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Добірка наукової літератури з теми "SIGNALLING MECHANISM"

Автор: Grafiati
Опубліковано: 11 вересня 2023

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Статті в журналах з теми "SIGNALLING MECHANISM"

1

BILLESTRUP, NILS, JOHNNY A. HANSEN, LONE H. HANSEN, ANNETTE H. MOLDRUP, ELISABETH D. GALSGAARD, and JENS H. NIELSEN. "Molecular Mechanism of Growth Hormone Signalling." Endocrine Journal 45, Suppl (1998): S41—S45. http://dx.doi.org/10.1507/endocrj.45.suppl_s41.

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2

Villalobos-Labra, Roberto, Luis Silva, Mario Subiabre, Joaquín Araos, Rocío Salsoso, Bárbara Fuenzalida, Tamara Sáez, et al. "Akt/mTOR Role in Human Foetoplacental Vascular Insulin Resistance in Diseases of Pregnancy." Journal of Diabetes Research 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/5947859.

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Insulin resistance is characteristic of pregnancies where the mother shows metabolic alterations, such as preeclampsia (PE) and gestational diabetes mellitus (GDM), or abnormal maternal conditions such as pregestational maternal obesity (PGMO). Insulin signalling includes activation of insulin receptor substrates 1 and 2 (IRS1/2) as well as Src homology 2 domain-containing transforming protein 1, leading to activation of 44 and 42 kDa mitogen-activated protein kinases and protein kinase B/Akt (Akt) signalling cascades in the human foetoplacental vasculature. PE, GDM, and PGMO are abnormal conditions coursing with reduced insulin signalling, but the possibility of the involvement of similar cell signalling mechanisms is not addressed. This review aimed to determine whether reduced insulin signalling in PE, GDM, and PGMO shares a common mechanism in the human foetoplacental vasculature. Insulin resistance in these pathological conditions results from reduced Akt activation mainly due to inhibition of IRS1/2, likely due to the increased activity of the mammalian target of rapamycin (mTOR) resulting from lower activity of adenosine monophosphate kinase. Thus, a defective signalling via Akt/mTOR in response to insulin is a central and common mechanism of insulin resistance in these diseases of pregnancy. In this review, we summarise the cell signalling mechanisms behind the insulin resistance state in PE, GDM, and PGMO focused in the Akt/mTOR signalling pathway in the human foetoplacental endothelium.
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3

Laurinen, P. I., and L. A. Olzak. "Functional Aspects of Border-Signalling Mechanisms." Perception 25, no. 1_suppl (August 1996): 92. http://dx.doi.org/10.1068/v96l1208.

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Multiple border-signalling mechanisms have been proposed in some models of object segregation. We investigated whether distinct functions of different border mechanisms could be isolated in human psychophysical tasks. The display was a low-spatial-frequency (1.5 cycles deg−1) sinusoidal grating. Two types of centre-surround stimuli were produced by (i) increasing or decreasing the mean luminance of a central patch of the grating to create a signed luminance border (LB), or (ii) by shifting the grating within the central patch 180° to create a sign-reversing border (PSB) without a change in mean luminance. Grating contrast was kept constant at 20%. Observers performed a spatial 2AFC task in each condition. The PSB stimulus served as the comparison stimulus. Test stimuli were either LB or PSB+LB. The mean luminance of the central test patches varied over trials to create border contrasts of −15% to 15% Michelson contrast. In separate sessions, subjects made four types of comparisons: which of the two central areas appeared (1) to differ more in depth from its surround; (2) to have greater modulation contrast of the sinusoid; (3) lighter/darker, (4) to have higher border contrast. Results depended strongly upon test border type and suggested that the mechanism responding to each has a distinct and different perceptual function, and the two may interact. Our results support the hypothesis that surface lightness is calculated by a sign-preserving mechanism, whereas a phase-insensitive mechanism is involved in percepts relating to segregation in depth.
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4

Pagliaro, P., and C. Penna. "Redox signalling and cardioprotection: translatability and mechanism." British Journal of Pharmacology 172, no. 8 (January 12, 2015): 1974–95. http://dx.doi.org/10.1111/bph.12975.

