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Zhou, Yixing Harden T. Kendall. "Cloning and characterization of a novel phospholipase C enzyme, human phospholipase C eta2." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1271.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.<br>Title from electronic title page (viewed Mar. 26, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Pharmacology." Discipline: Pharmacology; Department/School: Medicine.
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Lin, Gialih Hoffmann. "Stereochemistry and mechanism of phospholipase A2 and phosphatidylinositide-specific phospholipase C /." The Ohio State University, 1989. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487672245900381.
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Tong, Yun. "Phosphoinositide-phospholipase C in diabetic cardiomyopathy." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0001/MQ32268.pdf.
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Zhao, Li. "Mechanistic studies on phosphatidylinositol-specific phospholipase C." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1047485476.
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Thesis (Ph. D.)--Ohio State University, 2003.<br>Title from first page of PDF file. Document formatted into pages; contains xix, 135 p.; also includes graphics (some col.) Includes bibliographical references (p. 128-135). Available online via OhioLINK's ETD Center
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Donahue, Vicki S. "Phospholipase c activity in retinal pigment epithelium." Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1041916.
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The role of the retinal pigment epithelial cells on the viability and renewal of photoreceptors has been well demonstrated in the Royal College of Surgeons (RCS) strain of rat. These rats are characterized by an inherited time-dependent degeneration of their photoreceptors. This degeneration is apparently due to the inability of the retinal pigment epithelial cells to adequately ingest fragments of photoreceptor membrane that are shed during the course of photoreceptor membrane renewal. The buildup of photoreceptor material in the interphotoreceptor space ultimately leads to the degeneration of photoreceptors in these animals. With regard to the pigment epithelial cells, neither the mechanism mediating the ingestion process in normal rats nor the nature of the defect of this process in RCS rats is understood.It is the goal of this proposed research to assay for the presence of phospholipase C in retinal pigment epithelial (RPE) cells and to determine possible modulators of the enzyme in an attempt to associate this with the process of phagocytosis.<br>Department of Biology
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Clark, Graeme Christopher. "Characterisation and exploitation of clostridial phospholipase C." Thesis, Birkbeck (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406120.
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Blank, Jonathan Louis. "The phospholipase C specific for the phosphoinositides." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252943.
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Meldrum, Eric. "Isolation and characterization of mammalian phospholipase C." Thesis, Open University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.258438.
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Chrétien, Louise. "Régulation de l'activité de la phospholipase C par les récepteurs AT [indice] 1 de l'angiotensine II et B [indice] 2 de la bradykinine." Sherbrooke : Université de Sherbrooke, 1998.
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Nazih, Hassan. "Hdl3, plaquettes et seconds messagers : caracterisation et regulation du systeme de transduction." Lille 2, 1993. http://www.theses.fr/1993LIL2P261.
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Popovics, Petra. "Biochemical and functional characterisation of phospholipase C-η2". Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/3511.
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Phospholipase C enzymes are important cell signalling enzymes that catalyse the cleavage of phosphatidylinositol 4,5-bisphophate PI(4,5)P₂ into two biologically active second messenger molecules. These are the inositol 1,4,5-trisphosphate which initiates Ca²⁺ release from the endoplasmic reticulum and the diacylglycerol that activates protein kinase C. Although this basic function is shared between the different isoforms, the PLC family encompasses a diverse collection of proteins with various domain structures in addition to the PLC-specific domains. The neuron-specific “6th family” of these enzymes, PLCηs have most recently been identified with two members, PLCη1 and PLCη2. The aim of the thesis is to characterise the PLCη2 variant from several aspects. Firstly, it describes that PLCη2 possesses a high sensitivity towards Ca²⁺. Secondly, it investigates how the Ca²⁺-induced enzymatic activity of PLCη2 is controlled by its different domains. Also it provides evidence that the pleckstrin homology domain targets PLCη2 to membranes by recognising PI(3,4,5)P₃. Moreover, the uniquely structured EF-hand is responsible for the Ca²⁺-sensitivity of the enzyme. Finally, it is demonstrated that the C2 domain is important for activity. The initial biochemical characterisation is followed by the description of a physiological role for PLCη2. It is shown using a neuroblast model that PLCη2 is crucial for neuronal differentiation and neurite growth. Further efforts were made to assess how PLCη2 is responsible for this effect. It was revealed that it might be involved in regulating intracellular Ca²⁺ dynamics, transcriptional activity and actin reorganisation in differentiating neurons. As the functions of PLCη2 are just beginning to come to light, more aspects for future research are also suggested in the thesis. Hopefully, this and the data presented within the thesis will stimulate even greater interest in this fascinating new field of research.
