Relevant bibliographies by topics / Intracellular pathways

Academic literature on the topic 'Intracellular pathways'

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Published: 4 June 2021
Last updated: 15 February 2024

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Journal articles on the topic "Intracellular pathways"

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Waligora, E. A., C. R. Fisher, N. J. Hanovice, A. Rodou, E. E. Wyckoff, and S. M. Payne. "Role of Intracellular Carbon Metabolism Pathways in Shigella flexneri Virulence." Infection and Immunity 82, no. 7 (April 14, 2014): 2746–55. http://dx.doi.org/10.1128/iai.01575-13.

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ABSTRACTShigella flexneri, which replicates in the cytoplasm of intestinal epithelial cells, can use the Embden-Meyerhof-Parnas, Entner-Doudoroff, or pentose phosphate pathway for glycolytic carbon metabolism. To determine which of these pathways is used by intracellularS. flexneri, mutants were constructed and tested in a plaque assay for the ability to invade, replicate intracellularly, and spread to adjacent epithelial cells. Mutants blocked in the Embden-Meyerhof-Parnas pathway (pfkABandpykAFmutants) invaded the cells but formed very small plaques. Loss of the Entner-Doudoroff pathway geneedaresulted in small plaques, but the doubleeda eddmutant formed normal-size plaques. This suggested that the plaque defect of theedamutant was due to buildup of the toxic intermediate 2-keto-3-deoxy-6-phosphogluconic acid rather than a specific requirement for this pathway. Loss of the pentose phosphate pathway had no effect on plaque formation, indicating that it is not critical for intracellularS. flexneri. Supplementation of the epithelial cell culture medium with pyruvate allowed the glycolysis mutants to form larger plaques than those observed with unsupplemented medium, consistent with data from phenotypic microarrays (Biolog) indicating that pyruvate metabolism was not disrupted in these mutants. Interestingly, the wild-typeS. flexnerialso formed larger plaques in the presence of supplemental pyruvate or glucose, with pyruvate yielding the largest plaques. Analysis of the metabolites in the cultured cells showed increased intracellular levels of the added compound. Pyruvate increased the growth rate ofS. flexneriin vitro, suggesting that it may be a preferred carbon source inside host cells.
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Ulevitch, Richard J., David L. Dunn, Mitchell P. Fink, and Christopher E. Taylor. "ENDOTOXIN-RELATED INTRACELLULAR PATHWAYS." Shock 6, no. 1 (July 1996): 1–2. http://dx.doi.org/10.1097/00024382-199607000-00001.

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Benitah, Salvador Aznar. "Intracellular signalling pathways and carcinogenesis." Revista de Oncología 3, no. 5 (September 2001): 274–77. http://dx.doi.org/10.1007/bf02719890.

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Nahorski, Stefan R. "Pharmacology of intracellular signalling pathways." British Journal of Pharmacology 147, S1 (January 2006): S38—S45. http://dx.doi.org/10.1038/sj.bjp.0706468.

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Sanders-Bush, Elaine. "CONTROL OF INTRACELLULAR SIGNALING PATHWAYS." Behavioural Pharmacology 10, SUPPLEMENT 1 (August 1999): S80. http://dx.doi.org/10.1097/00008877-199908001-00203.

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LACOMBE, CATHERINE, ISABELLE DUSANTER, STÉPHANIE GOBERT, ODILE MULLER, SYLVIE GISSELBRECHT, and PATRICK MAYEUX. "Intracellular Pathways Activated by Erythropoietina." Annals of the New York Academy of Sciences 718, no. 1 (February 26, 2008): 223–31. http://dx.doi.org/10.1111/j.1749-6632.1994.tb55721.x.

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Castle, D., and A. Castle. "Intracellular Transport and Secretion of Salivary Proteins." Critical Reviews in Oral Biology & Medicine 9, no. 1 (January 1998): 4–22. http://dx.doi.org/10.1177/10454411980090010301.

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Intracellular transport and secretion of salivary proteins are major activities of salivary acinar cells. While the major intracellular pathway followed by salivary proteins following their synthesis has been described previously, there is only limited understanding of how this process is regulated at the molecular level. Studies of salivary proteins, especially proline-rich proteins, expressed in an endocrine cell line have begun to provide insight regarding intermolecular interactions during transport and the role played by structural signals during intracellular sorting. Analysis of the secretion of newly synthesized salivary proteins in parotid tissue has shown that there are multiple pathways of discharge from acinar cells. While granule exocytosis is the major pathway, at least two other pathways that export salivary proteins have been found to originate from maturing secretion granules. These pathways may contribute to other acinar cell functions, including secretion of proteins in the absence of acute stimulation and support of the secretory process for fluid and electrolytes.
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Xu, Wen, Bei Wang, Yisong Gao, Yuxuan Cai, Jiali Zhang, Zhiyin Wu, Jiameng Wei, Chong Guo, and Chengfu Yuan. "Alkaloids Exhibit a Meaningful Function as Anticancer Agents by Restraining Cellular Signaling Pathways." Mini-Reviews in Medicinal Chemistry 22, no. 7 (April 2022): 968–83. http://dx.doi.org/10.2174/1389557521666211007114935.

