Dissertations / Theses: 'Cellular signal transduction'

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Pat, Betty Kila. "Signal transduction pathways in renal fibrosis /." St. Lucia, Qld, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17739.pdf.

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Haugh, Jason Michael 1972. "Cellular compartmentation effects in receptor-mediated signal transduction." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85364.

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Leahy, Rachel A. "Signal Transduction and Cellular Differentiation in Airway Epithelium." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1352673026.

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Kim, Hyun Ji. "Development and signal transduction in Dictyostelium." Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:4ed80c6e-adc8-46d6-aeaf-c853cef7af77.

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Dictyostelium, is a simple eukaryote that multiplies as separate amoebae. However when nutrients are no longer available it embarks on a developmental programme in which the amoebae collect together by chemotaxis and the resulting aggregates eventually transform into fruiting bodies consisting of a cluster of spores held up on a cellular stalk. The entire process of development normally takes about 24 hours. However there are mutants, termed rapidly developing mutants (rde) which complete development in about two-thirds of this time. RdeA null mutants have been reported to have elevated levels of cyclic AMP that may lead to increased activity of the enzyme, cAMP dependent protein kinase (PKA). I started my work by measuring total cAMP levels in an rdeA mutant along with an aca-/rdeA- double mutant that is expected to have very low level of cAMP due to the absence of the adenylyl cyclase, AC A. Two Dictyostelium adenylyl cyclases were known at the beginning of my work; one is AC A the aggregative enzyme, and the other ACG, expressed only during spore germination. Contrary to expectation, I detected cAMP in aca-/rdeA cells. This raised the question of which enzyme was responsible for producing this cAMP. In collaboration with Dr.Pauline Schaap, I discovered a novel adenylyl cyclase that I initially detected in rdeA and regA mutants but not in wild-type cells. The product of the rdeA gene, RDEA was thought to be an H2-module histidine phosphotrasferase of the kind acting in multi-step phosphorelays. Similarly REGA was believed to be a response regulator associated with a cAMP-phosphodiesterase. It had been proposed that RDEA phosphorylates REGA in a multi-step phosphorelay and it had been shown that it is the phosphorylated form of REGA that is active as a cAMP-PDE. I therefore thought that cAMP produced by the novel AC could be protected in rdeA mutants by the absence of the REGA cAMP-PDE activity and this idea was supported by my finding that the enzyme activity could also be detected in wild-type (aca-) cells when REGA-PDE was inhibited by IBMX. In order to investigate further the proposed phosphorelay model, I tested for possible interaction between RDEA and REGA using the yeast two-hybrid system and also measured intracellular cAMP-phosphodiesterase activity in rdeA and regA mutants. I found that the interaction between RDEA and REGA appeared to be too transient to be detected in the two-hybrid system. In addition rdeA and regA mutants seemed to have levels of intracellular cAMP-phosphodiesterase activity similar to wild type. However REGA-PDE activity measured specifically by immuno-precipitation was completely absent in the regA mutant. It therefore appeared that there is another intracellular cAMP-phosphodiesterase, in addition to the REGA PDE, in Dictyostelium and that the latter cannot be easily detected in total cell lysates. One possible explanation is that the novel adenylyl cyclase exists together with REGA in a complex (that may also include PKA) and that REGA PDE preferentially destroys the cAMP made by the novel adenylyl cyclase. I conclude that rdeA and regA mutants may develop rapidly due to high PKA activity induced by the accumulation of cAMP made by the novel AC when the REGA cAMP-PDE activity is absent.

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Chang, Wen-Tsan. "Molecular studies of signal transduction and development." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360212.

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Brownlie, Zoe. "Regulation of signal transduction by RGS4." Connect to e-thesis, 2007. http://theses.gla.ac.uk/124/.

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Thesis (Ph.D.) - University of Glasgow, 2007. Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, 2007. Includes bibliographical references.

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Gammon, Benjamin Matthew. "Signal transduction in the cellular slime mould Dictyostelium discoideum." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279872.

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Manne, Bhanu Kanth. "CLEC-2 SIGNAL TRANSDUCTION IN PLATELET ACTIVATION." Diss., Temple University Libraries, 2015. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/340495.