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Raabe, Andreas Christian. "Rôle de la phospholipase C, des phosphoinositides et du calcium dans la gamétogenèse de Plasmodium berghei, parasite du paludisme." Montpellier 2, 2008. http://www.theses.fr/2008MON20081.
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Une étape cruciale dans le cycle de Plasmodium, parasite causal du paludisme est sa transmission de l'hôte vertébré au moustique vecteur. Seuls les stades sanguins sexués sont capables de se développer dans le moustique. Chez le moustique, le nouvel environnement déclenche une cascade de signalisation conduisant à la gamétogenèse. Les travaux de thèse ont pour objectifs d'élucider cette cascade de signalisation qui joue un rôle clé dans la transmission du paludisme. Des approches pharmacologiques biochimiques et génétiques ainsi que des études d'imagerie ont été utilisées et fournissent de multiples évidences d'une implication de la phospholipase C (PLC) au cours de la gamétogenèse mâle de Plasmodium berghei. Les études pharmacologiques impliquent le récepteur à la ryanodine pour un premier signal calcique qui active la PLC. Un marquage métabolique du PIP2 et des mesures d'inositol tris phosphate (IP3) montre la chronologie de l'activité PLC. Les données biochimiques ont été corroborées par imagerie des gamétocytes exprimant une protéine fluorescente liant PIP2 et IP3, et suggèrent que l'activation de la PLC agit comme amplificateur du signal calcique. En outre, nous avons développé une nouvelle méthode pour analyser la gamétogenèse mâle, basée sur le marquage radioactif de l'ADN nouvellement synthétisé. Cette méthode a donné de nouvelles informations sur la cinétique de la réplication de l'ADN au cours de la gamétogenèse. La méthode a été validée pour l'identification de composés qui interfèrent avec la gamétogenèse et éventuellement bloquerait la transmission du paludisme<br>A crucial step in the life cycle of Plasmodium, the causative agent of malaria, is its transmission from vertebrate host to mosquito vector. Only sexual blood stages, termed gametocytes, are capable to develop within the mosquito. Upon ingestion by a mosquito, cues from the new environment trigger an intracellular signalling cascade within the gametocytes leading to gametogenesis, the first developmental step in the mosquito. This study aimed to further our understanding of this signalling cascade, as it plays a key role in malaria transmission. Genetic, biochemical, pharmacological, and live cell imaging approaches were employed and provide multiple lines of evidence for phospholipase C (PLC) involvement in the signalling events during male gametogenesis of Plasmodium berghei. Pharmacological evidence suggests that ryanodine receptors mediate an initial release of calcium that activates PLC. Metabolic labelling of PIP2 was used in combination with sensitive IP3 detection and allowed to deduce a timeline of PLC activity during gametogenesis. Biochemical data were confirmed by live cell microscopy of gametocytes expressing a fluorescent reporter protein binding to PIP2 and IP3, and suggest that PLC acts as calcium signal amplifier. Furthermore, we developed a new method to analyse male gametogenesis, based on radioactive labelling of newly synthesised DNA. This method provided new insight into the kinetics of DNA replication during Plasmodium gametogenesis. This assay can now be used to identify compounds that interfere with gametogenesis and potentially block malaria transmission
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Day, James Edward Harvey. "The Design and Synthesis of Phospholipase C Gamma Inhibitors." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487209.
