Relevant bibliographies by topics / Signalling effect

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Signalling effect'

Author: Grafiati
Published: 5 June 2025
Last updated: 16 July 2025

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Journal articles on the topic "Signalling effect"

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Pirkl, Martin, Elisabeth Hand, Dieter Kube, and Rainer Spang. "Analyzing synergistic and non-synergistic interactions in signalling pathways using Boolean Nested Effect Models." Bioinformatics 32, no. 6 (2015): 893–900. http://dx.doi.org/10.1093/bioinformatics/btv680.

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Abstract Motivation: Understanding the structure and interplay of cellular signalling pathways is one of the great challenges in molecular biology. Boolean Networks can infer signalling networks from observations of protein activation. In situations where it is difficult to assess protein activation directly, Nested Effect Models are an alternative. They derive the network structure indirectly from downstream effects of pathway perturbations. To date, Nested Effect Models cannot resolve signalling details like the formation of signalling complexes or the activation of proteins by multiple alternative input signals. Here we introduce Boolean Nested Effect Models (B-NEM). B-NEMs combine the use of downstream effects with the higher resolution of signalling pathway structures in Boolean Networks. Results: We show that B-NEMs accurately reconstruct signal flows in simulated data. Using B-NEM we then resolve BCR signalling via PI3K and TAK1 kinases in BL2 lymphoma cell lines. Availability and implementation: R code is available at https://github.com/MartinFXP/B-NEM (github). The BCR signalling dataset is available at the GEO database (http://www.ncbi.nlm.nih.gov/geo/) through accession number GSE68761. Contact: martin-franz-xaver.pirkl@ukr.de, Rainer.Spang@ukr.de Supplementary information: Supplementary data are available at Bioinformatics online.
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Guerrero-Alba, Raquel, Eduardo E. Valdez-Morales, Nestor N. Jimenez-Vargas, et al. "Stress activates pronociceptive endogenous opioid signalling in DRG neurons during chronic colitis." Gut 66, no. 12 (2016): 2121–31. http://dx.doi.org/10.1136/gutjnl-2016-311456.

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Aims and backgroundPsychological stress accompanies chronic inflammatory diseases such as IBD, and stress hormones can exacerbate pain signalling. In contrast, the endogenous opioid system has an important analgesic action during chronic inflammation. This study examined the interaction of these pathways.MethodsMouse nociceptive dorsal root ganglia (DRG) neurons were incubated with supernatants from segments of inflamed colon collected from patients with chronic UC and mice with dextran sodium sulfate (cDSS)-induced chronic colitis. Stress effects were studied by adding stress hormones (epinephrine and corticosterone) to dissociated neurons or by exposing cDSS mice to water avoidance stress. Changes in excitability of colonic DRG nociceptors were measured using patch clamp and Ca2+imaging techniques.ResultsSupernatants from patients with chronic UC and from colons of mice with chronic colitis caused a naloxone-sensitive inhibition of neuronal excitability and capsaicin-evoked Ca2+responses. Stress hormones decreased signalling induced by human and mouse supernatants. This effect resulted from stress hormones signalling directly to DRG neurons and indirectly through signalling to the immune system, leading to decreased opioid levels and increased acute inflammation. The net effect of stress was a change endogenous opioid signalling in DRG neurons from an inhibitory to an excitatory effect. This switch was associated with a change in G protein-coupled receptor excitatory signalling to a pathway sensitive to inhibitors of protein kinase A-protein, phospholipase C-protein and G protein βϒ subunits.ConclusionsStress hormones block the inhibitory actions of endogenous opioids and can change the effect of opioid signalling in DRG neurons to excitation. Targeting these pathways may prevent heavy opioid use in IBD.
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Wang, Yishu, Enhang Lu, Riqiang Bao, et al. "Notch signalling regulates steroidogenesis in mouse ovarian granulosa cells." Reproduction, Fertility and Development 31, no. 6 (2019): 1091. http://dx.doi.org/10.1071/rd18281.

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The Notch signalling pathway in the mammalian ovary regulates granulosa cell proliferation. However, the effects of Notch signalling on steroidogenesis are unclear. In this study we cultured mouse ovarian granulosa cells from preantral follicles invitro and observed the effect of Notch signalling on steroidogenesis through overexpression, knockdown and inhibition of Notch signalling. Activation of Notch signalling decreased progesterone and oestrogen secretion. In contrast, inhibition of Notch signalling increased the production of progesterone and oestrogen. Expression of the genes for steroidogenic-related enzymes, including 3β-hydroxysteroid dehydrogenase, p450 cholesterol side-chain cleavage enzyme and aromatase, was repressed after stimulation of Notch signalling. The expression of upstream transcription factors, including steroidogenic factor 1 (SF1), Wilms’ tumour 1 (Wt1), GATA-binding protein 4 (Gata4) and Gata6, was also inhibited after stimulation of Notch signalling. Production of interleukin (IL)-6 was positively correlated with Notch signalling and negatively correlated with the expression of these transcription factors and enzymes. In conclusion, Notch signalling regulated progesterone and oestrogen secretion by affecting the expression of upstream transcription factors SF1, Wt1, Gata4 and Gata6, as well as downstream steroidogenic-related enzymes. IL-6, which may be regulated directly by Notch signalling, may contribute to this process. Our findings add to the understanding of the diverse functions of Notch signalling in the mammalian ovary.
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Šrámek, Jan, Vlasta Němcová-Fürstová та Jan Kovář. "Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells". International Journal of Molecular Sciences 22, № 8 (2021): 4285. http://dx.doi.org/10.3390/ijms22084285.