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Physiology Ph.D. Platelets are involved in many processes ranging from fighting microbial infections and triggering inflammation to promoting tumor angiogenesis and metastasis. Nevertheless, the primary physiological function of platelets is to act as essential mediators in maintaining homeostasis of the circulatory system by forming hemostatic thrombi that prevent blood loss and maintain vascular integrity. CLEC-2 is a C-type lectin-like receptor that is highly expressed in platelets and lesser extent, in other cell types such as activated dendritic cells and B cells. Rhodocytin was the first ligand used to identify CLEC-2 receptor and it’s signaling on platelets. In the first chapter we identified a new agonist for CLEC-2 receptor. Fucoidan, a sulfated polysaccharide from fucus vesiculosus, decreases bleeding time and clotting time in hemophilia, possibly through inhibition of tissue factor pathway inhibitor. However, its effect on platelets and the receptor by which fucoidan induces cellular processes has not been elucidated. In this study, we demonstrate that fucoidan induces platelet activation in a concentration-dependent manner. Fucoidan-induced platelet activation was completely abolished by the pan-Src family kinase (SFK) inhibitor, PP2, or when Syk is inhibited. PP2 abolished phosphorylation of Syk and Phospholipase Cγ−2. Fucoidan-induced platelet activation had a lag phase, which is reminiscent of platelet activation by collagen and CLEC-2 receptor agonists. Platelet activation by fucoidan was only slightly inhibited in FcRγ chain null mice, indicating that fucoidan was not acting primarily through GPVI receptor. On the other hand, fucoidan-induced platelet activation was inhibited in platelet-specific CLEC-2 knock-out murine platelets revealing CLEC-2 as a physiological target of fucoidan. Thus, our data show fucoidan as a novel CLEC-2 receptor agonist that activates platelets through a SFK-dependent signaling pathway. Furthermore, the efficacy of fucoidan in hemophilia raises the possibility that decreased bleeding times could be achieved through activation of platelets. Lipid rafts are distinct areas of the plasma membrane implicated in the regulation of signaling in a variety of cells including platelets. A previous study C-type lectin like receptor 2 (CLEC-2) has been reported to activate platelets through a lipid raft-dependent manner. Secreted ADP potentiates CLEC-2-mediated platelet aggregation. We have investigated whether the decrease in CLEC-2-mediated platelet aggregation, previously reported in platelets with disrupted rafts, is a result of the loss of agonist potentiation by ADP. We disrupted platelet lipid rafts with methyl-β-cyclodextrin (MβCD) and measured signaling events downstream of CLEC-2 activation. Lipid raft disruption decreases platelet aggregation induced by CLEC-2 agonists. The inhibition of platelet aggregation by the disruption of lipid rafts was rescued by the exogenous addition of epinephrine but not 2-methylthioadenosine diphosphate (2MeSADP), which suggests that lipid raft disruption effects P2Y12-mediated Gi activation but not Gz. Phosphorylation of Syk (Y525/526) and PLCγ2 (Y759), were not affected by raft disruption in CLEC-2 agonist-stimulated platelets. Furthermore, tyrosine phosphorylation of the CLEC-2 hemi-ITAM was not effected when MβCD disrupts lipid rafts. Lipid rafts do not directly contribute to CLEC-2 receptor activation in platelets. The effects of disruption of lipid rafts in in vitro assays can be attributed to inhibition of ADP feedback that potentiates CLEC-2 signaling. Tyrosine kinase pathways are known to play an important role in the activation of platelets. In particular, the GPVI and CLEC-2 receptors are known to activate Syk upon tyrosine phosphorylation of an Immune Tyrosine Activation Motif (ITAM) and hemi-ITAM, respectively. However, unlike GPVI, the CLEC-2 receptor contains only one tyrosine motif in the intracellular domain. The mechanisms by which this receptor activates Syk are not completely understood. In chapter 3, we identified a novel signaling mechanism in CLEC-2-mediated Syk activation. CLEC-2-mediated, but not GPVI-mediated, platelet activation and Syk phosphorylation were abolished by inhibition of PI3-Kinase, which demonstrates that PI3-Kinase regulates Syk downstream of CLEC-2. Ibrutinib, a Tec family kinase inhibitor, also completely abolished CLEC-2-mediated aggregation and Syk phosphorylation in human and murine platelets. Furthermore, embryos lacking both Btk and Tec exhibited cutaneous edema associated with blood-filled vessels in a typical lymphatic pattern similar to CLEC-2 or Syk-deficient embryos. Thus our data show, for the first time, that PI3-Kinase and Tec family kinases play a crucial role in the regulation of platelet activation and Syk phosphorylation downstream of CLEC-2 receptor. Temple University--Theses

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Hung, Hiu Wai. "Signal transduction mechanism in xenopus presynaptic differentiation /." View Abstract or Full-Text, 2003. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202003%20HUNG.