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Phospholipase C (PLC) catalyses the hydrolysis of phosphatidylinositoI4,5-biphosphate to two important secondary messengers which mediate downstream cell motility and cell proliferation. PLCy is of particular interest because of its involvement with growth factor mediated cell motility, which is a key process to both angiogenesis and tumour invasion. Experimental results provide compelling evidence that PLCy may be rate limiting in tumour invasion and angiogenesis. There is a need for efficacious and 'drug like' inhibitors ofPLCy. Two compounds CCT006000 and CCT007740 were identified from a high throughput biochemical screen against PLCy2. An initial investigation into their structure activity relationships led to the conclusion that CCT007740 (PLCy2 50% inhibitory concentration (ICso) 50 JlM) was a promising candidate for further development. A series of structural modifications to CCT007740 and subsequent optimisation produced CCTl29010 (PLCy2 ICso 1.7 JlM). Although CCTl29010 had improved potency, the compound was degraded rapidly by mouse liver microsomes (MLM) and lacked cellular activity. Further exploration and manipulation of CCTl29010 led to the discovery of CCTl30234 (PLCy2 ICso 480 nM). The compound displays the cellular signature expected that of a PLCy inhibitor; inhibiting growth factor induced HUVEC migration and calcium release. CCTl32034 is stable to MLM and has good pharmacokinetic properties. CCTl30234 significantly inhibited metastasis in a highly invasive prostate carcinoma model, further validating PLCy as an important cancer drug target.
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Klein, Ryan Reaves Thakker Dhiren R. "Regulation of tight junction barrier function by phospholipase C." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1380.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.<br>Title from electronic title page (viewed Apr. 25, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the School of Pharmacy." Discipline: Pharmacy; Department/School: Pharmacy.
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Mills, Lewis Nathan. "The role of phospholipase C in guard cell signalling." Thesis, Lancaster University, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429967.
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Blake, Robert A. "Regulation of the platelet phospholipase C by tyrosine phosphorylation." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240551.
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Treagus, Jane Elizabeth. "The translocation of phospholipase C-β1 into the nucleus". Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.625027.
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Shi, Xiaomeng. "Phosphatidylinositol-specific phospholipase C: Conformational changes upon membrane binding." Thesis, Boston College, 2010. http://hdl.handle.net/2345/1413.
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Thesis advisor: Mary F. Roberts<br>Phosphatidylinositol-specific phospholipase C (PI-PLC) from B. thuringiensis is activated by phosphatidylcholine (PC) surfaces for both phosphatidylinositol (PI) cleavage to inositol 1,2-(cyclic)-phosphate (cIP) and subsequent hydrolysis of cIP to inositol-1-phosphate. These enzyme kinetics strongly suggest that this PI-PLC has two discrete binding sites for phospholipids - the active site binding PI (or substrate competitors) and an activator site specific for PC. However, it is difficult to determine the orientation and conformation of peripheral membrane proteins when docked to target membranes, let alone where sites for these might be on the protein. In this thesis, various biophysical techniques were applied to this bacterial PI-PLC to obtain structural information in the absence and presence of membranes to characterize specific conformational changes that occur when the protein binds to activating membranes. The crystal structures of an interfacially impaired double mutant of PI-PLC, W47A/W242A, was solved and showed the protein as a homodimer. The major interactions came from four clustered surface tyrosine residues from each monomer. This structure suggested the possibility of PI-PLC dimerization on membrane surfaces as part of the mechanism for interfacial activation. Mutations of these tyrosines showed a loss of activity and membrane binding. Crystal structures of these mutant proteins showed no significant change in the proteins, consistent with either disruption of a dimerization interface of a specific PC binding motif. FRET was used to try and monitor oligomerization of PI-PLC, derivatized on a cysteine introduced at residue 280 (W280C) with either a donor or acceptor fluorophore, on vesicle surfaces. The results suggested some specific aggregation could occur on very PC-rich surfaces but not on phospholipid vesicles with at least 