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Pancreatic β-cell failure and death contribute significantly to the pathogenesis of type 2 diabetes. One of the main factors responsible for β-cell dysfunction and subsequent cell death is chronic exposure to increased concentrations of FAs (fatty acids). The effect of FAs seems to depend particularly on the degree of their saturation. Saturated FAs induce apoptosis in pancreatic β-cells, whereas unsaturated FAs are well tolerated and are even capable of inhibiting the pro-apoptotic effect of saturated FAs. Molecular mechanisms of apoptosis induction by saturated FAs in β-cells are not completely elucidated. Saturated FAs induce ER stress, which in turn leads to activation of all ER stress pathways. When ER stress is severe or prolonged, apoptosis is induced. The main mediator seems to be the CHOP transcription factor. Via regulation of expression/activity of pro- and anti-apoptotic Bcl-2 family members, and potentially also through the increase in ROS production, CHOP switches on the mitochondrial pathway of apoptosis induction. ER stress signalling also possibly leads to autophagy signalling, which may activate caspase-8. Saturated FAs activate or inhibit various signalling pathways, i.e., p38 MAPK signalling, ERK signalling, ceramide signalling, Akt signalling and PKCδ signalling. This may lead to the activation of the mitochondrial pathway of apoptosis, as well. Particularly, the inhibition of the pro-survival Akt signalling seems to play an important role. This inhibition may be mediated by multiple pathways (e.g., ER stress signalling, PKCδ and ceramide) and could also consequence in autophagy signalling. Experimental evidence indicates the involvement of certain miRNAs in mechanisms of FA-induced β-cell apoptosis, as well. In the rather rare situations when unsaturated FAs are also shown to be pro-apoptotic, the mechanisms mediating this effect in β-cells seem to be the same as for saturated FAs. To conclude, FA-induced apoptosis rather appears to be preceded by complex cross talks of multiple signalling pathways. Some of these pathways may be regulated by decreased membrane fluidity due to saturated FA incorporation. Few data are available concerning molecular mechanisms mediating the protective effect of unsaturated FAs on the effect of saturated FAs. It seems that the main possible mechanism represents a rather inhibitory intervention into saturated FA-induced pro-apoptotic signalling than activation of some pro-survival signalling pathway(s) or metabolic interference in β-cells. This inhibitory intervention may be due to an increase of membrane fluidity.
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Gleeson, Deborah J. "Context-dependent effect of social environment on immune response and sexual signalling in male zebra finches." Australian Journal of Zoology 54, no. 6 (2006): 375. http://dx.doi.org/10.1071/zo06001.

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Variation in avian immune response can be influenced by social environment. This is of particular interest in the context of immunomediated sexual behaviour because social environment may subsequently affect a bird’s relative investment in immunocompetence versus sexual signalling. I tested whether the effect of social environment on immune response and sexual signalling depends on socio-sexual status using male zebra finches (Taeniopygia guttata). To do this, I manipulated social environment (‘same sex’ versus ‘dual sex’) and socio-sexual status (‘high’ versus ‘low’) of the males. I then determined what effect these manipulations had on an index of immunocompetence, namely cell-mediated immune response, and two indices of sexual signalling (bill colour and song rate). I found that social environment influenced cell-mediated immune response and sexual signalling in low-status males. These males had lower immune responses and increased sexual signalling in the dual-sex environment compared with the same-sex environment. In contrast, high-status males had similar immune responses and sexual signalling regardless of social environment. These results suggest that social environment can influence immune response and sexual signalling; however, the nature of this effect was context-dependent, with low-status males more affected than high-status males.
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Benzler, Jonas, Goutham K. Ganjam, Manon Krüger та ін. "Hypothalamic glycogen synthase kinase 3β has a central role in the regulation of food intake and glucose metabolism". Biochemical Journal 447, № 1 (2012): 175–84. http://dx.doi.org/10.1042/bj20120834.

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GSK3β (glycogen synthase kinase 3β) is a ubiquitous kinase that plays a key role in multiple intracellular signalling pathways, and increased GSK3β activity is implicated in disorders ranging from cancer to Alzheimer's disease. In the present study, we provide the first evidence of increased hypothalamic signalling via GSK3β in leptin-deficient Lepob/ob mice and show that intracerebroventricular injection of a GSK3β inhibitor acutely improves glucose tolerance in these mice. The beneficial effect of the GSK3β inhibitor was dependent on hypothalamic signalling via PI3K (phosphoinositide 3-kinase), a key intracellular mediator of both leptin and insulin action. Conversely, neuron-specific overexpression of GSK3β in the mediobasal hypothalamus exacerbated the hyperphagia, obesity and impairment of glucose tolerance induced by a high-fat diet, while having little effect in controls fed standard chow. These results demonstrate that increased hypothalamic GSK3β signalling contributes to deleterious effects of leptin deficiency and exacerbates high-fat diet-induced weight gain and glucose intolerance.
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Strembitska, Anastasiya, Sarah Mancini, Jonathan Gamwell, Timothy Palmer, George Baillie, and Ian Salt. "A769662 Inhibits Insulin-Stimulated Akt Activation in Human Macrovascular Endothelial Cells Independent of AMP-Activated Protein Kinase." International Journal of Molecular Sciences 19, no. 12 (2018): 3886. http://dx.doi.org/10.3390/ijms19123886.

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Protein kinase B (Akt) is a key enzyme in the insulin signalling cascade, required for insulin-stimulated NO production in endothelial cells (ECs). Previous studies have suggested that AMP-activated protein kinase (AMPK) activation stimulates NO synthesis and enhances insulin-stimulated Akt activation, yet these studies have largely used indirect activators of AMPK. The effects of the allosteric AMPK activator A769662 on insulin signalling and endothelial function was therefore examined in cultured human macrovascular ECs. Surprisingly, A769662 inhibited insulin-stimulated NO synthesis and Akt phosphorylation in human ECs from umbilical veins (HUVECs) and aorta (HAECs). In contrast, the AMPK activators compound 991 and AICAR had no substantial inhibitory effect on insulin-stimulated Akt phosphorylation in ECs. Inhibition of AMPK with SBI-0206965 had no effect on the inhibition of insulin-stimulated Akt phosphorylation by A769662, suggesting the inhibitory action of A769662 is AMPK-independent. A769662 decreased IGF1-stimulated Akt phosphorylation yet had no effect on VEGF-stimulated Akt signalling in HUVECs, suggesting that A769662 attenuates early insulin/IGF1 signalling. The effects of A769662 on insulin-stimulated Akt phosphorylation were specific to human ECs, as no effect was observed in the human cancer cell lines HepG2 or HeLa, as well as in mouse embryonic fibroblasts (MEFs). A769662 inhibited insulin-stimulated Erk1/2 phosphorylation in HAECs and MEFs, an effect that was independent of AMPK in MEFs. Therefore, despite being a potent AMPK activator, A769662 has effects unlikely to be mediated by AMPK in human macrovascular ECs that reduce insulin sensitivity and eNOS activation.
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BHATTACHARYYA, Asima, Shresh PATHAK, Simanti DATTA, Santanu CHATTOPADHYAY, Joyoti BASU та Manikuntala KUNDU. "Mitogen-activated protein kinases and nuclear factor-κB regulate Helicobacter pylori-mediated interleukin-8 release from macrophages". Biochemical Journal 368, № 1 (2002): 121–29. http://dx.doi.org/10.1042/bj20020555.