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Abstract: Alkaloids are nitrogen-containing organic compounds widely found in natural products, which play an essential role in clinical treatment. Cellular signaling pathways in tumors are a series of enzymatic reaction pathways that convert extracellular signals into intracellular signals to produce biological effects. The ordered function of cell signaling pathways is essential for tumor cell proliferation, differentiation, and programmed death. This review describes the antitumor progression mediated by various alkaloids after inhibiting classical signaling pathways; related studies are systematically retrieved and collected through PubMed. We selected the four currently most popular pathways for discussion and introduced the molecular mechanisms mediated by alkaloids in different signaling pathways, including the NF-kB signaling pathway, PI3K/AKT signaling pathway, MAPK signaling pathway, and P53 signaling pathway. The research progress of alkaloids related to tumor signal transduction pathwa
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Pieper, Rembert, C. R. Fisher, Moo-Jin Suh, S. T. Huang, P. Parmar, and S. M. Payne. "Analysis of the Proteome of Intracellular Shigella flexneri Reveals Pathways Important for Intracellular Growth." Infection and Immunity 81, no. 12 (October 7, 2013): 4635–48. http://dx.doi.org/10.1128/iai.00975-13.

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ABSTRACTGlobal proteomic analysis was performed withShigella flexneristrain 2457T in association with three distinct growth environments:S. flexnerigrowing in broth (in vitro),S. flexnerigrowing within epithelial cell cytoplasm (intracellular), andS. flexnerithat were cultured with, but did not invade, Henle cells (extracellular). Compared toin vitroand extracellular bacteria, intracellular bacteria had increased levels of proteins required for invasion and cell-to-cell spread, including Ipa, Mxi, and Ics proteins. Changes in metabolic pathways in response to the intracellular environment also were evident. There was an increase in glycogen biosynthesis enzymes, altered expression of sugar transporters, and a reduced amount of the carbon storage regulator CsrA. Mixed acid fermentation enzymes were highly expressed intracellularly, while tricarboxylic acid (TCA) cycle oxidoreductive enzymes and most electron transport chain proteins, except CydAB, were markedly decreased. This suggested that fermentation and the CydAB system primarily sustain energy generation intracellularly. Elevated levels of PntAB, which is responsible for NADPH regeneration, suggested a shortage of reducing factors for ATP synthesis. These metabolic changes likely reflect changes in available carbon sources, oxygen levels, and iron availability. Intracellular bacteria showed strong evidence of iron starvation. Iron acquisition systems (Iut, Sit, FhuA, and Feo) and the iron starvation, stress-associated Fe-S cluster assembly (Suf) protein were markedly increased in abundance. Mutational analysis confirmed that the mixed-acid fermentation pathway was required for wild-type intracellular growth and spread ofS. flexneri. Thus, iron stress and changes in carbon metabolism may be key factors in theS. flexneritransition from the extra- to the intracellular milieu.
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Frühbeck, Gema. "Intracellular signalling pathways activated by leptin." Biochemical Journal 393, no. 1 (December 12, 2005): 7–20. http://dx.doi.org/10.1042/bj20051578.

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Leptin is a versatile 16 kDa peptide hormone, with a tertiary structure resembling that of members of the long-chain helical cytokine family. It is mainly produced by adipocytes in proportion to fat size stores, and was originally thought to act only as a satiety factor. However, the ubiquitous distribution of OB-R leptin receptors in almost all tissues underlies the pleiotropism of leptin. OB-Rs belong to the class I cytokine receptor family, which is known to act through JAKs (Janus kinases) and STATs (signal transducers and activators of transcription). The OB-R gene is alternatively spliced to produce at least five isoforms. The full-length isoform, OB-Rb, contains intracellular motifs required for activation of the JAK/STAT signal transduction pathway, and is considered to be the functional receptor. Considerable evidence for systemic effects of leptin on body mass control, reproduction, angiogenesis, immunity, wound healing, bone remodelling and cardiovascular function, as well as on specific metabolic pathways, indicates that leptin operates both directly and indirectly to orchestrate complex pathophysiological processes. Consistent with leptin's pleiotropic role, its participation in and crosstalk with some of the main signalling pathways, including those involving insulin receptor substrates, phosphoinositide 3-kinase, protein kinase B, protein kinase C, extracellular-signal-regulated kinase, mitogen-activated protein kinases, phosphodiesterase, phospholipase C and nitric oxide, has been observed. The impact of leptin on several equally relevant signalling pathways extends also to Rho family GTPases in relation to the actin cytoskeleton, production of reactive oxygen species, stimulation of prostaglandins, binding to diacylglycerol kinase and catecholamine secretion, among others.
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Dissertations / Theses on the topic "Intracellular pathways"

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Wilson, Rona Kirstin. "Intracellular pathways in prion peptide trafficking." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433105.

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`Arnold, Claire. "Intracellular signalling pathways in myeloproliferative neoplasms." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680884.