50 mol% anionic phospholipids, strongly suggesting that a stable dimer was not forming when the enzyme was bound to vesicles mimicking conditions where enzyme specific activity is high. If dimerization occurs on surfaces, it must be transient. To examine which portions of the PI-PLC are interacting with membrane and to further explore if there is any evidence for PI-PLC dimerization on membrane surface, deuterium exchange coupled by mass spectrometry experiments were carried out with wild type PI-PLC, W47A/W242A and a covalent dimer formed from W242C that is more active than wild type enzyme. Results showed (i) a stable short helix B (containing an exposed tryptophan thought to insert into membranes) in wild type PI-PLC and its complete destabilization in W47A/W242C, (ii) a flexible surface loop (containing another tryptophan thought to partition into the membrane) that became protected when the protein was bound to vesicles, and (iii) reduced deuterium exchange for the peptide containing the tyrosines that either mediate transient dimerization or form a PC binding site.. These observations modify how we envision the protein anchoring to substrate-containing membranes<br>Thesis (PhD) — Boston College, 2010<br>Submitted to: Boston College. Graduate School of Arts and Sciences<br>Discipline: Chemistry
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Blachier, François. "Activation de la phospholipase c par trois agents insulinotropes." Paris 6, 1988. http://www.theses.fr/1988PA066085.
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Blachier, François. "Activation de la phospholipase C par trois agents insulinotropes." Grenoble 2 : ANRT, 1988. http://catalogue.bnf.fr/ark:/12148/cb37611958m.
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De, Filippis Lidia. "The phospholipase C signalling system : study of the role of the Go protein and identification of a novel variant of Phospholipase C β4." Thesis, Open University, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270087.
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Bühler, Anja [Verfasser]. "Molecular mechanisms regulating phospholipase C-gamma 2 activity / Anja Bühler." Ulm : Universität Ulm. Fakultät für Naturwissenschaften, 2016. http://d-nb.info/1094889202/34.
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Rezaei, Effat. "Regulation of phospholipase C in human megakaryocyte-like cell lines." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337499.
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Hodson, Elizabeth Anne Marie. "G protein regulation of phospholipase C in vascular smooth muscle." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390487.
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Leslie, Dario Lyall. "Genetic analysis of alpha toxin (phospholipase C) from Clostridium perfringens." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.346420.
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Nomikos, Michail. "Molecular and enzymatic characterization of mammalian phospholipase C zeta (PLCzeta)." Thesis, Cardiff University, 2006. http://orca.cf.ac.uk/55522/.
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In mammalian oocytes, the fertilising sperm evokes intracellular calcium (Ca2+) oscillations that are essential for the initiation of egg activation and embryonic development. Although the exact mechanism leading to the initiation of Ca2+ oscillations is still unclear, accumulating evidence suggests that sperm-specific phospholipase C zeta (PLC zeta) is delivered from the fertilising sperm into the ooplasm, triggering the Ca2+ oscillations through the inositol 1,4,5-trisphosphate (InsP3) pathway. PLC zeta is the smallest known mammalian PLC isoform comprising of two EF hand, a C2 and the X and Y catalytic core domains. In this study we examined the biochemical properties of recombinant bacterially expressed mouse PLC zeta (m PLC zeta) using the well-characterised rat PLC zeta1 (rPLC zeta1) as control. Using a PtdInsP2 hydrolysis assay we showed that both isoforms had a similar Km for PtdIns(4,5)P2 and that PLC zeta had a much higher Ca2+ sensitivity, which would predict it to be active at resting Ca2+ concentrations in eggs. PLC zeta bound with high affinity to PtdIns(3,5)P2 and PtdIns(4,5)P2 even though it lacks a PH domain from its sequence, which targets PLC zeta1 to PtdIns(4,5)P2. A series of domain deletion constructs of PLC zeta were used to demonstrate the role of the EF hands on the Ca2+ sensitivity of PLC zeta and the role of C2 domain and XY linker on its binding to PtdInsP2. Luminescent PLC constructs were generated to examine their potential to elicit Ca2+ oscillations, quantifying their expression levels in mouse eggs. Anti-human PLC zeta (h PLC zeta) monoclonal antibodies were produced and their ability to block the in vitro hydrolysing activity of recombinant h PLC zeta was tested.