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Gastric infection, as well as inflammation, caused by Helicobacter pylori, activates the production of cytokines and chemokines by mononuclear cells; interleukin-8 (IL-8) is one of the major inflammatory chemokines. Since H. pylori does not invade mucosal tissue, we observed the effect of the water extract of H. pylori (HPE), containing shed factors, on the production of IL-8 by human peripheral blood monocytes and the human monocyte cell line THP-1. HPE-treatment induced activation of the mitogen-activated protein kinases (MAPKs) ERK (extracellular signal-regulated kinase), p38 and JNK (c-Jun N-terminal kinase), an effect which was not dependent on the presence of the cag pathogenicity island. p38 MAPK activation was sustained. The specific inhibitors, U0126 (for ERK1/2 signalling) and SB203580 (for p38 MAPK signalling), both abrogated IL-8 secretion from HPE-treated THP-1. Dominant-negative mutants of the upstream kinases MEK1 (MAPK/ERK kinase 1), MKK (MAPK kinase) 6 and MKK7 also inhibited IL-8 secretion, pointing to a role of all three MAPKs in HPE-mediated IL-8 release. The inhibitory effects of polymyxin B and anti-CD14 antibody suggested that the effect of HPE on MAPKs was mediated by H. pylori lipopolysaccharide (LPS). By analysis of IL-8-promoter-driven luciferase gene expression, we observed that the effects of HPE-induced nuclear factor-κB (NF-κB) activation and MAPK signalling were mediated at the level of the IL-8 promoter. While ERK1/2 activation could be linked to enhanced DNA binding of activator protein-1 (AP-1), p38 MAPK signalling did not affect AP-1 DNA binding. Taken together, these results provide the first evidence that LPS from H. pylori stimulates IL-8 release from cells of the monocytic lineage through activation of NF-κB and signalling along MAPK cascades. The stimulation of MAPK signalling in macrophages by LPS of H. pylori amplifies the inflammatory response associated with gastric H. pylori infection and needs to be taken into consideration when developing therapeutics based on these signalling pathways.
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Elbialy, Abdalla. "The role of antioxidants in restoring MAPK 14 and a DNA damage marker level following autophagy suppression." Open Biology 10, no. 12 (2020): 200253. http://dx.doi.org/10.1098/rsob.200253.

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Autophagy is a lysosomal degradation mechanism for elimination and recycling of damaged intracellular organelles and proteins. Recent studies have shown that autophagy could help reduce oxidative stress by removing oxidized proteins and damaged mitochondria. Autophagy deficiency is associated with the disruption of many intracellular biological processes. Using bioinformatics tools and fibroblast immunostaining technology, I tried to investigate whether oxidative stress is involved in mediating the effect of autophagy suppression on certain cell biological processes and signalling pathways. Many pharmaceutical components have different modes of action to suppress autophagy. In this study, I performed analysis on autophagy suppression induced by neutralizing lysosomal pH (NH 4 Cl and bafilomycin A1). Bioinformatics analysis of GEO data, GSE60570 accession number, revealed that p38 signalling induction and DNA damage response are among the main disrupted signalling pathways in bafilomycin A1-treated RPE-1 cells. Likewise, fibroblast immunostaining showed that autophagy deficiency established by ammonium chloride (NH 4 Cl) has significantly increased P38 signalling, DNA damage marker (H2A.X), and oxidative stress marker (dityrosine). I therefore investigated the role of oxidative stress and whether antioxidants treatment could reverse autophagy suppression effects on p38 signalling and DNA damage response. Importantly, antioxidant treatment clearly restored P38 signalling and H2A.X levels in autophagy-suppressed fibroblast cells. Indicating that oxidative stress might be associated with the harmful effect of autophagy suppression.
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Zhang, Jiandi. "Resveratrol inhibits insulin responses in a SirT1-independent pathway." Biochemical Journal 397, no. 3 (2006): 519–27. http://dx.doi.org/10.1042/bj20050977.

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Resveratrol mimics calorie restriction to extend lifespan of Caenorhabditis elegans, yeast and Drosophila, possibly through activation of Sir2 (silent information regulator 2), a NAD+-dependent histone deacetylase. In the present study, resveratrol is shown to inhibit the insulin signalling pathway in several cell lines and rat primary hepatocytes in addition to its broad-spectrum inhibition of several signalling pathways. Resveratrol effectively inhibits insulin-induced Akt and MAPK (mitogen-activated protein kinase) activation mainly through disruption of the interactions between insulin receptor substrates and its downstream binding proteins including p85 regulatory subunit of phosphoinositide 3-kinase and Grb2 (growth factor receptor-bound protein 2). The inhibitory effect of resveratrol on insulin signalling is also demonstrated at mRNA level, where resveratrol reverses insulin effects on phosphoenolpyruvate carboxykinase, glucose-6-phosphatase, fatty acid synthase and glucokinase. In addition, RNA interference experiment shows that the inhibitory effect of resveratrol on insulin signalling pathway is not weakened in cells with reduced expression of SirT1, the mammalian counterpart of Sir2. These observations raise the possibility that resveratrol may additionally modulate lifespan through inhibition of insulin signalling pathway, independently of its activation of SirT1 histone deacetylase. Furthermore, the present study may help to explain a wide range of biological effects of resveratrol, and provides further insight into the molecular basis of calorie restriction.
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Dissertations / Theses on the topic "Signalling effect"

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Steinwald, Hannah. "Effect of signalling a positive reinforcer on contextual conditioning." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59864.