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5

Ye, Hong, Joseph R. Arron, Betty Lamothe, Maurizio Cirilli, Takashi Kobayashi, Nirupama K. Shevde, Deena Segal, et al. "Distinct molecular mechanism for initiating TRAF6 signalling." Nature 418, no. 6896 (July 2002): 443–47. http://dx.doi.org/10.1038/nature00888.

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6

ROBBINS, EDWARD HENRY, and JOHN D. SCHATZBERG. "Callable Bonds: A Risk-Reducing Signalling Mechanism." Journal of Finance 41, no. 4 (September 1986): 935–49. http://dx.doi.org/10.1111/j.1540-6261.1986.tb04558.x.

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7

Broz, Petr, and Vishva M. Dixit. "Inflammasomes: mechanism of assembly, regulation and signalling." Nature Reviews Immunology 16, no. 7 (June 13, 2016): 407–20. http://dx.doi.org/10.1038/nri.2016.58.

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8

García-Padilla, Carlos, Estefanía Lozano-Velasco, Carmen López-Sánchez, Virginio Garcia-Martínez, Amelia Aranega, and Diego Franco. "Non-Coding RNAs in Retinoic Acid as Differentiation and Disease Drivers." Non-Coding RNA 7, no. 1 (February 17, 2021): 13. http://dx.doi.org/10.3390/ncrna7010013.

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Анотація:
All-trans retinoic acid (RA) is the most active metabolite of vitamin A. Several studies have described a pivotal role for RA signalling in different biological processes such as cell growth and differentiation, embryonic development and organogenesis. Since RA signalling is highly dose-dependent, a fine-tuning regulatory mechanism is required. Thus, RA signalling deregulation has a major impact, both in development and disease, related in many cases to oncogenic processes. In this review, we focus on the impact of ncRNA post-transcriptional regulatory mechanisms, especially those of microRNAs and lncRNAs, in RA signalling pathways during differentiation and disease.
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9

Winterbourn, Christine C. "Hydrogen peroxide reactivity and specificity in thiol-based cell signalling." Biochemical Society Transactions 48, no. 3 (May 15, 2020): 745–54. http://dx.doi.org/10.1042/bst20190049.

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Reversible oxidation of thiol proteins is an important cell signalling mechanism. In many cases, this involves generation or exposure of the cells to H2O2, and oxidation of proteins that are not particularly H2O2-reactive. There is a conundrum as to how these proteins are oxidised when other highly reactive proteins such as peroxiredoxins are present. This article discusses potential mechanisms, focussing on recent evidence for oxidation being localised within the cell, redox relays involving peroxiredoxins operating in some signalling pathways, and mechanisms for facilitated or directed oxidation of specific targets. These findings help define conditions that enable redox signalling but there is still much to learn regarding mechanisms.
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10

Tsydenova, Irina A., Daria S. Dolgasheva, Ksenia A. Gaptulbarova, Marina K. Ibragimova, Matvei M. Tsyganov, Ekaterina A. Kravtsova, Anna A. Nushtaeva, and Nikolai V. Litviakov. "WNT-Conditioned Mechanism of Exit from Postchemotherapy Shock of Differentiated Tumour Cells." Cancers 15, no. 10 (May 15, 2023): 2765. http://dx.doi.org/10.3390/cancers15102765.

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Background: the present study aims to prove or disprove the hypothesis that the state of copy number aberration (CNA) activation of WNT signalling pathway genes accounts for the ability of differentiated tumour cells to emerge from postchemotherapy shock. Methods: In the first step, the CNA genetic landscape of breast cancer cell lines BT-474, BT-549, MDA-MB-231, MDA-MD-468, MCF7, SK-BR-3 and T47D, which were obtained from ATCC, was examined to rank cell cultures according to the degree of ectopic activation of the WNT signalling pathway. Then two lines of T47D with ectopic activation and BT-474 without activation were selected. The differentiated EpCAM+CD44-CD24-/+ cells of these lines were subjected to IL6 de-differentiation with formation of mammospheres on the background of cisplatin and WNT signalling inhibitor ICG-001. Results: it was found that T47D cells with ectopic WNT signalling activation after cisplatin exposure were dedifferentiated to form mammospheres while BT-474 cells without ectopic WNT-signalling activation did not form mammospheres. The dedifferentiation of T47D cells after cisplatin exposure was completely suppressed by the WNT signalling inhibitor ICG-001. Separately, ICG-001 reduced, but did not abolish, the ability to dedifferentiate in both cell lines. Conclusions: these data support the hypothesis that the emergence of differentiated tumour cells from postchemotherapy shock after chemotherapy is due to ectopic activation of WNT signalling pathway genes.
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Дисертації з теми "SIGNALLING MECHANISM"