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Chang, Wei-Chiao. "Ca²+-dependent-regulation of phospholipase A² and leukotriene C⁴ secretion." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670084.
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Jäger, Karin. "Glycosyl-phosphatidylinositol-anchored acetyl-cholinesterase and phosphatidylinositol-specific phospholipase C /." Bern, 1990. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Ladas, Ioannis. "The role of phospholipase C enzymes in health and disease." Thesis, Cardiff University, 2015. http://orca.cf.ac.uk/75723/.
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Phospholipases C (PLCs) are a large family of enzymes that regulate the cleavage of phosphatidylinositol-4,5- bisphosphate into Inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). This project included research on PLCζ and PLCβ1 on male infertility and thyroid cancer respectively. Human PLCζ (hPLCζ) is the key protein for egg activation following sperm-egg fusion and triggers the release of Ca2+ producing a series of oscillations which initiate embryogenesis. Defects in hPLCζ lead to infertility, thus the project aimed at its expression and enrichment suitable for biomedical applications. The results included 1) Comparison of hPLCζ bacterial expression from twenty four plasmid constructs with varying protein tags. 2) Expression of active soluble hPLCζ, free from its bacterial solubility partners. The PLCβ1 project involved a novel InDel (1076 bp deletion, ATAA junction insertion) identified in the 3rd intron of PLCβ1 (Chr 20) by genome-wide linkage analysis (GWLA, LOD score 3.01) of a large kindred with multinodular goitre (MNG) progressing to papillary thyroid cancer (PTC). Affected individuals exhibited increased PLCβ1 transcript levels in their thyroids and the InDel has a putative ERα binding site. The project aimed to, 1) Develop a genotyping technique for high-throughput PLCβ1 InDel screening in large cohorts 2) Determine the InDel’s mechanism of action in modifying thyrocyte proliferation. 3) Next generation sequencing (NGS) of the chr20 region identified by GWLA to identify potential variants responsible for MNG. 1) A QPCR genotyping method was established and the InDel identified in patients with benign thyroid disease. 2) Reporter gene assays suggested silencer elements within the InDel. 3) PLCβ1 knockdown using siRNA exhibited a trend in inhibiting proliferation of a thyroid cell-line. 4) NGS of the 20cM-Chr20 GWLA identified region found no additional disease loci confirming a role for the PLCβ1 InDel. The InDel provides a biomarker for MNG patients most likely to develop PTC.
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Hergenrother, Paul Joseph. "The catalytic mechanism of phospholipase C and the total synthesis of erythromycin B /." Digital version accessible at:, 1999. http://wwwlib.umi.com/cr/utexas/main.
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Remmal, Adnane. "Métabolisme des phospholipides dans les plaquettes du rat spontanément hypertendu." Paris 11, 1987. http://www.theses.fr/1987PA112275.