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Three experiments used an appetitive Pavlovian conditioning procedure to investigate the ability of the context to generate excitation. Discrete stimuli (CSs) signalling food unconditioned stimuli (USs) were used to decrease contextual conditioning. Detailed observations of the behaviours of rats during and immediately preceding the presentation of CSs, and in an event-free period were analysed. Experiment 1 showed that a discrete visual CS was able to interfere with contextual conditioning because it was a more efficient cue for food than the context. Experiment 2 found that an auditory CS could reduce contextual conditioning in a similar manner but the topography of responding during the event-free period was specific to the modality of the CS. Experiment 3 demonstrated that signal-appropriate responding during the event-free period occurred only if the CS was a signal for reinforcement.
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Hopkinson, Helen Elizabeth. "Beta←2-adrenoceptor signalling and the effect of insulin." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301070.

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Scott, Sarah Anne. "The effect of glial signalling on dopamine neuronal differentiation." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612827.

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Wong, Tin Lok. "Mechanism of action of silicon in cell signalling." Thesis, University of Cambridge, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709339.

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Giuliano, Simon 1975. "Calcium signalling regulating platelet adhesion and thrombus growth." Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/7875.

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Pandey, Vibhor. "Quality signalling: The effect of innovation programs on innovation-driven enterprises." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/209165/1/Vibhor_Pandey_Thesis.pdf.

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This thesis takes a novel approach to evaluate the impact of the public policies of innovation and entrepreneurship on individual firms. This evaluation research uses 10-year time series data on Queensland businesses, Advance Queensland (AQ) program data and public datasets to investigate what types of companies get selected for the AQ program and the overall impact of these policies on innovation-driven entrepreneurship. The study found corrective general market behaviour and had a significant effect on the firms. The thesis contributes to the theory of entrepreneurial “Quality Signalling” and the government’s approach to the “Picking Winners” and “Picking the Willing” phenomenon.
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Wadley, Glenn, and mikewood@deakin edu au. "Regulation of insulin signalling by exercise in skeletal muscle." Deakin University. School of Health Sciences, 2003. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050826.111050.

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Regular physical activity improves insulin action and is an effective therapy for the treatment and prevention of type 2 diabetes. However, little is known of the mechanisms by which exercise improves insulin action in muscle. These studies investigate the actions of a single bout of exercise and short-term endurance training on insulin signalling. Twenty-four hours following the completion of a single bout of endurance exercise insulin action improved, although greater enhancement of insulin action was demonstrated following the completion of endurance training, implying that cumulative bouts of exercise substantially increase insulin action above that seen from the residual effects of an acute bout of prior exercise. No alteration in the abundance and phosphorylation of proximal members of the insulin-signalling cascade in skeletal muscle, including the insulin receptor and IRS-1 were found. A major finding however, was the significant increase in the serine phosphorylation of a known downstream signalling protein, Akt (1.5 fold, p ≤0.05) following an acute bout of exercise and exercise training. This was matched by the observed increase in protein abundance of SHPTP2 (1.6 fold, p ≤0.05) a protein tyrosine phosphatase, in the cytosolic fraction of skeletal muscle following endurance exercise. These data suggest a small positive role for SHPTP2 on insulin stimulated glucose transport consistent with transgenic mice models. Further studies were aimed at examining the gene expression following a single bout of either resistance or endurance exercise. There were significant transient increases in IRS-2 mRNA concentration in the few hours following a single bout of both endurance and resistance exercise. IRS-2 protein abundance was also observed to significantly increase 24-hours following a single bout of endurance exercise indicating transcriptional regulation of IRS-2 following muscular contraction. One final component of this PhD project was to examine a second novel insulin-signalling pathway via c-Cbl tyrosine phosphorylation that has recently been shown to be essential for insulin stimulated glucose uptake in adipocytes. No evidence was found for the tyrosine phosphorylation of c-Cbl in the skeletal muscle of Zucker rats despite demonstrating significant phosphorylation of the insulin receptor and Akt by insulin treatment and successfully immunoprecipitating c-Cbl protein. Surprisingly, there was a small but significant increase in c-Cbl protein expression following insulin-stimulation, however c-Cbl tyrosine phosphorylation does not appear to be associated with insulin or exercise-mediated glucose transport in skeletal muscle.
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Al-Abri, Abdulrahim. "Investigating the effect of PIP4K2a overexpression in insulin signalling in L6 myotubes." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-effect-of-pip4k2a-overexpression-in-insulin-signalling-in-l6-myotubes(1dd2d1dd-c765-4830-9b66-cf32a64d7de9).html.