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Gong, Yunchen 1965. "Analyses of alternative cell signal transduction pathways." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85552.

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Living cells keep sensing the changes in their environments, mostly, via cell surface receptors for different ligands. Attachment-dependent cells are sensitive to alterations in extracellular matrix (ECM). ECM is not only required for cell survival, but also prerequisite for epidermal growth factor (EGF) to stimulate cell proliferation. The receptors for the majority of ECM components are integrins and the receptor for EGF is EGF receptor (EGFR). When bound by their ligands, integrins and EGFR induce signal transduction cascades composed of alternative pathways. A quantitative assessment of relative contributions of alternative pathways to one final cell signaling will help understand designing principles of the network. Unfortunately, a methodology for such assessment is still not available, partly because of lack of relatively mature mathematical models. On the other hand, in most biochemical cascades, existence of alternative pathways increases the complexity and thus the robustness of networks. The relationships between the topology and robustness of large-scale biochemical networks have been studied intensively recently. In small-scale networks, while feedback has been revealed as an important contributor for adaptation and robustness, the quantitative correlation between the topology/pathway redundancy of small networks and their robustness remains unknown. In this thesis, apoptosis of bovine mammary gland epithelial cells was demonstrated to be induced when fibronectin, one of the major components of ECM, was degraded by overexpressed tPA via two potential ways: deprivation of attachment and the effects of fibronectin fragments. Secondly, a mathematical model for EGFR activation of the MAPK cascade, in which alternative pathways exist, was explored and it was found that the Shc-dependent pathway is both redundant and dominant. We hypothesize that the Shc-dependent pathway is important for EGFR to compete with other receptors, which need Shc to transduce cell signals; and this pathway is not aimed to increase the robustness of the EGFR cascade. Finally, for the general importance of alternative pathways to the network topology and robustness, several concepts have been proposed to decompose and quantitatively characterize the networks. We demonstrate that the pathnet score is a better assessment for robustness than the molecular connectivity.

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Ulrich, Luke. "Comparative Genomics of Microbial Signal Transduction." Diss., Georgia Institute of Technology, 2005. http://hdl.handle.net/1853/7632.

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High-throughput genome processing, sophisticated protein sequence analysis, programming, and information management were used to achieve two major advances in the comparative genomics of microbial signal transduction. First, an integrated and flexible bioinformatics platform and the Microbial Signal Transduction database (MiST) were developed, which facilitated the genome-wide analysis of bacterial signal transduction. This platform was used successfully for the high-throughput identification and classification of signal transduction proteins in more than 300 archaeal and bacterial organisms. Second, analysis of information encoded in prokaryotic genomes revealed that the majority of signal transduction systems consist of one-component systems a single protein containing both input and output domains but lacking phosphotransfer domains typical of two-component systems. The prevalence of one-component systems is a paradigm-shifting discovery because two-component systems are currently viewed as the primary mode of signal transduction in prokaryotes. One-component systems are more widely distributed among bacteria and archaea and display a greater diversity of domains than two-component systems. Additionally, in-depth bioinformatic analyses were performed that further characterized the function of two, input, signaling domains. In summary, this systematic, high-throughput delineation of microbial signal transduction is another step forward in our understanding of the genomic basis of life.

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Wong, Wai-lap. "Signal transduction pathways of ret receptor tuyrosine kinase." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22786478.

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王偉立 and Wai-lap Wong. "Signal transduction pathways of ret receptor tuyrosine kinase." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31225354.

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Roberts, Craig Dane. "cAMP Signaling in Chemosensory Transduction." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/161.