1

Promel, Simone. "Investigating the molecular mechanism of latrophilin signalling." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.533843.

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2

Lewis, Miranda Faye. "Dissecting the molecular mechanism of toll signalling." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707987.

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3

Nyamay'Antu, Alengo. "Elucidating the mechanism of angiopoeitin-mediated Tie2 signalling." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/elucidating-the-mechanism-of-angiopoeitinmediated-tie2-signalling(4269f3c3-fc71-455d-ae5b-4bc47dda78ca).html.

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Research on angiogenesis has been focused on developing anti-angiogenic therapies to target endothelial cell-specific signalling pathways, as a mean to limit tumour outgrowth and metastasis. One of the main targets is the endothelial cell-specific Tie2 receptor and its ligands, the angiopoietins, which controls the later stages of angiogenesis. Although the angiopoietin/Tie2 signalling pathways have been well characterized, the molecular mechanism by which the ligands regulate Tie2 activity remains unclear. To address this question, we determined whether the activation mechanism of Tie2 is induced by dimerisation alone, or whether subsequent relative rotation of the kinase domain is required. Here we employed a coiled-coiled based protein engineering approach to identify the relative orientations of the kinase domains that are optimal for Tie2 activation. By replacing the extracellular domain of Tie2 with the dimeric parallel coiled-coil motif Put3cc, we generated ligand-independent homodimers of the kinase domains Put3cc-Tie2 I-VII that have distinct orientations. We show that dimerisation is sufficient to induce Tie2 activation and downstream activation of Akt, and that varying the interface of the kinase domain in Tie2 dimers can increase its catalytic efficiency. In addition we examined for the presence of potential dimerisation within the transmembrane and intracellular domain of Tie2. We show that the KD and potentially the TM contain dimerisation motifs that stabilise Tie2 in the inactive and active conformations. In addition, we show that deletion of the potential coiled-coil motif in the JM does not disrupt dimerisation but decreases the catalytic efficiency of Tie2. Finally, we propose that the activation mechanism of Tie2 may be similar to the previously described asymmetric dimer formation of EGFR and FGFR receptors.
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4

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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5

Seymour, Lyndsey A. "Characterising the signalling mechanism of the mTOR-dependent phosphatase." Thesis, Cardiff University, 2011. http://orca.cf.ac.uk/55115/.

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The mechanistic Target of Rapamycin Complex 1 (mTORC1) complex is central in the regulation of many crucial cellular processes including translation, transcription, proliferation and autophagy. Deregulation of the complex is evident in a number of diseases including Tuberous Sclerosis, Alzheimer's Disease and cancer. Whilst the signalling events leading to activation of mTORC1 are well understood, the inhibitory phosphatase activity that prevents aberrant signalling has received comparatively little attention. In yeast, phosphatases are an integral part of TORC1 signalling. Poor nitrogen supply leads to activation of the phosphatases Pph21/22 and Sit4 and subsequent dephosphorylation of TORC1 substrates. Under these conditions, the phosphatase negative regulatory protein Tap42 is sequestered by Tip41. In good nitrogen supply, TORC1 phosphorylatesTip41 leading to release of Tap42 and subsequent inhibition of Pph21/22 and Sit4. This allows the accumulation of phosphorylated TORC1 substrates. This thesis investigated the role of Tip41 in mTORC1 signalling. Purification of Tip41 identified direct interaction with PP2Ac (human Pph21/22). As overexpression of Tip41 resulted in inhibition of mTORC1 signalling, Tip41 is proposed as a bona fide positive regulatory subunit of PP2Ac. Further investigation indicated that hypophosphorylated PP2A-rjp4i may directly oppose Rheb-mediated activation of mTORC1 thus promoting Raptor degradation. In addition, a specific nuclear isoform of Tip41 was identified, which may specifically regulate the transcription factor HIF1. Studies using the adenoviral protein E40RF4 also identified the PP2ABa complex in regulation of mTORC1 signalling. The data in this thesis show that PP2ABa acts downstream of the TSC 1/2 complex to inhibit mTORC1. Results also indicate that PP2ABa may be negatively regulated by ubiquitin-mediated proteasomal degradation of Ba in an mTORC1-specific manner. Therefore PP2ABa may be subject to an mTORC1 feedback mechanism that is required for activation of downstream substrates. These data indicate that phosphatase activity is critical in regulation of mTORC1, reflecting the mechanism in yeast.
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6