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Insulin signalling is an essential process in humans by which the level of plasma glucose is maintained within the physiologically healthy range. Insulin activates the phosphoinositide 3 kinase (PI3K) signalling pathway that generates the phospholipid messenger PtdIns(3,4,5)P3, which in turn enhances the activity of two important proteins, AKT and Rac1. This then leads to increase the presence of the glucose transporter 4 (GLUT4) at the plasma membrane that enhances the intake of glucose, particularly in skeletal muscle cells and adipocytes. Insulin signalling also triggers interconversion of several other phosphoinositides (PIs) which play pivotal roles in different steps of glucose regulation. PtdIns5P is an important PI that is robustly increased after insulin treatment in the skeletal muscle cell line, L6 myotubes. Many of PtdIns5P`s functions are not fully understood. To gain more knowledge of the role of PtdIns5P in insulin signalling in muscle cells, the PtdIns5P kinase phosphatidylinositol-5-phosphate 4-kinase a (PIP4K2a) was over-expressed in L6 myotubes as a way of removing PtdIns5P, and the consequences in insulin signalling were studied. Although PtdIns5P is converted by PIP4K2a to PtdIns(4,5)P2 which is a precursor of the potent PI PtdIns(3,4,5)P3, previous studies revealed that the increase in PtdIns(3,4,5)P3 induced by insulin in control cells is diminished in cells overexpressing PIP4K2a, for unknown reasons. Additionally, although the phosphorylation of the serine/threonine protein kinase AKT was not affected in these L6 cells, glucose uptake was attenuated. The current study investigates the possible causes of attenuating glucose uptake in PIP4K overexpressing myotubes by examining the small GTPase Rac1 which plays an important role in the cytoskeleton re-arrangement that is necessary for GLUT4 translocation. Furthermore, the possible roles of PI phosphatases that may cause the disturbance on the levels of PIs in response to insulin were evaluated. Additionally, the potential role of PtdIns5P in Rac1 activation in L6 myotubes was further investigated by delivering synthetic PtdIns5P using a carrier-based delivery approach. The results showed that the attenuation of glucose uptake documented in previous studies occurred as a result of a defect in the process of translocating GLUT4 from intracellular storage to the plasma membrane. Rac1 activity was significantly reduced in cells expressing PIP4K2a. Quantifying the level of PIs suggested that PIP4K2a expression increases the removal of PtdIns(3,4,5)P3 by the PI 5-phosphatase, SKIP. Silencing the expression of SKIP by siRNA restored the level of PtdIns(3,4,5)P3 but Rac1 activity and the attenuation GLUT4 translocation were not rescued possibly as a result of removing PtdIns5P by PIP4K2a. On the other hand, exogenous delivery of PtdIns5P in L6 myotubes activates both Rac1 and GLUT4 translocation in the absence of insulin. However, activating GLUT4 translocation by the exogenous PtdIns5P requires PI3K activity since redistribution of GLUT4 to the plasma membrane is inhibited by the PI3K inhibitor, wortmannin. Removing PtdIns5P reduces Rac1 activity and stimulates SKIP that inhibits PtdIns(3,4,5)P3 increase which attenuates GLUT4 translocation and hence glucose uptake. These results emphasise the critical role played by PtdIns5P which seems to serve as a regulator of insulin signalling, both directly and/or by regulating other enzymes involved in the metabolism of PIs.
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Ali, Tarek Adel. "Effect of implant surface roughness on the NFkB signalling pathway in macrophages." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2436.

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Physical stress such as the surface roughness of the implants may activate the NFkB signalling pathway in macrophages. This activation is intimately related to the mechanism(s) by which the macrophage interacts with the surface through serum proteins and/or the formation of membrane rafts. This thesis examines the role of surface topography on activation of the NFkB signalling pathway in macrophages. We examined the effect of implant surface topography on activating the NFkB signalling pathway in the RAW 264.7 macrophage cell line. We also examined the effect surface roughness had on the adhesion of the macrophages using the different media. To finish, we observed the effect the different media and the surface roughness had on the morphology of the macrophages by Scanning Electron Microscopy. Activation of the NFkB pathway was surface topography dependent. The Smooth surface showed the highest level of activation followed by the Etched then the SLA. Addition of suboptimal concentrations of LPS mildly enhanced the response by signalling through the Toll receptor. Activation of NFKB occurred in the absence of fetal calf sera, although to a lesser extent. All three surfaces had very few cells with nuclear translocation at the 5 minutes time point with no significant statistical differences between the surfaces. After 30 minutes, translocation reached comparable levels to those surfaces tested with complete medium. Disruption of the lipid rafts affected the triggering and signalling of the NFkB pathway. This inhibitory effect was concentration and time dependent. Smooth surfaces bound more macrophages in the 30 minutes assay. Fetal calf serum appeared to be very critical for adhesion and spreading of the macrophages on the various surfaces examined. Removal of cholesterol did not affect adhesion or spreading on their respective surfaces. We have clearly demonstrated that the lipid rafts along with surface topography play a role in the activation on NFKB. This in-vitro study has demonstrated that surface topography modulated activation of the NFKB signalling pathway in a time-dependent manner. However, at present, it is unclear through which receptor(s) / surface structure the signal pathway is initiated.
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Zihni, Ceniz. "The effect of adrenomedullin on growth-associated signalling pathways in vascular cells." Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396311.

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Books on the topic "Signalling effect"

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N, Verkhratskiĭ A., and Toescu Emil C, eds. Integrative aspects of calcium signalling. Plenum Press, 1998.

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Tuominen-Gustafsson, Helena Birgitta. Calcium signalling pathways in human neutrophils. Åbo Akademis Förlag, 1998.

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D, Houslay Miles, and Milligan Graeme, eds. G-proteins as mediators of cellular signalling processes. Wiley, 1990.

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Paul, Mattson Mark, ed. Calcium homeostasis and signalling in aging. Elsevier, 2002.

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Ernesto, Carafoli, and Brini Marisa, eds. Calcium signalling and disease: Molecular pathology of calcium. Springer, 2007.

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Ramzan, Mohammad. An analysis of the effect of intra-firm exchange offer and stock swap announcements on stockholder's wealth: A signalling approach under asymmetric information. University College Dublin, 1995.

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Lee, Won Heum. The effect of exchange offers and stock swaps on equity risk and shareholders' wealth: A signalling model approach : a dissertation submitted in partial satisfaction of the requirements for the degree of Doctor of Philosophy in Management. UMI Dissertation Services, 1992.

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Horowitz, John. The effects of hypergravic fields on neural signalling in the hippocampus. National Aeronautics and Space Administration, 1991.

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H, Michell R., Drummond Alan H, and Downes C. Peter, eds. Inositol lipids in cell signalling. Academic Press, 1989.

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

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Book chapters on the topic "Signalling effect"

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Kondo, Sylvia, Colin J. Wilde, Gillian D. Bryant-Greenwood, Eleanor Taylor, Malcolm Peaker, and Lynn M. Boddy-Finch. "Effect of Relaxin on Primary Cultures of Goat Mammary Epithelial Cells." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_17.

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Purup, Stig, Yael Sandowski, and Kris Sejrsen. "Endocrine Effect of IGF-I on Mammary Growth in Prepubertal Heifers." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_20.