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cAMP is a second messenger in a variety of chemosensory receptors, including taste buds and glucose-sensitive pancreatic beta-cells. cAMP is modulated during taste transduction, yet the significance of cAMP changes and the taste cell types in which they occur (Type I glial-like; Type II Receptor; Type III Presynaptic) remain unclear. I developed techniques to image real-time changes in intracellular cAMP in taste cells using genetically-encoded cAMP reporters. This FRET-based reporter permits one to measure single-cell cAMP levels with excellent spatial and temporal resolution (Zaccolo & Pozzan 2002, Science 295:1711). Using a biolistic approach I have transfected rat fungiform taste buds with cAMP reporter plasmids. Focal application of bitter tastant to living fungiform tastebuds in situ produced a decrease in [cAMP]i within individual taste receptor cells. These results are qualitatively similar to previous biochemical measurements from homogenized taste tissue (Yan et al. 2001, Am J Physiol Cell Physiol 280:C742) but are now allowing us to examine the cAMP response in individual, identified cells. I next explored the effect of elevating cAMP on calcium levels, using Fura-2 imaging of isolated mouse vallate taste buds. Elevating [cAMP]i in taste buds evoked calcium responses in presynaptic/Type III taste cells, which do not express GAD1. cAMP induced responses were generated by calcium influx. Using pharmacological antagonists, I determined that the calcium influx triggered by cAMP is through L-type calcium channels, whereas influx following depolarization is primarily through P/Q-type calcium channels. Consistent with these data, single cell RT-PCR showed that the L-type subunit (alpha 1C) was expressed primarily in GAD-negative Presynaptic cells, while the P/Q-type (alpha 1A) was expressed in all Presynaptic cells. Thus, cAMP may modulate the function of synapses in some taste cells. Finally, we have developed a mouse strain expressing a cAMP reporter in a tissue-specific and tetracycline-inducible manner. We crossed this mouse with another strain expressing tet-activator in beta cells of the pancreas. Such islets responded to increasing concentrations of glucose (5.5 to 35mM) with an increase in cAMP levels. The half maximum of 9mM glucose for the cAMP response corresponds well with reported glucose concentrations that elicit insulin release from whole islets. Stimulating pancreatic islets with glucose is known to drive calcium influx into beta-cells. When we simultaneously imaged both second messengers, we found that cAMP changes precede and are independent of calcium changes. In conclusion, these studies have outlined novel potential functions for cAMP signaling in the transduction of both primary tastant and plasma glucose information. In addition, the flexibility of the tet-system will enable cAMP reporter expression in numerous cell types, including those which mediate gustatory transduction.

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Richard, Jessica. "The two-component signal transduction systems of Pseudomonas aeruginosa." Thesis, Montana State University, 2008. http://etd.lib.montana.edu/etd/2008/richard/RichardJ0508.pdf.

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Two-component signal transduction systems are important components for bacteria, because they allow the bacteria to sense environmental conditions and rapidly adapt to changes in the environment. Two-component systems generally contain a sensor histidine kinase, which detects an environmental signal and responds by autophosphorylation at a histidine residue using ATP as the phosphate donor. The phosphate group is then transferred to an aspartate residue in the receiver domain of the second component, the response regulator, which in its activated form responds by stimulating or repressing gene expression or motility, as needed for the physiological responses of the cell. The structural versatility of two-component systems reflects the wide range of signals to which bacteria respond. Despite this versatility, histidine kinases and response regulators show a conserved mechanism of signal transfer. Pseudomonas aeruginosa is a versatile organism that can use a variety of nutrient sources and is found in many different environments. It is a human pathogen in nosocomial infections as well as in pulmonary fluid of patients with cystic fibrosis. P. aeruginosa encodes genes for over 60 two-component regulatory systems. In this review, I discuss the structure and function of two-component systems in bacteria, and conduct a phylogenetic analysis of the P. aerugionsa two-component systems. Finally, I develop a model of the calcium-responsive two-component system of P. aeruginosa, PA2656/PA2657, which is closely related to the magnesium responsive PmrAB and phosphate responsive PhoPQ two-component systems. The results provide insight on how P. aeruginosa is able to detect and respond to changing environmental conditions.

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Tsui, Michelle Grace, and 徐善婷. "PDZD2, a candidate for brachydactyly type A1, encodes a secreted protein that negatively modulates hedgehog signaling." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/209211.