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Vicario, Chiara. "Magnetogenetic Control of Intracellular Signaling Pathways." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066581/document.

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Le contrôle de l'organisation spatiotemporelle des biomolécules à l'intérieur des cellules vivantes est fondamental pour déchiffrer les mécanismes qui règlent les voies de signalisation cellulaire et leur régulation. Dans ce projet de thèse nous présentons une nouvelle méthode pour induire une perturbation très spécifique et locale des voies de signalisation à l'intérieur des cellules vivantes: la magnétogénétique. Elle est basée sur l'utilisation de nanoparticules magnétiques biofonctionnalisée, pour induire et maintenir des gradients de protéines à l'intérieur des cellules vivantes.Nous avons modifié la taille et la surface de deux différentes types de particules, les nanoparticules superparamagnétiques synthétiques avec couche de silice et les nanoparticules basées sur la protéine GFP-ferritine, afin d'assurer une mobilité libre dans le cytosol. Ces nanoparticules peuvent être localisées rapidement dans les cellules vivantes grâce à leur diffusion biaisée par des forces magnétiques faibles, dans l'ordre du fN. En combinaison avec une fonctionnalisation de surface spécifique pour la capture des protéines d'intérêt ainsi que un chargement efficace des nanoparticules dans le cytoplasme, nous présentons une technologie capable de contrôler des gradients de protéines intracellulaires avec une résolution spatiale du micromètre et une résolution temporelle de quelques dizaines de secondes.Dans ce travail nous avons montré la possibilité de contrôler avec précision la perturbation des voies de signalisation associées aux petites protéines Rho GTPases et nous avons quantifié la propagation du signal en termes de recrutement des effecteurs et des changement morphologiques
Controlling the spatio-temporal organization of biomolecules inside living cells is a major rerequisite for deciphering mechanisms governing cell signaling and its regulation. In this thesis project, a new method to induce a highly specific and local perturbation of signaling pathways inside living cells is presented: magnetogenetics. It is based on the use of biofunctionalized magnetic nanoparticles, to induce and maintain protein gradients inside living cells. We tailored the size and surface properties of both synthetic silica core shell nanoparticles and superparamagnetic GFP-ferritin-based nanoparticles in order to ensure unhindered mobility in the cytosol. These nanoparticles can be rapidly localized in living cells by exploiting biased diffusion at weak magnetic forces in the fN range. In combination with nanoparticles' surface functionalization for specific in situ capturing of target proteins as well as efficient delivery into the cytosplasm, this work presents a novel technology for controlling intracellular protein gradients with a spatial resolution of micrometers and a temporal resolution of a few tens of seconds. In this work we showed the possibility to precisely control the perturbation of the signaling pathways associated to the small Rho GTPases proteins with relative quantification on signal propagation in terms of effector recruitment and morphological changes
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Hutchinson, James Lawrence. "Salmonella interactions with host intracellular trafficking pathways." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611631.

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Nesbeth, Darren Nicholas. "Biochemical studies of intracellular trafficking pathways in eukaryotes." Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313830.

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Romero, Alirio Jose Melendez. "Intracellular signalling pathways activated by Fc#gamma#RI." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266462.

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Cullen, Peter J. "A study of the regulation of intracellular calcium." Thesis, University of East Anglia, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.277302.

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Behar, Marcelo S. Dohlman Henrik G. "Dynamic regulation and information transfer in intracellular-signaling pathways." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1546.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Physics and Astronomy." Discipline: Physics and Astronomy; Department/School: Physics and Astronomy.
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Pouliot, Philippe. "Implication of intracellular signalling pathways in allergic asthma pathogenesis." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115896.