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Bowden, Christine E., Karen Plaut, and Rhonda L. Maple. "Effect of Plane of Nutrition on Mammary Gland Development in Prepubertal Goats." In Intercellular Signalling in the Mammary Gland. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_9.

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Caré, Bertrand R., and Hédi A. Soula. "The Effect of Membrane Receptor Clustering on Spatio-temporal Cell Signalling Dynamics." In Information Processign in Cells and Tissues. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-28792-3_8.

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Degitz, C., S. Reime, and O. Thews. "Effect of Acidosis-Induced Signalling Pathways on Mitochondrial O2 Consumption of Tumour Cells." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-14190-4_38.

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M�ller, W. E., A. Eckert, H. Hartmann, and H. F�rstl. "The Amplifying Effect of β-Amyloid on Cellular Calcium Signalling in Alzheimer's Disease." In Basic and Clinical Science of Mental and Addictive Disorders. KARGER, 1997. http://dx.doi.org/10.1159/000059504.

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Amato, M., S. Aterini, S. Pacini, and M. Ruggiero. "Effect of Vitamin E Conjugated to Dialysis Membranes on Immunohematopoietic Cell Growth and Signalling." In Contributions to Nephrology. KARGER, 1999. http://dx.doi.org/10.1159/000059996.

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Raghul, E. I., and K. Aravindan. "Chemotherapeutic Effect of Lutein on TGFβ/Smad2 Signalling Molecules Gene Expression in Oral Cancer Cells." In Recent Developments in Microbiology, Biotechnology and Pharmaceutical Sciences. CRC Press, 2025. https://doi.org/10.1201/9781003618140-7.

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De Pauw, Ines, Carolien Boeckx, and An Wouters. "Mechanisms of Cetuximab Resistance and How to Overcome It." In Critical Issues in Head and Neck Oncology. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_3.

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AbstractDeregulated or increased signalling of the epidermal growth factor receptor (EGFR) plays an integral role in the development of various cancer types, including head and neck squamous cell carcinoma (HNSCC), making it a compelling drug target. However, after initially promising results of EGFR-targeted therapies, such as the monoclonal antibody cetuximab, it became clear that both intrinsic and acquired therapeutic resistance are major roadblocks in the field of personalised cancer treatments.In order to unravel and overcome resistance to cetuximab, at least two strategies can be adopted.Firstly, therapeutic resistance to anti-EGFR therapy may arise from mechanisms that can compensate for reduced EGFR signalling and/or mechanisms that can modulate EGFR-dependent signalling. In this chapter, we discuss which mechanisms of cetuximab resistance are already known and which ones deserve further investigation. This enhanced knowledge will guide us to rationally design and test novel combination therapies that overcome resistance to EGFR-targeting agents in cancer treatment.Secondly, an urgent need remains to develop novel targeted treatments for single-agent or combined therapy use. In this view, due to the particular mode of activation of the EGFR receptor, involving ligand-induced homo- and heterodimerization of the four HER receptors, an increased inhibition scope of HER receptors most likely results in a more potent blockade of the HER network, preventing premature emergence of resistance and leading to a more pronounced therapeutic benefit. We discuss two multitargeted compounds, being MEHD7945A (duligotuzumab) and afatinib, in this chapter.Despite the huge efforts to unravel the molecular landscape of HNSCC, the main clinically validated target remains EGFR. However, immune checkpoints, like programmed cell death protein 1 (PD-1), are gaining clinical approvals as well. We underscore the importance of adopting rational drug combinations to enhance the therapeutic effect of the EGFR-inhibitor cetuximab and highlight the ongoing search for predictive biomarkers, with the ultimate goal of delivering individualized cancer therapy to HNSCC patients.
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Kortstee, Anne, Fred Rook, and Sjef Smeekens. "Sucrose is a signalling molecule in plants." In Photosynthesis: Mechanisms and Effects. Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-3953-3_653.

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Conference papers on the topic "Signalling effect"

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Setiani Sumardiko, Dwi, Purwo Sri Rejeki, and Gadis Meinar Sari. "The Effect of Osteocyte Signalling on Osteocyte Apoptosis." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007333000720075.

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Rose, Ralph. "The structural signalling effect of silent and filled pauses." In The 9th Workshop on Disfluency in Spontaneous Speech. ELTE Faculty of Humanities, 2019. http://dx.doi.org/10.21862/diss-09-006-rose.

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Gallardo Hernandez, E. A., J. Cotter, R. Lewis, and D. T. Eadie. "The Effect of Friction Modifiers on Wheel/Rail Isolation." In IEEE/ASME/ASCE 2008 Joint Rail Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/jrc2008-63030.

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Train detection, for signalling purposes, is often by means of track circuits. Signalling block occupancy is triggered by the wheelset of the train ‘shorting out’ the track circuit, i.e. the wheels and axle act as a shunt. Contamination on the track such as ballast dust, rust, oil, or leaves as well as substances designed to improve train operation such as friction modifiers or sand may cause the contact between the wheelsets and the track to be compromised, inhibiting train identification. In previous work a twin disc approach has been used to study the effect of sand (used to improve adhesion) and leaves on wheel/rail isolation. Friction modifiers are of significant current interest in wheel/rail research. Introducing a new material into the tread/top of rail interface can raise questions about the impact on signalling systems. Although no significant effects have been observed in practical operation on a range of railway systems, the intention in this work was to evaluate conductance between wheel and rail in a more controlled and systematic fashion using the previously established methodology. Using the twin disc technique, friction modifier, in the form of a solid stick, was applied using a spring loaded device to the rotating wheel disc to generate a visible film. Tests were run to measure contact impedance at typical loads and slips. Static tests were also carried out using discs pre-conditioned with a friction modifier film. The electrical circuit used was a modified simplified simulation of audio frequency track circuit. No significant difference was observed in the measured impedance for dry conditions with no friction modifier, versus tests where friction modifier was applied, regardless of percentage slip or input voltage. The analysis suggests that the introduction of friction modifier into the existing wheel/rail interfacial film does not result in increased impedance with all other factors being equal.
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Abadi, Mojtaba Mansour, Zabih Ghassemlooy, Manav R. Bhatnagar, Stanislav Zvanovec, Mohammad-Ali Khalighi, and Ali-Reza Maheri. "Using differential signalling to mitigate pointing errors effect in FSO communication link." In 2016 ICC - 2016 IEEE International Conference on Communications Workshops (ICC). IEEE, 2016. http://dx.doi.org/10.1109/iccw.2016.7503779.