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Hedgehog (Hh) is an important morphogen that dictates tissue patterning during embryonic development. Recent studies showed that mutation in Indian Hedgehog(IHH)resulted in Brachydactyly type A1(BDA1);however, the disease pathogenesis in patients without IHH mutation remained unknown. PDZD2 is a multi-PDZ domain-containing protein of unknown function in early development. Human PDZD2 is mapped to chromosome 5p13.2, which co-localizes with the disease-associated gene in a family of BDA1 patients, suggesting involvement of PDZD2 in limb development. In situ hybridization revealed that Pdzd2 was expressed in the distal mesenchyme partially overlapping with Shh expressionin mouse limb bud. During digit patterning, Pdzd2 was expressed in the interzone regions that flanked the Ihh/Gli1-expressing phalanx condensation. Moreover,Pdzd2 was expressed in the paraxial mesoderm adjacent to the differentiating neural tube. Pdzd2expression in various Hh-active tissues in mouse and chicken suggested an evolutionary conserved role of PDZD2 in modulating general Hh signaling during early development. Interestingly, PDZD2 protein was detected at the neural tube away from its site of synthesis, suggesting a non-cell autonomous role of PDZD2 possibly via its secreted form, sPDZD2. Functional studies showed that overexpression of sPDZD2 in the chicken neural tube leads to down-regulation ofNKX2.2andOLIG2expression.sPDZD2 was shown to counteract the ectopic NKX2.2 expression induced by long-range signaling of ectopic HH. Consistently, sPDZD2exhibited an inhibitory effect on SHH-induced reporter activity in a Gli-luciferase cell line. For in vivo analysis, a transgenic mouse line carrying a floxed Pdzd2 allele (Pdzd2fl) was generated to ablate Pdzd2 expression.Pdzd2+/fl mice were crossed with Protamine-cre to generate the null allele (Pdzd2-). However, heterozygous intercross yielded no homozygous mutant as early as E9.5, suggesting early embryonic lethality. Thus, conditional Pdzd2 knock-out in the limb was pursuedusingPrx1-cre.However, no significant perturbation of Hh signaling was observed in Pdzd2fl/fl:Prx1-cre limb buds, which might be due to incomplete knock-out of Pdzd2, or functional redundancy among Hh modulators. To study the relevance of Pdzd2in the development of BDA1, Pdzd2-/fl mouse was crossed with the BDA1 mouseIhhE95K/E95Kto study the effect of reducing Pdzd2expression under defective Hh signaling. Preliminary analysis of the Pdzd2+/-, Ihh+/E95K compound mutants showed more severe phenotypes comparing with IhhE95K/E95K. These included delayed limb development and further diffusion ofGli1expression in the digits, suggestive of a direct involvement of Pdzd2in BDA1. It was speculated that Pdzd2negatively modulated Ihh signaling and restricted Hh signals from entering the interzone, which was required for normal digit patterning. Depletion of Pdzd2might result in an expansion of Ihh signaling into the interzone, leading to the BDA1phenotypessimilar to the current BDA1 disease model proposed forIhhE95Kmutation. Taken together, my study revealed the novel expression of Pdzd2in close proximity to multiple Hh-active tissues during early development and provided the first evidence that PDZD2/sPDZD2 is a negative modulator of general Hh signaling. These data strongly supported PDZD2as a disease-associated locus in the family of BDA1 patients that do not carry IHHmutations. published_or_final_version Biochemistry Doctoral Doctor of Philosophy

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17

Wangorsch, Gaby Verfasser], and Thomas [Akademischer Betreuer] [Dandekar. "Mathematical modeling of cellular signal transduction / Gaby Wangorsch. Betreuer: Thomas Dandekar." Würzburg : Universität Würzburg, 2013. http://d-nb.info/1107217032/34.

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Pliego-Rivero, Francisco Bernardo. "Thy-1 : cellular compartmentalization during development and participation in signal transduction." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.358073.

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Wangorsch, Gaby [Verfasser], and Thomas [Akademischer Betreuer] Dandekar. "Mathematical modeling of cellular signal transduction / Gaby Wangorsch. Betreuer: Thomas Dandekar." Würzburg : Universität Würzburg, 2013. http://d-nb.info/1107217032/34.

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Rogers, Laura Ann. "Membranes as a hub for cellular signaling /." Access full-text from WCMC, 2007. http://proquest.umi.com/pqdweb?did=1481668281&sid=2&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Madan, Namrata. "Role of Different Isoforms of Na/K-ATPase in Signal Transduction." University of Toledo Health Science Campus / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=mco1418318054.