Bryan, Andrea. "A study of electrophysiological and pathological signalling mechanism in the Xenopus laevis oocyte." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267991.

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7

Jethwa, Susanna Anjali. "Exosomes : vesicular carriers of autotaxin, a novel mechanism of LPA signalling." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608189.

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8

Jopling, Helen Mary. "A Mechanism for VEGFR2 Trafficking, Signalling and Degradation in Human Endothelial Cells." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.515561.

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9

McDowell, Natasha. "The mechanism of long-range signalling between cells of the Xenopus embryo." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624744.

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McLaughlin, Declan. "Investigation into the mechanism of Nox2 NADPH oxidase-dependent signalling in doxorubicin cardiotoxicity." Thesis, Queen's University Belfast, 2014. https://pure.qub.ac.uk/portal/en/theses/investigation-into-the-mechanism-of-nox2-nadph-oxidasedependent-signalling-in-doxorubicin-cardiotoxicity(4250d47c-175c-48d9-bc79-7d1a5ab01443).html.

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Although the antibiotic, doxorubicin (DOX), is a widely-used and successful first-line treatment for cancers, it can induce cardiotoxicity which is associated with increased production of myocardial reactive oxygen species (ROS). Recent work has suggested that ROS generated specifically from Nox2 NADPH oxidase, contributes to key processes underlying cardiac dysfunction associated with chronic DOX treatment. The aim of this study was therefore (1) to characterise the role of Nox2 NADPH oxidase-derived ROS in DOX-induced cardiotoxicity in a 4 week murine experimental model as the basis for detailed mechanistic studies, (2) identify Nox2-regulated genes and signalling pathways which may play a key role in the development of DOX-induced cardiotoxicity in vivo, and (3) investigate detailed Nox2-dependent signalling mechanisms in DOX-treated cardiomyocytes in vitro. Wild type (WT) and Nox2-/y mice were treated with or without DOX (4mg/kg) and studied after 4 weeks. DOX-induced cardiac contractile dysfunction and cardiomyocyte remodelling was attenuated in Nox2-/y as compared to WT mice. Furthermore, DOX treatment was found to increase Nox2 mRNA expression in WT mice, whilst Nox2 mRNA was not detected in Nox2-/y animals and was not induced by DOX. Inhibitor studies conducted in WT animals confirmed that the observed effects were mediated by ROS. Taken together, these data give further support to our previous data suggesting that ROS specifically-derived from Nox2 NADPH oxidase make a significant contribution DOX-induced cardiac remodelling and provide a solid basis for use of the 4 week experimental model for detailed mechanistic studies. In this regard, a whole-genome gene expression array (Illumina MouseWG-6 v2.0) was performed on ventricular tissue from these animals in order to identify key Nox2-regulated pathways which may mediate protection against DOX cardiotoxicity. Pathway analysis identified 156 differentially expressed genes (P<0.1) and highlighted ‘Cell Death and Survival’ as the network of most significance to the dataset. Further examination using heat maps highlighted cell death and survival functions, with a focus on 5 genes associated with cardiomyocyte apoptosis. Of these genes, peroxisome proliferator-activated receptor-gamma co-activator 1 alpha (PGC1α), and the mitochondrial membrane protein, mitofusin 2 (Mfn2), which is known to be up- vi regulated by PGC1α, were selected as good candidates for further investigation. qPCR confirmed increased expression of Mfn2 mRNA in hearts from WT (1.3-fold) but not Nox2-/y DOX-treated animals, although no changes in PGC1α mRNA were apparent between groups. To further investigate the signalling mechanism by which Mfn2 may mediate the protective effects of Nox2, an in vitro model of DOX-induced apoptosis in HL-1 cardiomyocytes was employed. Initial characterization studies showed that DOX treatment for 24 hours resulted in increased expression of both Nox2 and Mfn2 and superoxide production. Targeted siRNA knockdown of Nox2 and Mfn2 produced significant downregulation of protein expression, and exhibited a protective effect against DOX-induced decreases in cell viability and caspase/viability activity. Furthermore, pharmacological inhibition of NADPH oxidase using the inhibitor, VAS2870, significantly reduced DOX-induced HL-1 cardiomyocyte apoptosis and cytotoxicity. Taken together, the findings of this study add further support to a key role for Nox2 NADPH oxidase-derived ROS in DOX cardiotoxicity, and suggest that apoptotic cell death may represent a central mechanism in this process, which may involve mitochondrial fusion, thereby contributing to the associated contractile dysfunction.
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Книги з теми "SIGNALLING MECHANISM"