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Barter, W. A. M. "ERTMS Level 2: effect on capacity compared with “best practice” conventional signalling." In COMPRAIL 2008. WIT Press, 2008. http://dx.doi.org/10.2495/cr080221.

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Guler, Egecan, Callum Geldard, Amy Baldwin, and Wasiu Popoola. "A Demonstration of Frequency-Shift Keying in Underwater Optical Wireless Communications." In CLEO: Applications and Technology. Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleo_at.2022.jw3b.104.

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This paper experimentally demonstrates the resilience of frequency-shift keying (FSK) signalling to turbulence effect in underwater optical wireless communications. The findings offer valuable insight into the design trade-off between spectral efficiency and resistance to turbulence.
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Ouboussad, Lylia, Chi Wong, Laura Hunt, et al. "03.24 Effect of tocilizumab therapy on il-6 signalling pathway in early rheumatoid arthritis patients." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211049.24.

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Lebedeva, Elena S., Natalya N. Kuzubova, Olga N. Titova, and Elena A. Surkova. "Effect of cyclooxygenase-2 inhibition on lung inflammation and hypoxia-inducible factor-1 signalling in COPD model." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3926.

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Yang, Jasemine S., Sima Allahverdian, Gurpreet K. Singhera, Ruth MacRedmond, and Delbert Dorscheid. "IL-13R±2 / AP-1 Complex Signalling Mediates Airway Epithelial Repair With No Effect On Remodeling Pathways." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2489.

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Rider, Christopher F., Suharsh Shah, David D. Gaunt, et al. "TNF±-Induced Glucocorticoid Resistance: Inhibition Of Inflammatory Signalling And The Effect On Full And Partial GR Agonists." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6267.

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Reports on the topic "Signalling effect"

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Hambur, Jonathan, and Qazi Haque. Can We Use High-frequency Yield Data to Better Understand the Effects of Monetary Policy and Its Communication? Yes and No! Reserve Bank of Australia, 2023. http://dx.doi.org/10.47688/rdp2023-04.

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Understanding the effects of monetary policy and its communication is crucial for a central bank. This paper explores a new approach to identifying the effects of monetary policy using high-frequency data around monetary policy decisions and other announcements that allows us to explore different facets of monetary policy, specifically: current policy action; signalling or forward guidance about future rates; and the effect on uncertainty and term premia. The approach provides an intuitive lens through which to understand how policy and its communication affected expectations for rates and risks during certain historical periods, and more generally. For example, it suggests that: (i) signalling/forward guidance shocks tended to raise expected future policy rates in the mid-2010s as the RBA highlighted rising risks in housing markets; (ii) COVID-19-era monetary policy worked mainly through affecting term premia rather than expectations for future policy rates, unlike pre-COVID-19 policy; and (iii) shocks to the expected path of rates are predictable based on data available at the time, which suggests that markets systematically misunderstand how the RBA reacts to data, highlighting the importance of clear communication. We also explore the macroeconomic effects of these different shocks. The effects of shocks to current policy are similar to those estimated in previous papers, and existing issues such as the 'price puzzle' remain, while the effects of other shocks are imprecisely estimated. Although the approach provides little new information on the macroeconomic effects of monetary policy, it does highlight the importance of these other facets of policy in moving interest rates and suggests additional work in this space could be valuable.
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Luo, Fang, han-han Chen, Jun-Jie Feng, et al. Effect of acupuncture on insulin signalling pathway and mitochondrial AMPK pathway in animal model of type 2 diabetes mellitus:A systematic evaluation and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2023. http://dx.doi.org/10.37766/inplasy2023.11.0086.

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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, 2010. http://dx.doi.org/10.32747/2010.7592116.bard.

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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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Wan, Wilfred, and Nivedita Raju. Escalation Risks at the Space–Nuclear Nexus. Stockholm International Peace Research Institute, 2024. http://dx.doi.org/10.55163/fzdw6296.

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Space systems are essential for nuclear and non-nuclear missions for China, Russia and the United States, with the space domain central in their national security strategies. Amid the strategic competition and rivalry between the three states, their threat perceptions exhibit unprecedented levels of worst-case scenario thinking, signalling a preparedness to respond with force in case of attacks or incidents involving space systems. Escalation risks in outer space, even possibly extending to the use of nuclear weapons, thus appear to be growing, especially as the deterrent role of such weapons is expanding to account for more capabilities with strategic effect. While different variables will impact escalation dynamics at the intersection of outer space, nuclear weapons and related systems (the ‘space–nuclear nexus’), some factors clearly contribute to the risk of escalation. These include strategic ambiguity and unclear red lines on what actions could result in potential nuclear retaliation. These fuzzy red lines are further blurred by the many uncertainties in space operations, such as congestion of orbits, considerations of potential civilian harm, the role of commercial actors in space, and the integration of artificial intelligence into space systems. Additional space–nuclear-related risk reduction measures are therefore vital. This paper proposes measures at the multilateral, bilateral and unilateral levels for China, Russia and the USA to consider.
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Granot, David, Richard Amasino, and Avner Silber. Mutual effects of hexose phosphorylation enzymes and phosphorous on plant development. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7587223.bard.