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Braun, David Meyer. "Maize receptor-like protein kinase signal transduction and function /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841268.

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Joyce, Kevin Michael. "Cellular and genomic effects of long-wavelength laser irradiation." Thesis, University of Ulster, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267791.

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Liu, Wei. "Role of axin in TGF-[beta] signaling pathway and characterization of axin mutant proteins in axinF̳u̳ mice /." View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20LIUW.

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Han, Shujie. "Regulation of phorbol ester-induced Ras/Raf/Erk signaling pathway in EL4 cells." Online access for everyone, 2008. http://www.dissertations.wsu.edu/Dissertations/Summer2008/s_han_1062508.pdf.

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Wang, Kepeng. "The involvement of JAK2/STAT2/STAT3 in myogenic differentiation /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20WANGK.

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Chan, Yuen-yee Kathy. "Functional segregation of the highly conserved basic motifs within the third endoloop of the human secretin receptor /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B23621473.

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Kallenberger, Stefan M. [Verfasser], and Roland [Akademischer Betreuer] Eils. "Variability in cellular signal transduction networks / Stefan Matthias Kallenberger ; Betreuer: Roland Eils." Heidelberg : Universitätsbibliothek Heidelberg, 2014. http://d-nb.info/1177810905/34.

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Knapp, Bettina, and Lars Kaderali. "Reconstruction of Cellular Signal Transduction Networks Using Perturbation Assays and Linear Programming." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-127239.

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Perturbation experiments for example using RNA interference (RNAi) offer an attractive way to elucidate gene function in a high throughput fashion. The placement of hit genes in their functional context and the inference of underlying networks from such data, however, are challenging tasks. One of the problems in network inference is the exponential number of possible network topologies for a given number of genes. Here, we introduce a novel mathematical approach to address this question. We formulate network inference as a linear optimization problem, which can be solved efficiently even for large-scale systems. We use simulated data to evaluate our approach, and show improved performance in particular on larger networks over state-of-the art methods. We achieve increased sensitivity and specificity, as well as a significant reduction in computing time. Furthermore, we show superior performance on noisy data. We then apply our approach to study the intracellular signaling of human primary nave CD4+ T-cells, as well as ErbB signaling in trastuzumab resistant breast cancer cells. In both cases, our approach recovers known interactions and points to additional relevant processes. In ErbB signaling, our results predict an important role of negative and positive feedback in controlling the cell cycle progression.

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Knapp, Bettina, and Lars Kaderali. "Reconstruction of Cellular Signal Transduction Networks Using Perturbation Assays and Linear Programming." Public Library of Science, 2013. https://tud.qucosa.de/id/qucosa%3A27289.

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Perturbation experiments for example using RNA interference (RNAi) offer an attractive way to elucidate gene function in a high throughput fashion. The placement of hit genes in their functional context and the inference of underlying networks from such data, however, are challenging tasks. One of the problems in network inference is the exponential number of possible network topologies for a given number of genes. Here, we introduce a novel mathematical approach to address this question. We formulate network inference as a linear optimization problem, which can be solved efficiently even for large-scale systems. We use simulated data to evaluate our approach, and show improved performance in particular on larger networks over state-of-the art methods. We achieve increased sensitivity and specificity, as well as a significant reduction in computing time. Furthermore, we show superior performance on noisy data. We then apply our approach to study the intracellular signaling of human primary nave CD4+ T-cells, as well as ErbB signaling in trastuzumab resistant breast cancer cells. In both cases, our approach recovers known interactions and points to additional relevant processes. In ErbB signaling, our results predict an important role of negative and positive feedback in controlling the cell cycle progression.

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Hartgraves, Morri D. "Carbachol- and ACPD-Induced Phosphoinositide Responses in the Developing Rat Neocortex." Thesis, University of North Texas, 2000. https://digital.library.unt.edu/ark:/67531/metadc2640/.

