, continued public acceptance, especially for nuclear energy, matters in the durability of such a pathway. France is a traditional and currently global leader in nuclear energy, ranking the highest among countries for its share of domestic electricity derived from nuclear power at 76% of total electricity in 2015 (IAEA, n.d.b). France is highly ranked for the size of its nuclear reactor fleet and amount of nuclear generation, second only to the United States. In 2016, this nation of 67 million people and economy of $2.7 trillion had 58 nuclear power reactors (CIA, n.d.; IAEA, n.d.b). Due to the level of nuclear energy in its power mix, France has some of the lowest carbon emissions per person for electricity (IEA, 2016a). France is also one of the largest net exporters of electricity in Europe, with 61.7 TWh exported (Réseau de Transport d’électricité [RTE], 2016), producing roughly $3.3 billion in annual revenue (World Nuclear Association [WNA], n.d). This European country has the largest reprocessing capacity for spent fuel, with roughly 17% of its electricity powered from recycled fuel (WNA, n.d.).
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Turyamuhika, Laban, Agaba Bosco, Asiimwe Moses, Musinguzi Benson, and Okek Erick. "Functioning and Control of Phagocytosis." In Phagocytosis - Main Key of Immune System. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.110511.
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Phagocytosis is a very complex and versatile process that contributes to immunity through a series of events that is it’s sometimes referred to the Come and Eat me process. Due to the recognition ingestion and digestion then destruction. It’s also central to tissue homeostasis and remodeling by clearing dead cells. This ability of phagocytes to perform such diverse functions rests in large part on their vast repertoire of receptors. In this book chapter we looked at the processes used by phagocyte to perform there phagocytosis function. This is made possible by the binding of opsonins on the microbes like the C3b of the complement. This works as a chemo attractant to the phagocytes to come and initiate the process of eating. On recognition this microbe or dead cell interacts with the phagocyte with the help of a very big repertoire of receptors the microbe is engulfed with in the phagosome. As microbes interact with the phagocyte receptors a cascade of signaling events downstream that then activate phagocytosis. This membrane and cytoskeleton remodulation lead to the formation of pseudopods that cover the entire microbe forming a phagocytic cup which closes a few minutes to take up the microbe completely. The signal cascade is most known for the Fc receptor activities. Crosslinking of the Fc receptor on the surface of phagocyte activate phagocytosis and any other effector functions such as activation of the oxidative burst, degranulation, antibody dependent cell mediated cytotoxicity and activation of genes for cytokine/chemokine production that are beneficial in microbe destruction and initiation of inflammation. This starts once the interaction of phagocytes receptors and their ligands on the target microbes takes place appropriately. The phagocyte receptors will then aggregate to activate a series of pathways that regulate actin cytoskeleton which helps in the formation of a new vesicle which comes out of the membrane to enclose the microbe. In here a number of processes and stages take place all aimed at killing and denaturing the particle. They include early phagosome, intermediate phagosome, phagolysosome formation and the late phagosome all these participate in eliminating the phagocytized microbe. However with all the above phagocytic efficiency, some pathogens evade phagocytosis using different means and presence of certain capacities that facilitate evasion examples of organisms that evade phagocytosis include Mycobacterium tuberculosis, Listeria monocytogens Escherichia coli etc. all these use different means in evasion. Therefore the concept and science of Phagocytes used to be studied more to explore more pharmaceutical products based on the evasion mechanisms.
Conference papers on the topic "Complement-like pathway"
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Povelones, Michael. "Specificity of complement-like pathway activation inAnopheles gambiae." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92449.
Full textReports on the topic "Complement-like pathway"
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Friedman, Haya, Julia Vrebalov, James Giovannoni, and Edna Pesis. Unravelling the Mode of Action of Ripening-Specific MADS-box Genes for Development of Tools to Improve Banana Fruit Shelf-life and Quality. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592116.bard.
Full textAbstract:
Fruit deterioration is a consequence of a genetically-determined fruit ripening and senescence programs, in which developmental factors lead to a climacteric rise of ethylene production in ethylene-sensitive fruits such as tomato and banana. Breeding of tomato with extended fruit shelf life involves the incorporation of a mutation in RIN, a MADS-box transcription factor participating in developmental control signalling of ripening. The RIN mode of action is not fully understood, and it may be predicted to interact with other MADS-box genes to execute its effects. The overall goal of this study was to demonstrate conservation of ripening control functions between banana and tomato and thus, the potential to genetically extend shelf-life in banana based on tools developed in tomato. The specific objectives were: 1. To increase the collection of potential RIN-like genes from banana; 2. To verify their action as developmental regulators; 3. To elucidate MADS-box gene mode of action in ripening control; 4. To create transgenic banana plants that express low levels of endogenous Le-RIN- like, MaMADS- gene(s). We have conducted experiments in banana as well as in tomato. In tomato we have carried out the transformation of the tomato rin mutant with the MaMADS1 and MaMADS2 banana genes. We have also developed a number of domain swap constructs to functionally examine the ripening-specific aspects of the RIN gene. Our results show the RIN-C terminal region is essential for the gene to function in the ripening signalling pathway. We have further explored the tomato genome databases and recovered an additional MADS-box gene necessary for fruit ripening. This gene has been previously termed TAGL1 but has not been functionally characterized in transgenic plants. TAGL1 is induced during ripening and we have shown via RNAi repression that it is necessary for both fleshy fruit expansion