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The regulation of systemic immune responses is dependent on individual cell responses that will concur to induce a coherent response against a stimulus. In turn, cell response is dependent on the processing of intracellular signals generated at the cell membrane and transmitted through successive protein modifications to the nucleus in order to activate gene transcription. This is referred to as intracellular signalling. Tight control of these mechanisms is required to generate an appropriate cell response to environmental stimulations and globally to establish an appropriate immune response. Among protein modifications used to transmit a signal to the nucleus, protein tyrosine phosphorylation represents a pivotal method used by immune cells to rapidly induce signalling. While protein tyrosine kinases (PTKs) phosphorylate proteins, protein tyrosine phosphatases (PTPs) regulate the signalling by removing the phosphate group. The goal of this study was to better characterize intracellular signalling events involved in allergic asthma, a chronic inflammatory disease involving a Th2 immune response. In a first time, we investigated the role of PTPs in the development of asthma. We show that inhibition of global PTP activity in mice, during either the allergen sensitization or the allergen challenge phase, reduces asthma development and is linked to an increased Th1 response in the spleen and lung. Secondly, we revealed that TC-PTP inhibition reduces asthma development, while PTP-1B inhibition exacerbates inflammatory cells recruitment to the lung. Inhibition of either SHP-1 or PTP-PEST activity did not significantly modulate asthma development in our model. In a third set of experiments, we got interested in the signalling pathways triggered by the pro-inflammatory molecules myeloid-related proteins (MRPs) 8 and 14. MRPs are small cytosolic proteins recently described to have extracellular functions. MRP8 expression is resistant to corticosteroid treatment, and potentially promotes inflammation in corticosteroid-treated patients. We identified that MRPs induce signal through the action of TLR-4 and trigger the activation of MEK/ERK and JNK pathways that lead to NF-kappaB translocation. Collectively, our data provide a new characterization of signalling pathways engaged in allergic asthma. This should be helpful in the elaboration of new therapeutic approaches targeting precise pathways to inhibit mechanisms of inflammation.
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Fitzgerald, Jonathan Basil. "Chondrocyte gene expression and intracellular signaling pathways in cartilage mechanotransduction." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33869.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2005.
Includes bibliographical references (p. 152-167).
Chondrocytes respond to in vivo mechanical loads by regulating the composition of the cartilage extracellular matrix. This study utilized three loading protocols that span the range of forces and flows induced by in vivo loading. Constant (static) compression of cartilage explants induces a transient hydrostatic pressure buildup and fluid exudation from the compacted matrix until relaxation leads to a new equilibrium compressed state. Dynamic compression induces cyclic matrix deformation, hydrostatic pressures, fluid flows, and streaming currents. Dynamic tissue shear causes cyclic matrix deformation only. After applying these loading protocols to intact cartilage explants for 1 to 24 hours, we used real-time PCR to measure the temporal expression profiles of selected genes associated with cartilage homeostasis. In concurrent experiments, we assessed the involvement of intracellular signaling pathways using molecular inhibitors. In order to interpret the results we developed two techniques that reliably clustered intermediate-sized datasets using principal component analysis and k-means clustering. Mechanical loading regulated a variety of genes including matrix proteins, proteases, protease inhibitors, transcription factors, cytokines, and growth factors. Static compression transiently upregulated matrix proteins, however, mRNA levels were suppressed by 24 hours.
(cont.) Dynamic compression and dynamic shear increased matrix protein transcription particularly after 24 hours. In contrast, matrix proteases were upregulated by all 24 hour loading regimes, particularly static compression. Taken together these results demonstrate the functionally-coordinated regulation of chondrocyte gene transcription in response to mechanical forces, and support the hypothesis that dynamic loading is anabolic for cartilage and static loading is anti-anabolic. Intracellular calcium release, cAMP activation of protein-kinase-A, and the phosphorylation of MAP kinases (ERK1/2, p38), were all identified as signaling events necessary for mechanically-induced transcription. In addition, we measured the immediate, transient increase in mRNA levels of transcription factors downstream of the MAP kinase pathway (c-Fos and c-Jun), in response to all three loading types. The prevention of protein synthesis during static compression suppressed mechanically-induced transcription suggesting that signaling molecules are synthesized in response to mechanical forces. Comparison of this well characterized model of normal cartilage mechanotransduction to what occurs within diseased cartilage will hopefully provide insight into the mechanisms driving the progression of osteoarthritis.
by Jonathan Basil Fitzgerald.
Ph.D.
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Books on the topic "Intracellular pathways"

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Perkins, Jonathan Edwards. A study of EGF-induced intracellular signalling pathways and effects in first trimester trophoblast. Birmingham: University of Birmingham, 2003.

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Conroy, Louise Anne. The development of t-lymphocytes within the murine foetal thymus: The role of intracellular signalling pathways. Birmingham: University of Birmingham, 1992.

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Groschner, Klaus, Wolfgang F. Graier, and Christoph Romanin. Store-operated Ca2+ entry (SOCE) pathways: Emerging signaling concepts in human (patho)physiology. Wien: Springer, 2012.

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Wilks, Andrew F., and Ailsa G. Harpur. Intracellular Signal Transduction: The JAK-STAT Pathway. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22050-4.

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Wilks, Andrew F. Intracellular signal transduction: The JAK-STAT pathway. New York: Springer, 1996.

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Idestrup, Chris. P2Y-and P2U-purinoceptor activation cause intracellualr CA2+ release in dorsal spinal astrocytes via the phospholipase C[BETA]/IP3 pathway. Ottawa: National Library of Canada, 1996.

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Newell-Price, John, Alia Munir, and Miguel Debono. Normal function of the endocrine system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0182.

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Endocrinology is the study of hormones (and their glands of origin), their receptors, the intracellular signalling pathways they invoke, and their associated diseases. The clinical specialty of endocrinology focuses specifically on the endocrine organs, that is, the organs whose primary function is hormone secretion, including the hypothalamus, the pituitary, the thyroid, the parathyroid, the adrenal glands, the pancreas, and the reproductive organs.
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Powell, Craig M. PTEN and Autism With Macrocepaly. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0010.