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Signal transduction via the phosphoinositide (PI) second messenger system has key roles in the development and plasticity of the neocortex. The present study localized PI responses to individual cortical layers in slices of developing rat somatosensory cortex. The acetylcholine agonist carbachol and the glutamate agonist trans-1-amino-1,3-cyclopentanedicarboxylic acid (ACPD) were used to stimulate PI turnover. The PI responses were compared to the distribution of the corresponding PI-linked receptors in order to investigate the regional ontogeny of PI coupling to receptors in relation to neural development. The method for assessing PI turnover was modified from Hwang et al. (1990). This method images the PI response autoradiographically through the localizaton of [3H]cytidine that has been incorporated into the membrane-bound intermediate, cytidine diphosphate diacylglycerol. In each age group (postnatal days 4-30), carbachol resulted in more overall labeling than ACPD. For both agonists, the response peaked on postnatal day 10 (P10) and was lowest in the oldest age group. The laminar distribution of the carbachol PI response from P4-P16 corresponded fairly well with the laminar distribution of [3H]quinuclidinyl benzilate binding (Fuchs, 1995). However, in the subplate layer the carbachol response was strong while receptor binding was minimal. The carbachol response decreased after postnatal day 10, while the overall levels of receptor binding continued to increase. From P5 - P14, PI-linked metabotropic glutamate receptors are most concentrated in layer IV (Blue et al., 1997), whereas only on P6 was there a correspondingly high ACPD-initiated PI response in this layer. Unlike receptors, the PI response was strong in upper V (P4 - P12) and within layers II/III (P8 - P16). From P4 - P21, the subplate showed relatively high PI labeling compared to receptor binding. The several differences between the distribution of PI response and receptors suggest spatiotemporal heterogeneity of receptor coupling to second messenger systems.

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Harding, Angus Silas. "A biochemical analysis of the MAP kinase pathway in mammalian cells /." A biochemical analysis of the MAP kinase pathway in mammalian cellsRead the abstract of the thesis, 2003. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17885.pdf.

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Lee, Tae Weon. "Regulation of expression of signal transduction cascade elements by G-protein coupled receptors." Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321070.

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Hudson, Christine Cecilia. "Isolation of signal transduction inhibitors by bioassay-directed fractionation of plant extracts." Diss., Georgia Institute of Technology, 1996. http://hdl.handle.net/1853/30636.

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Nikolaou, Elissavet. "Phylogenetic diversity of fungal stress signaling pathways." Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources, 2008. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=24849.

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Keane, John F. "A framework for molecular signal processing and detection in biological cells /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6126.

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Miljan, Erik Armand Jaan. "Molecular and cellular characterization of ganglioside-stimulated protein kinase." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B29957618.

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Mayeenuddin, Linnia H. "Modulation of PTH-mediated signal transduction in osteoblasts by factors regulating cellular growth." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28803.pdf.

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Small, Nadine Veronica. "Mechanism of signal transduction for chemotaxis of the cellular slime mould Dictyostelium discoideum." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315786.

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Chahal, Manpreet Singh. "Roles for PLD2 in growth factor-mediated signal transduction in EL4 lymphoma cells." Pullman, Wash. : Washington State University, 2008. http://www.dissertations.wsu.edu/Dissertations/Fall2008/m_chahal_080808.pdf.

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Thesis (Ph. D.)--Washington State University, December 2008. Title from PDF title page (viewed on Oct. 22, 2009). "Pharmacology/Toxicology Graduate Program." Includes bibliographical references (p. 90-97).

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Rentel, Maike Christina. "Signal transduction in response to active oxygen species in Arabidopsis thaliana." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:5dc0b7f5-5aa9-4633-a8dd-89ca2dcb3982.

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Many environmental stresses result in increased generation of active oxygen species (AOS) in plant cells, leading to the induction of protective mechanisms. In this study, signalling components linking AOS perception to downstream responses were examined, with particular emphasis on H2O2 signalling. All AOS investigated had an early [Ca2+]cyt peak in common, but differed in other aspects of their Ca2+ signatures, indicating that the plant is able to discriminate between different types of AOS. An early event in AOS signal transduction may involve changes in the cellular redox balance as reduction of glutathione levels prior to stress application increased the height of the first [Ca2+]cyt peak. Inhibiting or enhancing the height of the H2O2-triggered Ca2+ signature lead to inhibition or enhancement of GST1 and APX1 induction, respectively, demonstrating that the Ca2+ signature is required for induction of genes encoding antioxidant enzymes. OX1, encoding a putative ser/thr kinase, was shown to be involved in signal transduction in response to H2O2-generating stresses. Transcript levels of OX1 were increased upon treatment with H2O2 and a range of abiotic and biotic stresses as well as ABA, all of which have been shown to result in H2O2 accumulation. Inhibition of stress-induced [Ca2+]cyt elevations inhibited OX1 induction, placing the OX1 kinase downstream of Ca2+ in the signalling chain. OX1 is required for full activation of AtMPKS and AtMPK6 in response to ozone fumigation, indicating that OX1 functions upstream of these MAP kinases. An ox1 null-mutant displayed enhanced susceptibility to infection with a virulent Peronospora parasitica isolate as well as reduced induction of several defence genes. In addition, the ox1 mutant exhibited shorter root hairs and an early flowering phenotype. AOS treatment induced several genes encoding AtERF transcription factors, but did not have an effect on other members of this family. Induction occurred in an ethylene-independent but Ca2+-dependent manner.