and subsequent ripening. In banana we have cloned the full length of six MaMADS box genes from banana and determined their spatial and temporal expression patterns. We have created antibodies to MaMADS2 and initiated ChI assay. We have created four types of transgenic banana plants designed to reduce the levels of two of the MaMADS box genes. Our results show that the MaMADS-box genes expression in banana is dynamically changing after harvest and most of them are induced at the onset of the climacteric peak. Most likely, different MaMADS box genes are active in the pulp and peel and they are differently affected by ethylene. Only the MaMADS2 box gene expression is not affected by ethylene indicating that this gene might act upstream to the ethylene response pathway. The complementation analysis in tomato revealed that neither MaMADS1 nor MaMADS2 complement the rin mutation suggesting that they have functionally diverged sufficiently to not be able to interact in the context of the tomato ripening regulatory machinery. The developmental signalling pathways controlling ripening in banana and tomato are not identical and/or have diverged through evolution. Nevertheless, at least the genes MaMADS1 and MaMADS2 constitute part of the developmental control of ripening in banana, since transgenic banana plants with reduced levels of these genes are delayed in ripening. The detailed effect on peel and pulp, of these transgenic plants is underway. So far, these transgenic bananas can respond to exogenous ethylene, and they seem to ripen normally. The response to ethylene suggest that in banana the developmental pathway of ripening is different than that in tomato, because rin tomatoes do not ripen in response to exogenous ethylene, although they harbor the ethylene response capability This study has a major contribution both in scientific and agricultural aspects. Scientifically, it establishes the role of MaMADS box genes in a different crop-the banana. The developmental ripening pathway in banana is similar, but yet different from that of the model plant tomato and one of the major differences is related to ethylene effect on this pathway in banana. In addition, we have shown that different components of the MaMADS-box genes are employed in peel and pulp. The transgenic banana plants created can help to further study the ripening control in banana. An important and practical outcome of this project is that we have created several banana transgenic plants with fruit of extended shelf life. These bananas clearly demonstrate the potential of MaMADS gene control for extending shelf-life, enhancing fruit quality, increasing yield in export systems and for improving food security in areas where Musaspecies are staple food crops.
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Weiss, David, and Neil Olszewski. Manipulation of GA Levels and GA Signal Transduction in Anthers to Generate Male Sterility. United States Department of Agriculture, 2000. http://dx.doi.org/10.32747/2000.7580678.bard.
Full textAbstract:
The original objectives of the research were: i. To study the role of GA in anther development, ii. To manipulate GA and/or GA signal transduction levels in the anthers in order to generate male sterility. iii. To characterize the GA signal transduction repressor, SPY. Previous studies have suggested that gibberellins (GAs) are required for normal anther development. In this work, we studied the role of GA in the regulation of anther development in petunia. When plants were treated with the GA-biosynthesis inhibitor paclobutrazol, anther development was arrested. Microscopic analysis of these anthers revealed that paclobutrazol inhibits post-meiotic developmental processes. The treated anthers contained pollen grains but the connective tissue and tapetum cells were degenerated. The expression of the GA-induced gene, GIP, can be used in petunia as a molecular marker to: study GA responses. Analyses of GIP expression during anther development revealed that the gene is induced only after microsporogenesis. This observation further suggests a role for GA in the regulation of post-meiotic processes during petunia anther development. Spy acts as a negative regulator of gibberellin (GA) action in Arabidopsis. We cloned the petunia Spy homologue, PhSPY, and showed that it can complement the spy-3 mutation in Arabidopsis. Overexpression of Spy in transgenic petunia plants affected various GA-regulated processes, including seed germination, shoot elongation, flower initiation, flower development and the expression of a GA- induced gene, GIP. In addition, anther development was inhibited in the transgenic plants following microsporogenesis. The N-terminus of Spy contains tetratricopeptide repeats (TPR). TPR motifs participate in protein-protein interactions, suggesting that Spy is part of a multiprotein complex. To test this hypothesis, we over-expressed the SPY's TPR region without the catalytic domain in transgenic petunia and generated a dominant- negative Spy mutant. The transgenic seeds were able to germinate on paclobutrazol, suggesting an enhanced GA signal. Overexpression of PhSPY in wild type Arabidopsis did not affect plant stature, morphology or flowering time. Consistent with Spy being an O-GlcNAc transferase (OGT), Spy expressed in insect cells was shown to O-GlcNAc modify itself. Consistent with O-GlcNAc modification playing a role in GA signaling, spy mutants had a reduction in the GlcNAc modification of several proteins. After treatment of the GA deficient, gal mutant, with GA3 the GlcNAc modification of proteins of the same size as those affected in spy mutants exhibited a reduction in GlcNAcylation. GA-induced GlcNAcase may be responsible for this de-GlcNAcylation because, treatment of gal with GA rapidly induced an increase in GlcNAcase activity. Several Arabidopsis proteins that interact with the TPR domain of Spy were identified using yeast two-hybrids screens. One of these proteins was GIGANTEA (GI). Consistent with GI and Spy functioning as a complex in the plant the spy-4 was epistatic to gi. These experiments also demonstrated that, in addition to its role in GA signaling, Spy functions in the light signaling pathways controlling hypocotyl elongation and photoperiodic induction of flowering. A second Arabidopsis OGT, SECRET AGENT (SCA), was discovered. Like SPY, SCA O-GlcNAc modifies itself. Although sca mutants do not exhibit dramatic phenotypes, spy/sca double mutants exhibit male and female gamete and embryo lethality, indicating that Spy and SCA have overlapping functions. These results suggest that O-GlcNAc modification is an essential modification in plants that has a role in multiple signaling pathways.