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Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al., 2007; Goffin, Hoefsloot, Bosgoed, Swillen, & Fryns, 2001; Herman, Butter, et al., 2007; McBride et al., 2010; Orrico et al., 2009; Stein, Elias, Saenz, Pickler, & Reynolds, 2010; Varga, Pastore, Prior, Herman, & McBride, 2009; Zori, Marsh, Graham, Marliss, & Eng, 1998). This chapter examines the role of PTEN in intracellular signaling, the link between PTEN signaling pathways and other autism-related genes and signaling pathways, the genetic relationship between PTEN and autism, model systems in which effects of Pten deletion on the brain have been studied, and promising preclinical data identifying therapeutic targets for patients with autism/macrocephaly associated with PTEN mutations.
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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Harpur, Ailsa G., and Andrew F. Wilks. Intracellular Signal Transduction: The JAK-STAT Pathway. Springer, 2013.

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Book chapters on the topic "Intracellular pathways"

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Heineke, Jörg. "Inter- and Intracellular Signaling Pathways." In Congenital Heart Diseases: The Broken Heart, 121–37. Vienna: Springer Vienna, 2016. http://dx.doi.org/10.1007/978-3-7091-1883-2_11.

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Šebestík, Jaroslav, Milan Reiniš, and Jan Ježek. "Dendrimers Regulating Intracellular Signaling Pathways." In Biomedical Applications of Peptide-, Glyco- and Glycopeptide Dendrimers, and Analogous Dendrimeric Structures, 197–98. Vienna: Springer Vienna, 2012. http://dx.doi.org/10.1007/978-3-7091-1206-9_21.

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Thiriet, Marc. "Signaling Pathways." In Intracellular Signaling Mediators in the Circulatory and Ventilatory Systems, 821–909. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4370-4_11.

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Contreras, Monica Sanchez, and Fernando Cardozo-Pelaez. "Chapter 13. Intracellular Signaling Pathways in Parkinson's Disease." In Extracellular and Intracellular Signaling, 247–82. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733434-00247.

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Gómez, Rodolfo, Javier Conde, Morena Scotece, and Oreste Gualillo. "Chapter 3. One Receptor for Multiple Pathways: Focus on Leptin Signaling." In Extracellular and Intracellular Signaling, 44–56. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733434-00044.

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Artemov, Dmitri, and Zaver M. Bhujwalla. "The Tumor Microenvironment in Nanoparticle Delivery and the Role of Imaging to Navigate Roadblocks and Pathways." In Intracellular Delivery III, 301–22. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-43525-1_12.

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Ochoa-Alvarez, Jhon Alberto, Candacy George, Harini Krishnan, Xiaoxuan Wu, and Gary S. Goldberg. "Chapter 6. Contact Normalization: Mechanisms and Pathways to Biomarkers and Chemotherapeutic Targets." In Extracellular and Intracellular Signaling, 105–15. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849733434-00105.

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Romanelli, Robert J., John T. Williams, and Kim A. Neve. "Dopamine Receptor Signaling: Intracellular Pathways to Behavior." In The Dopamine Receptors, 137–73. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-333-6_6.

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Tokarev, Andrei A., Aixa Alfonso, and Nava Segev. "Overview of Intracellular Compartments and Trafficking Pathways." In Trafficking Inside Cells, 3–14. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-93877-6_1.

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Saklatvala, J., A. Clark, and J. Dean. "The Intracellular Signaling Pathways of Inflammatory Stress." In Mechanisms of Organ Dysfunction in Critical Illness, 137–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-56107-8_9.

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Conference papers on the topic "Intracellular pathways"

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Dörner, Thomas. "09 Novel intracellular pathways." In 9th Annual Meeting of the Lupus Academy. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-la.9.

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"04 Targeting novel intracellular pathways." In 8th ANNUAL MEETING OF THE LUPUS ACADEMY, Warsaw, Poland, September 6–8, 2019. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-la.16.

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Bando, Kazuki, Katsumasa Fujita, Nicholas Smith, Jun Ando, and Satoshi Kawata. "3D Dynamic SERS Imaging of Intracellular Transport Pathways." In JSAP-OSA Joint Symposia. Washington, D.C.: OSA, 2013. http://dx.doi.org/10.1364/jsap.2013.19p_d4_7.

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Archała, Aneta, and Anita Płazińska. "β2-adrenergic receptor polymorphism in intracellular signalling pathways." In 1st International Electronic Conference on Biomedicine. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecb2021-10265.

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Jinghua Gu, Chen Wang, Le-Ming Shih, Tian-Li Wang, Yue Wang, R. Clarke, and Jianhua Xuan. "GIST: A Gibbs sampler to identify intracellular signal transduction pathways." In 2011 33rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2011. http://dx.doi.org/10.1109/iembs.2011.6090677.

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Bartholome, Kilian, Jens Timmer, and Markus Kollmann. "Design principles of signal transduction pathways to compensate intracellular perturbations." In 2006 IEEE Conference on Computer Aided Control System Design, 2006 IEEE International Conference on Control Applications, 2006 IEEE International Symposium on Intelligent Control. IEEE, 2006. http://dx.doi.org/10.1109/cacsd-cca-isic.2006.4776902.

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Bartholome, Kilian, Jens Timmer, and Markus Kollmann. "Design Principles of Signal Transduction Pathways to compensate Intracellular Perturbations." In 2006 IEEE International Conference on Control Applications. IEEE, 2006. http://dx.doi.org/10.1109/cca.2006.286134.