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1927-, Segawa Tomio, ed. Physiology and pharmacology of transmembrane signalling: Proceedings of the Uehara Memorial Foundation Symposium on the Mechanism of Transmembrane Signalling, Tokyo, Japan May 12-14, 1988. Amsterdam: Excerpta Medica, 1989.

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2

1945-, Cohen P., and Houslay Miles D, eds. Molecular mechanisms of transmembrane signalling. Amsterdam: Elsevier, 1985.

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3

Frank, Entschladen, and Zänker Kurt S, eds. Cell migration: Signalling and mechanisms. Basel: Karger, 2010.

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4

M, Harnett Margaret, and Rigley Kevin P, eds. Lymphocyte signalling: Mechanisms, subversion, and manipulation. Chichester: J. Wiley, 1997.

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5

Wirtz, Karel W. A., ed. Molecular Mechanisms of Signalling and Membrane Transport. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60799-8.

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6

Brumell, John H. Phosphorylation-dependent signalling mechanisms in human neutrophils. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1997.

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7

Packer, Lester, and Karel W. A. Wirtz, eds. Signalling Mechanisms — from Transcription Factors to Oxidative Stress. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3.

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8

Davies, Clare Charlotte. Mechanisms of CD40 signalling and apoptosis in carcinoma cells. Birmingham: University of Birmingham, 2003.

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9

O'Connor, Rodney Philip. A relationship between the amplitude and spectral characteristics of the geomagnetic field and the occurrence of sudden infant death in Canada: A possible cellular mechanism supported by a mathematical modeland experimental evidence for involvement of calcium signalling and nitric oxide. Sudbury, Ont: Laurentian University, Department of Biology, 2001.

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10

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

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Частини книг з теми "SIGNALLING MECHANISM"

1

Dubey, Reena, and Deepti Tiwari. "Molecular Mechanism of Brassinosteroids in Boosting Crop Yield." In Brassinosteroids Signalling, 269–92. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5743-6_16.

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2

Abbas, Hafiz Muhammad Khalid, Syed Muhammad Hassan Askri, Sajid Ali, Ammara Fatima, Muhammad Tahir ul Qamar, Shu-Dan Xue, Zafarullah Muhammad, Waheed Akram, and Yu-Juan Zhong. "Mechanism Associated with Brassinosteroids Crosstalk with Gibberellic Acid in Plants." In Brassinosteroids Signalling, 101–15. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5743-6_6.

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3

Bakshi, Palak, Shagun Bali, Pooja Sharma, Mohd Ibrahim, Kamini Devi, Neerja Sharma, Ashutosh Sharma, Amrit Pal Singh, Bilal Ahmad Mir, and Renu Bhardwaj. "Mechanism Associated with Brassinosteroids-Mediated Detoxification of Pesticides in Plants." In Brassinosteroids Signalling, 203–21. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-5743-6_12.

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Manju and Pranav Kumar Prabhakar. "Targeting Molecular and Cellular Mechanism in Rhinovirus Infection." In Targeting Cellular Signalling Pathways in Lung Diseases, 485–500. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6827-9_22.