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Research objectives 1) Analyze the combined effects of hexose phosphorylation and P level in tomato and Arabidopsis plants 2) Analyze the combined effects of hexose phosphorylation and P level in pho1 and pho2 Arabidopsis mutants 3) Clone and analyze the PHO2 gene 4) Select Arabidopsis mutants resistant to high and low P 5) Analyze the Arabidopsis mutants and clone the corresponding genes 6) Survey wild tomato species for growth characteristics at various P levels Background to the topic Hexose phosphorylating enzymes, the first enzymes of sugar metabolism, regulate key processes in plants such as photosynthesis, growth, senescence and vascular transport. We have previously discovered that hexose phosphorylating enzymes might regulate these processes as a function of phosphorous (P) concentration, and might accelerate acquisition of P, one of the most limiting nutrients in the soil. These discoveries have opened new avenues to gain fundamental knowledge about the relationship between P, sugar phosphorylation and plant development. Since both hexose phosphorylating enzymes and P levels affect plant development, their interaction is of major importance for agriculture. Due to the acceleration of senescence caused by the combined effects of hexose phosphorylation and P concentration, traits affecting P uptake may have been lost in the course of cultivation in which fertilization with relatively high P (30 mg/L) are commonly used. We therefore intended to survey wild tomato species for high P-acquisition at low P soil levels. Genetic resources with high P-acquisition will serve not only to generate a segregating population to map the trait and clone the gene, but will also provide a means to follow the trait in classical breeding programs. This approach could potentially be applicable for other crops as well. Major conclusions, solutions, achievements Our results confirm the mutual effect of hexose phosphorylating enzymes and P level on plant development. Two major aspects of this mutual effect arose. One is related to P toxicity in which HXK seems to play a major role, and the second is related to the effect of HXK on P concentration in the plant. Using tomato plants we demonstrated that high HXK activity increased leaf P concentration, and induced P toxicity when leaf P concentration increases above a certain high level. These results further support our prediction that the desired trait of high-P acquisition might have been lost in the course of cultivation and might exist in wild species. Indeed, in a survey of wild species we identified tomato species that acquired P and performed better at low P (in the irrigation water) compared to the cultivated Lycopersicon esculentum species. The connection between hexose phosphorylation and P toxicity has also been shown with the P sensitive species VerticordiaplumosaL . in which P toxicity is manifested by accelerated senescence (Silber et al., 2003). In a previous work we uncovered the phenomenon of sugar induced cell death (SICD) in yeast cells. Subsequently we showed that SICD is dependent on the rate of hexose phosphorylation as determined by Arabidopsis thaliana hexokinase. In this study we have shown that hexokinase dependent SICD has many characteristics of programmed cell death (PCD) (Granot et al., 2003). High hexokinase activity accelerates senescence (a PCD process) of tomato plants, which is further enhanced by high P. Hence, hexokinase mediated PCD might be a general phenomena. Botrytis cinerea is a non-specific, necrotrophic pathogen that attacks many plant species, including tomato. Senescing leaves are particularly susceptible to B. cinerea infection and delaying leaf senescence might reduce this susceptibility. It has been suggested that B. cinerea’s mode of action may be based on induction of precocious senescence. Using tomato plants developed in the course of the preceding BARD grant (IS 2894-97) and characterized throughout this research (Swartzberg et al., 2006), we have shown that B. cinerea indeed induces senescence and is inhibited by autoregulated production of cytokinin (Swartzberg et al., submitted). To further determine how hexokinase mediates sugar effects we have analyzed tomato plants that express Arabidopsis HXK1 (AtHXK1) grown at different P levels in the irrigation water. We found that Arabidopsis hexokinase mediates sugar signalling in tomato plants independently of hexose phosphate (Kandel-Kfir et al., submitted). To study which hexokinase is involved in sugar sensing we searched and identified two additional HXK genes in tomato plants (Kandel-Kfir et al., 2006). Tomato plants have two different hexose phosphorylating enzymes; hexokinases (HXKs) that can phosphorylate either glucose or fructose, and fructokinases (FRKs) that specifically phosphorylate fructose. To complete the search for genes encoding hexose phosphorylating enzymes we identified a forth fructokinase gene (FRK) (German et al., 2004). The intracellular localization of the four tomato HXK and four FRK enzymes has been determined using GFP fusion analysis in tobacco protoplasts (Kandel-Kfir et al., 2006; Hilla-Weissler et al., 2006). One of the HXK isozymes and one of the FRK isozymes are located within plastids. The other three HXK isozymes are associated with the mitochondria while the other three FRK isozymes are dispersed in the cytosol. We concluded that HXK and FRK are spatially separated in plant cytoplasm and accordingly might play different metabolic and perhaps signalling roles. We have started to analyze the role of the various HXK and FRK genes in plant development. So far we found that LeFRK2 is required for xylem development (German et al., 2003). Irrigation with different P levels had no effect on the phenotype of LeFRK2 antisense plants. In the course of this research we developed a rapid method for the analysis of zygosity in transgenic plants (German et al., 2003).
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Yu, Mei, Pengyu Wang, Binbin Li, et al. NRSF Negatively Regulates Microglial Pro-Inflammatory Activation. Progress in Neurobiology, 2024. http://dx.doi.org/10.60124/j.pneuro.2024.20.02.

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Microglial activation contributes to neurological disorders like Parkinson’s disease (PD), and modulating this activation is a potential therapeutic approach. The neuron-restrictive silencer factor (NRSF) functions as a negative regulator of gene transcription through epigenetic modifications. While previous research has primarily examined the role of NRSF in neuronal differentiation and injury, emerging evidence indicates that NRSF also plays a significant role in maintaining the phenotype of glial cells. In this study, we explored the role and underlying mechanisms of NRSF in lipopolysaccharide (LPS)-induced pro-inflammatory or interleukin-4 (IL4)-induced anti-inflammatory phenotype of microglial activation. Following LPS stimulation, the nuclear localization of NRSF increased in BV2 microglial cells, primary mouse microglia, and microglia within the substantia nigra of PD mice. Knockdown of NRSF enhanced the expression of inflammation-related factors induced by LPS via the mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) and nuclear factor-κB (NF-κB) p65 signalling pathways in BV2 cells. Moreover, the culture medium from LPS-treated NRSF knockdown BV2 cells exerted greater toxic effects on human neuroblastoma SH-SY5Y cells compared to the control. However, NRSF knockdown exerted inconsistent effects on the expression of anti-inflammatory-related genes in IL4-treated BV2 cells. Our findings suggest that NRSF knockdown promotes microglial pro-inflammatory activation.
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