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Lu, X. Lucas, Bo Huo, Andrew D. Baik, and X. Edward Guo. "Intercellular Calcium Wave Propagation in Linear and Circuit-Like Bone Cell Networks." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19365.

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Intracellular calcium ([Ca2+]i) transients in response to mechanical stimulation can be propagated to neighboring cells in bone cell networks, which provides an essential mechanism for cell-cell communication in bone. Transfer of intracellular second messengers (e.g., IP3 and Ca2+) through gap junction pores and the diffusion of extracellular ATP to activate membrane receptors have long been conjectured as the two major pathways for intercellular Ca2+ wave propagation [1]. In this study, by comparing the calcium wave in open-end linear and looped circuit-like cell chains, the roles of gap junction intercellular communication (GJIC) and extracellular ATP diffusion in calcium wave propagation in bone cell networks were examined. The results were further confirmed with pathway-inhibitor studies performed on linear cell chains.
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Wu, Yicong, Wei Zheng, and Jianan Y. Qu. "Monitoring cellular metabolic pathways by wavelength- and time-resolved intracellular autofluorescence." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/ecbo.2007.6628_5.

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Wu, Yicong, Wei Zheng, and Jianan Y. Qu. "Monitoring cellular metabolic pathways by wavelength- and time-resolved intracellular autofluorescence." In European Conference on Biomedical Optics, edited by Dietrich Schweitzer and Maryann Fitzmaurice. SPIE, 2007. http://dx.doi.org/10.1117/12.727610.

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Reports on the topic "Intracellular pathways"

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Naim, Michael, Andrew Spielman, Shlomo Nir, and Ann Noble. Bitter Taste Transduction: Cellular Pathways, Inhibition and Implications for Human Acceptance of Agricultural Food Products. United States Department of Agriculture, February 2000. http://dx.doi.org/10.32747/2000.7695839.bard.

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Historically, the aversive response of humans and other mammals to bitter-taste substances has been useful for survival, since many toxic constituents taste bitter. Today, the range of foods available is more diverse. Many bitter foods are not only safe for consumption but contain bitter constituents that provide nutritional benefits. Despite this, these foods are often eliminated from our current diets because of their unacceptable bitterness. Extensive technology has been developed to remove or mask bitterness in foods, but a lack of understanding of the mechanisms of bitterness perception at the taste receptor level has prevented the development of inhibitors or efficient methods for reducing bitterness. In our original application we proposed to: (a) investigate the time course and effect of selected bitter tastants relevant to agricultural products on the formation of intracellular signal molecules (cAMP, IP3, Ca2+) in intact taste cells, in model cells and in membranes derived therefrom; (b) study the effect of specific bitter taste inhibitors on messenger formation and identify G-proteins that may be involved in tastant-induced bitter sensation; (c) investigate interactions and self-aggregation of bitter tastants within membranes; (d) study human sensory responses over time to these bitter-taste stimuli and inhibitors in order to validate the biochemical data. Quench-flow module (QFM) and fast pipetting system (FPS) allowed us to monitor fast release of the aforementioned signal molecules (cGMP, as a putative initial signal was substituted for Ca2+ ions) - using taste membranes and intact taste cells in a time range below 500 ms (real time of taste sensation) - in response to bitter-taste stimulation. Limonin (citrus) and catechin (wine) were found to reduce cellular cAMP and increase IP3 contents. Naringin (citrus) stimulated an IP3 increase whereas the cheese-derived bitter peptide cyclo(leu-Trp) reduced IP3 but significantly increased cAMP levels. Thus, specific transduction pathways were identified, the results support the notion of multiple transduction pathways for bitter taste and cross-talk between a few of those transduction pathways. Furthermore, amphipathic tastants permeate rapidly (within seconds) into liposomes and taste cells suggesting their availability for direct activation of signal transduction components by means of receptor-independent mechanisms within the time course of taste sensation. The activation of pigment movement and transduction pathways in frog melanophores by these tastants supports such mechanisms. Some bitter tastants, due to their amphipathic properties, permeated (or interacted with) into a bitter tastant inhibitor (specific phospholipid mixture) which apparently forms micelles. Thus, a mechanism via which this bitter taste inhibitor acts is proposed. Human sensory evaluation experiments humans performed according to their 6-n-propyl thiouracil (PROP) status (non-tasters, tasters, super-tasters), indicated differential perception of bitterness threshold and intensity of these bitter compounds by different individuals independent of PROP status. This suggests that natural products containing bitter compounds (e.g., naringin and limonin in citrus), are perceived very differently, and are in line with multiple transduction pathways suggested in the biochemical experiments. This project provides the first comprehensive effort to explore the molecular basis of bitter taste at the taste-cell level induced by economically important and agriculturally relevant food products. The findings, proposing a mechanism for bitter-taste inhibition by a bitter taste inhibitor (made up of food components) pave the way for the development of new, and perhaps more potent bitter-taste inhibitors which may eventually become economically relevant.
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Bazer, Fuller W., Arieh Gertler, and Elisha Gootwine. Role of Placental Lactogen in Sheep. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7574339.bard.