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5

Chatterjee, Antra, Alok Kumar Shrivastava, Sonia Sen, Shweta Rai, Shivam Yadav, Ruchi Rai, Shilpi Singh, and LC Rai. "UVR8 Signalling, Mechanism and Integration with other Pathways." In UV-B Radiation, 289–307. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119143611.ch15.

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6

Gopal, Gayathri, Shibi Muralidar, and Senthil Visaga Ambi. "Targeting Molecular and Cellular Mechanism of Influenza A Virus." In Targeting Cellular Signalling Pathways in Lung Diseases, 447–69. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6827-9_20.

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7

Brownlee, C. "Intracellular Signalling During Ferilisation and Polarisation in Fucoid Algae." In Mechanism of Fertilization: Plants to Humans, 579–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83965-8_39.

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Dastidar, Debabrata Ghosh, Dipanjan Ghosh, Swarnasree Ghosh, and Gopal Chakrabarti. "Drug Delivery in Respiratory Diseases: Current Opportunities, Molecular and Cellular Mechanism, and Future Challenges." In Targeting Cellular Signalling Pathways in Lung Diseases, 847–902. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6827-9_38.

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9

Md Ahsan Ul Bari, Julie Gaburro, Agnes Michalczyk, M. Leigh Ackland, Catherine Williams, and Asim Bhatti. "Mechanism of Docosahexaenoic Acid in the Enhancement of Neuronal Signalling." In Series in BioEngineering, 99–117. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3957-7_5.

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Pinxteren, Jef A., Antony J. O’Sullivan, and Bastien D. Gomperts. "A role for G-protein βγ-subunits in the secretory mechanism of rat peritoneal mast cells." In Molecular Mechanisms of Signalling and Membrane Transport, 89–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60799-8_6.

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Тези доповідей конференцій з теми "SIGNALLING MECHANISM"

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Novikova, M., N. Khromova, V. Rybko, B. Kopnin, and P. Kopnin. "PO-267 Notch-dependent tumourigenic mechanism associated with exosome signalling." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.781.

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Ali, A. H., and R. L. Brewster. "Efficient handover signalling for microcellular environments using packet access mechanism." In IEE Colloquium on Antennas and Propagation for Future Mobile Communications. IEE, 1998. http://dx.doi.org/10.1049/ic:19980133.

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Sljoka, Adnan, and Nobuyuki Tsuchimura. "Exploring Protein Flexibility and Allosteric Signalling Mechanism with Rigidity Theory." In 2016 3rd Asia-Pacific World Congress on Computer Science and Engineering (APWC on CSE). IEEE, 2016. http://dx.doi.org/10.1109/apwc-on-cse.2016.047.

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Priyadarsini, Madhukrishna, Padmalochan Bera, and M. Ashiqur Rahman. "A Signalling Game-Based Security Enforcement Mechanism for SDN Controllers." In 2019 10th International Conference on Computing, Communication and Networking Technologies (ICCCNT). IEEE, 2019. http://dx.doi.org/10.1109/icccnt45670.2019.8944843.

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Wong, Kai-Juan, and D. K. Arvind. "A Hybrid Wakeup Signalling Mechanism for Periodic-Listening MAC Algorithms." In 2007 15th IEEE International Conference on Networks. IEEE, 2007. http://dx.doi.org/10.1109/icon.2007.4444131.

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Ibrahim, Ali, Luca Muscariello, and James Roberts. "A Single Channel Signalling Mechanism for Power/Rate Control in WLANs." In 2009 Next Generation Internet Networks (NGI). IEEE, 2009. http://dx.doi.org/10.1109/ngi.2009.5175752.

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Gupta, Pankaj K., R. V. Rajakumar, C. S. Kumar, and Goutam Das. "Analytical evaluation of signalling cost on power saving mechanism in mobile networks." In 2013 IEEE TENCON Spring Conference. IEEE, 2013. http://dx.doi.org/10.1109/tenconspring.2013.6584475.