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Cao, Yang. "Macromolecular crowding effects on the activity of the extracellular signal regulated kinase 2 /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?CHEM%202008%20CAO.

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Yu, Lu. "Multiple signaling pathways cooperate to activate skeletal muscle differentiation /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20YU.

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Xu, Weiguang. "Solution structure of [Alpha]-syntrophin PH-PDZ tandem domain /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20XU.

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Zhou, Liying. "Studying the mitochondria-dependent apoptotic signaling pathway in mammalian cells /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20ZHOU.

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Ma, Chun-Wai. "Aboav-Weaire law in complex network and its applications in bioinformatics /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?PHYS%202005%20MA.

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Jamie, Hajierah. "Possible crosstalk between signal transduction pathways in the induction of differentiation in HT-29 cells." Thesis, University of Port Elizabeth, 2000. http://hdl.handle.net/10948/d1019684.

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The investigation into the mechanisms by which compounds such as butyrate induce differentiation in HT-29 cells, is lacking. The colonic carcinoma cell line, HT-29, undergoes differentiation induction in the presence of butyrate and acetoacetate. The Caco-2 cell line spontaneously differentiates on contact inhibition. In this study, a signal transduction pathway involving ATP, cAMP, Ca2+ and the transcriptional factor CREB was investigated following suggestions that the energy state of the cell and diffferentiation are linked. The activity of the MAP kinase cascade, including possible crosstalk that may exist between these pathways was determined. The HT-29 cells were exposed to 5 mM acetoacetate, butyrate, DMSO and propionate. The results of this differentiation induction were compared to Caco-2 and HeLa cells, which are cervical carcinoma cells. It was found that ATP levels are decreased on differentiation induction in HT-29 cells, which, in turn affected the cAMP concentrations. Theoretically, the inducers do not have any effect on PDE 4 activity, and may facilitate the interaction between cAMP and PKA. Influx of Ca2+ into the cells was inhibited to a degree by the inducers, which was possibly overcome by crosstalk between the cAMP and Ca2+ pathways. CREB activation, lineage-specific gene expression, ERK activity and c-myc expression were all dependent on both the inducers used and the cell-type. PKA played a major role in CREB activation in acetoacetate- and butyrate -induced HT-29, Caco-2 and HeLa cells, while a2+/Calmodulin-dependent kinases I/IV may have a secondary role. Alkaline phosphatase expression in HeLa cells was independent of CREB. Evidence that crosstalk between the MAP kinase cascade and the REBactivation pathways exist, was illustrated by increased CREB activation on ERK inhibition in acetoacetate- and butyrate-induced HT-29 and HeLa cells. Also, the role that ERK played in the cells differed with inducer and cell-type. The dependence of cmyc expression on c-jun and c-fos, appeared to be differentiation induction- and celltype specific. Results from this study indicate the potential use of acetoacetate and butyrate as anti-cancer compounds.

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Geng, Hao. "ResDE-dependent transcriptional control in response to oxygen limitation /." Full text open access at:, 2007. http://content.ohsu.edu/u?/etd,256.

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Chan, Yuen-yee Kathy, and 陳婉儀. "Functional segregation of the highly conserved basic motifs within thethird endoloop of the human secretin receptor." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B3124290X.

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Chiu, Yung-tuen, and 趙容端. "Studying the role of androgen receptor signaling in the development, progression and therapeutic approach of prostate cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B4559692X.

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Dissertations / Theses on the topic 'Cellular signal transduction'

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