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Central problems in sheep and dairy cattle production are reproductive failure due to embryonic/fetal mortality and low birth weights, especially in prolific breeds, and reduced milk yields which adversely affect neonatal survival and economy of production. The sheep placenta expresses lactogenic (ovine placental lactogen, oPL) and somatogenic (ovine placental growth hormone, oGH) hormones. Our research has focused on the biological roles of oPL and oGH in function of the uterine endometrium during gestation and the mammary gland during pregnancy and lactation. Major conclusions were that: ( 1 ) immunization of prepubertal ewes against oPL resulted in increased birth weights of their lambs and their milk production during lactation; (2) neither oPL nor oGH had an antiluteolytic effect on uterine endometrium to affect lifespan of the corpus luteum; (3) only sequential exposure of the progesterone stimulated uterus to oIFNt and oPL or oGH increased endometrial gland proliferation and secretory protein gene expression; (4) oPL signals through a homodimer of ovine prolactin receptor (PRL-R) and heterodimer of oPRL-R and growth hormone receptor (GH-R); (5) exogenous recombinant oPL and oGH stimulated mammogenesis and milk yield during lactation; and (6) mutation of oPL and oGH was used to define specific biological effects and a rational basis for design of a specific receptor agonists or antagonists. This project was very productive in elucidating basic biological effects of oPL and oGH on intracellular signal transduction pathways, uterine development and secretory function, as well as mammogenesis and lactogenesis. We determined that immunization of prepubertal ewes against roPL increased birth weights of their lambs, especially those born as twins and triplets, as well as enhanced lactational performance. These studies significantly extended our knowledge of uterine and fetal-placental physiology and provided a foundation for new strategies to enhance reproductive and lactation efficiency. Based on these results, the major achievements were: 1) creation of a practical and cost effective management tool for producers to increase reproductive performance, neonatal survival, and milk yield of ewes in commercial flocks; and 2) define, for the first time, biological effects of oPL on endometrial functions and gene expression by uterine gland epithelium.
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Or, Etti, David Galbraith, and Anne Fennell. Exploring mechanisms involved in grape bud dormancy: Large-scale analysis of expression reprogramming following controlled dormancy induction and dormancy release. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7587232.bard.

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The timing of dormancy induction and release is very important to the economic production of table grape. Advances in manipulation of dormancy induction and dormancy release are dependent on the establishment of a comprehensive understanding of biological mechanisms involved in bud dormancy. To gain insight into these mechanisms we initiated the research that had two main objectives: A. Analyzing the expression profiles of large subsets of genes, following controlled dormancy induction and dormancy release, and assessing the role of known metabolic pathways, known regulatory genes and novel sequences involved in these processes B. Comparing expression profiles following the perception of various artificial as well as natural signals known to induce dormancy release, and searching for gene showing similar expression patterns, as candidates for further study of pathways having potential to play a central role in dormancy release. We first created targeted EST collections from V. vinifera and V. riparia mature buds. Clones were randomly selected from cDNA libraries prepared following controlled dormancy release and controlled dormancy induction and from respective controls. The entire collection (7920 vinifera and 1194 riparia clones) was sequenced and subjected to bioinformatics analysis, including clustering, annotations and GO classifications. PCR products from the entire collection were used for printing of cDNA microarrays. Bud tissue in general, and the dormant bud in particular, are under-represented within the grape EST database. Accordingly, 59% of the our vinifera EST collection, composed of 5516 unigenes, are not included within the current Vitis TIGR collection and about 22% of these transcripts bear no resemblance to any known plant transcript, corroborating the current need for our targeted EST collection and the bud specific cDNA array. Analysis of the V. riparia sequences yielded 814 unigenes, of which 140 are unique (keilin et al., manuscript, Appendix B). Results from computational expression profiling of the vinifera collection suggest that oxidative stress, calcium signaling, intracellular vesicle trafficking and anaerobic mode of carbohydrate metabolism play a role in the regulation and execution of grape-bud dormancy release. A comprehensive analysis confirmed the induction of transcription from several calcium–signaling related genes following HC treatment, and detected an inhibiting effect of calcium channel blocker and calcium chelator on HC-induced and chilling-induced bud break. It also detected the existence of HC-induced and calcium dependent protein phosphorylation activity. These data suggest, for the first time, that calcium signaling is involved in the mechanism of dormancy release (Pang et al., in preparation). We compared the effects of heat shock (HS) to those detected in buds following HC application and found that HS lead to earlier and higher bud break. We also demonstrated similar temporary reduction in catalase expression and temporary induction of ascorbate peroxidase, glutathione reductase, thioredoxin and glutathione S transferase expression following both treatments. These findings further support the assumption that temporary oxidative stress is part of the mechanism leading to bud break. The temporary induction of sucrose syntase, pyruvate decarboxylase and alcohol dehydrogenase indicate that temporary respiratory stress is developed and suggest that mitochondrial function may be of central importance for that mechanism. These finding, suggesting triggering of identical mechanisms by HS and HC, justified the comparison of expression profiles of HC and HS treated buds, as a tool for the identification of pathways with a central role in dormancy release (Halaly et al., in preparation). RNA samples from buds treated with HS, HC and water were hybridized with the cDNA arrays in an interconnected loop design. Differentially expressed genes from the were selected using R-language package from Bioconductor project called LIMMA and clones showing a significant change following both HS and HC treatments, compared to control, were selected for further analysis. A total of 1541 clones show significant induction, of which 37% have no hit or unknown function and the rest represent 661 genes with identified function. Similarly, out of 1452 clones showing significant reduction, only 53% of the clones have identified function and they represent 573 genes. The 661 induced genes are involved in 445 different molecular functions. About 90% of those functions were classified to 20 categories based on careful survey of the literature. Among other things, it appears that carbohydrate metabolism and mitochondrial function may be of central importance in the mechanism of dormancy release and studies in this direction are ongoing. Analysis of the reduced function is ongoing (Appendix A). A second set of hybridizations was carried out with RNA samples from buds exposed to short photoperiod, leading to induction of bud dormancy, and long photoperiod treatment, as control. Analysis indicated that 42 genes were significant difference between LD and SD and 11 of these were unique.
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Wang, X. F., and M. Schuldiner. Systems biology approaches to dissect virus-host interactions to develop crops with broad-spectrum virus resistance. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134163.bard.