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Guay, Wei Lin, Sven-Arne Reinemo, Bjorn Dag Johnsen, Tor Skeie, and Ola Torudbakken. "A Scalable Signalling Mechanism for VM Migration with SR-IOV over Infiniband." In 2012 IEEE 18th International Conference on Parallel and Distributed Systems (ICPADS). IEEE, 2012. http://dx.doi.org/10.1109/icpads.2012.60.

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Edan, Naktal Moaid, Ali Al-Sherbaz, and Scott Turner. "WebNSM: A Novel Scalable WebRTC Signalling Mechanism for Many-to-Many Video Conferencing." In 2017 IEEE 3rd International Conference on Collaboration and Internet Computing (CIC). IEEE, 2017. http://dx.doi.org/10.1109/cic.2017.00015.

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Jathal, Maitreyee K., Thomas M. Steele, Salma Siddiqui, Benjamin A. Mooso, Leandro S. D’Abronzo, Christiana M. Drake, and Paramita M. Ghosh. "Abstract 1303: In vivo analysis of EGFR family signalling as a bypass mechanism in prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1303.

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Звіти організацій з теми "SIGNALLING MECHANISM"

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Morse, Alexander. Bioinformatics experiments. Exp 1. Analysis of mechanisms of Cd+2 impact on MAPK-signalling through DUSPs. Part 1. Theory. ResearchHub Technologies, Inc., September 2022. http://dx.doi.org/10.55277/researchhub.9y5bc33g.

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Wagner, D. Ry, Eliezer Lifschitz, and Steve A. Kay. Molecular Genetic Analysis of Flowering in Arabidopsis and Tomato. United States Department of Agriculture, May 2002. http://dx.doi.org/10.32747/2002.7585198.bard.

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The primary objectives for the US lab included: the characterization of ELF3 transcription and translation; the creation and characterization of various transgenic lines that misexpress ELF3; defining genetic pathways related to ELF3 function regulating floral initiation in Arabidopsis; and the identification of genes that either interact with or are regulated by ELF3. Light quality, photoperiod, and temperature often act as important and, for some species, essential environmental cues for the initiation of flowering. However, there is relatively little information on the molecular mechanisms that directly regulate the developmental pathway from the reception of the inductive light signals to the onset of flowering and the initiation of floral meristems. The ELF3 gene was identified as possibly having a role in light-mediated floral regulation since elj3 mutants not only flower early, but exhibit light-dependent circadian defects. We began investigating ELF3's role in light signalling and flowering by cloning the ELF3 gene. ELF3 is a novel gene only present in plant species; however, there is an ELF3 homolog within Arabidopsis. The Arabidopsis elj3 mutation causes arrhythmic circadian output in continuous light; however, we show conclusively normal circadian function with no alteration of period length in elj3 mutants in dark conditions and that the light-dependent arrhythmia observed in elj3 mutants is pleiotropic on multiple outputs regardless of phase. Plants overexpressing ELF3 have an increased period length in constant light and flower late in long-days; furthermore, etiolated ELF3-overexpressing seedlings exhibit a decreased acute CAB2 response after a red light pulse, whereas the null mutant is hypersensitive to acute induction. This finding suggests that ELF3 negatively regulates light input to both the clock and its outputs. To determine whether ELF3's action is phase dependent, we examined clock resetting by light pulses and constructed phase response curves. Absence of ELF3 activity causes a significant alteration of the phase response curve during the subjective night, and overexpression of ELF3 results in decreased sensitivity to the resetting stimulus, suggesting that ELF3 antagonizes light input to the clock during the night. Indeed, the ELF3 protein interacts with the photoreceptor PHYB in the yeast two-hybrid assay and in vitro. The phase ofELF3 function correlates with its peak expression levels of transcript and protein in the subjective night. ELF3 action, therefore, represents a mechanism by which the oscillator modulates light resetting. Furthermore, flowering time is dependent upon proper expression ofELF3. Scientifically, we've made a big leap in the understanding of the circadian system and how it is coupled so tightly with light reception in terms of period length and clock resetting. Agriculturally, understanding more about the way in which the clock perceives and relays temporal information to pathways such as those involved in the floral transition can lead to increased crop yields by enabling plants to be grown in suboptimal conditions.
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Sionov, Edward, Nancy Keller, and Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604292.bard.

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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.
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