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More than 60% of plant viruses are positive-strand RNA viruses that cause billion-dollar losses annually and pose a major threat to stable agricultural production, including cucumber mosaic virus (CMV) that infects numerous vegetables and ornamental trees. A highly conserved feature among these viruses is that they form viral replication complexes (VRCs) to multiply their genomes by hijacking host proteins and remodeling host intracellular membranes. As a conserved and indispensable process, VRC assembly also represents an excellent target for the development of antiviral strategies that can be used to control a wide-range of viruses. Using CMV and a model virus, brome mosaic virus (BMV), and relying on genomic tools and tailor-made large-scale resources specific for the project, our original objectives were to: 1) Identify host proteins that are required for viral replication complex assembly. 2) Dissect host requirements that determine viral host range. 3) Provide proof-of-concept evidence of a viral control strategy by blocking the viral replication complex-localized phospholipid synthesis. We expect to provide new ways and new concepts to control multiple viruses by targeting a conserved feature among positive-strand RNA viruses based on our results. Our work is going according to the expected timeline and we are progressing well on all aims. For Objective 1, among ~6,000 yeast genes, we have identified 96 hits that were possibly play critical roles in viral replication. These hits are involved in cellular pathways of 1) Phospholipid synthesis; 2) Membrane-shaping; 3) Sterol synthesis and transport; 4) Protein transport; 5) Protein modification, among many others. We are pursuing several genes involved in lipid metabolism and transport because cellular membranes are primarily composed of lipids and lipid compositional changes affect VRC formation and functions. For Objective 2, we have found that CPR5 proteins from monocotyledon plants promoted BMV replication while those from dicotyledon plants inhibited it, providing direct evidence that CPR5 protein determines the host range of BMV. We are currently examining the mechanisms by which dicot CPR5 genes inhibit BMV replication and expressing the dicot CPR5 genes in monocot plants to control BMV infection. For Objective 3, we have demonstrated that substitutions in a host gene involved in lipid synthesis, CHO2, prevented the VRC formation by directing BMV replication protein 1a (BMV 1a), which remodels the nuclear membrane to form VRCs, away from the nuclear membrane, and thus, no VRCs were formed. This has been reported in Journal of Biological Chemistry. Based on the results from Objective 3, we have extended our plan to demonstrate that an amphipathic alpha-helix in BMV 1a is necessary and sufficient to target BMV 1a to the nuclear membrane. We further found that the counterparts of the BMV 1a helix from a group of viruses in the alphavirus-like superfamily, such as CMV, hepatitis E virus, and Rubella virus, are sufficient to target VRCs to the designated membranes, revealing a conserved feature among the superfamily. A joint manuscript describing these exciting results and authored by the two labs will be submitted shortly. We have also successfully set up systems in tomato plants: 1) to efficiently knock down gene expression via virus-induced gene silencing so we could test effects of lacking a host gene(s) on CMV replication; 2) to overexpress any gene transiently from a mild virus (potato virus X) so we could test effects of the overexpressed gene(s) on CMV replication. In summary, we have made promising progress in all three Objectives. We have identified multiple new host proteins that are involved in VRC formation and may serve as good targets to develop antiviral strategies; have confirmed that CPR5 from dicot plants inhibited viral infection and are generating BMV-resistance rice and wheat crops by overexpressing dicot CPR5 genes; have demonstrated to block viral replication by preventing viral replication protein from targeting to the designated organelle membranes for the VRC formation and this concept can be further employed for virus control. We are grateful to BARD funding and are excited to carry on this project in collaboration.
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