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Afin de rechercher une origine moléculaire du dérèglement de l'homéostasie calcique observé dans la cellule du muscle lisse vasculaire dans l'hypertension primaire, nous avons étudié et comparé le métabolisme des phospholipides membranaire chez le Rat spontanément hypertendu (SHR) et son témoin normo tendu WKY. En raison des nombreuses analogies existantes entre les cellules du muscle lisse vasculaire et les plaquettes sanguines, ces dernières constituent un modèle intéressant pour étudier le métabolisme du calcium chez le sujet hypertendu et pour tenter d'identifier l'anomalie qui pourrait intervenir dans la pathogénèse de l'hypertension. Dans les plaquettes, comme d'ailleurs dans nombre d'autres cellules où les réponses physiologiques sont dépendantes de la concentration en ions calcium libre dans le cytosol, il est maintenant bien établi que c'est le déclenchement du métabolisme des phospholipides contenant l'Inositol (C'est-à-dire phosphoinositides) qui constitue l'étape initiale dans la mobilisation de calcium. Les phosphoinositides comprennent le phosphatidyl inositol (PI), la phosphatidylinositol 4 phosphate (PIP) et le phosphatidylinositol 4,5 bi phosphate (PIP2). Lors de la stimulation des plaquettes par la thrombine par exemple, c'est l'hydrolyse de PIP2 par une phospholipase C qui initie le processus d'activation cellulaire. Dans la 1ère partie de ce travail, nous avons donc étudié et comparé le métabolisme des phosphoinositides dans les plaquettes du Rat SHR et de son témoin normo tendu WKY : à l'état basal, dans les plaquettes au repos c'est à dire non stimulées et lors de l'activation plaquettaire par la thrombine. Pour ce faire, les plaquettes isolées sont marquées au 32p et la mesure de la radioactivité associée à PI, PIP, PIP2 et à l'acide phosphatidique (PA), permet l'analyse quantitative et comparative du métabolisme de ces lipides dans les deux souches. De rats. Des réponses physiologiques à la thrombine telles que l'agrégation et la sécrétion de sérotonine (SHT) sont mesurées en parallèle. Nos résultats montrent que dans les plaquettes non activées, le métabolisme basal des phosphoinositides est identique et suggèrent que les quantités de PI, PIP, PIP2 et PA sont identiques. Lors de l'activation par la thrombine nos résultats montrent que comparées aux plaquettes de WKY, celles de SHR se sont avérées plus réactives en ce qui concerne les réponses physiologiques (Agrégation et sécrétion de Sérotonine) et en ce qui concerne l'Hydrolyse et la resynthèse des phosphoinositides. Nos résultats montrent donc une hyperréactivité des plaquettes de SHR vis à vis de la thrombine. Cette hyperréactivité serait due à l'activité accrue de la phospholipase C que nous avons montrée chez SHR. Puisque les plaquettes libèrent un grand nombre de substances vase actives, leur hyperréactivité chez SHR peut être liée au spasme artériolaire observé dans l'HTA primaire, et aux thombi vasculaires fréquentes dans cette pathologie. Afin d'essayer de déceler une cause éventuelle de l'altération de cette enzyme qui agit au niveau membranaire nous avons dans la 2ème partie de ce travail, étudié et comparé le métabolisme des autres phospholipides dans les plaquettes des deux souches en faisant des marquages isotopiques avec différents précurseurs radioactifs ( 32P,3H glycérol, H choline). Nos résultats montrent que dans les plaquettes de SHR, non stimulées le marquage de la PC est plus rapide que dans celles de WKY. La composition des membranes plaquettaire de phospholipides s'est avérée similaire entre les 2 souches. Ceci montre donc que le marquage accru de PC que nous avons observé· représentait une vitesse de renouvellement rapide et non une synthèse nette. Ce renouvellement rapide mettant en jeu t9ute la tête polaire de PC serait dû à l'activité accru d'une phospholipase C spécifique pour PC. Cette enzyme n'avait jamais été décrite dans. La plaquette sanguine. Ce renouvellement rapide de PC chez SHR pourrait provoquer des anomalies membranaires pouvant expliquer plusieurs altérations observées dans plusieurs métabolismes membranaires dans l'hypertension artérielle. Chacune de ces deux phospholipase C hyperactives chez SHR pourrait être impliquée directement ou indirectement dans la génèse et (ou) le maintien de l'hypertension artérielle chez le rat spontanément hypertendu
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Nomura, Wataru. "Methylglyoxal-induced activation of protein kinase C through phospholipase C and TORC2 in Saccharomyces cerevisiae." Kyoto University, 2010. http://hdl.handle.net/2433/120466.
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Kyoto University (京都大学)<br>0048<br>新制・課程博士<br>博士(農学)<br>甲第15423号<br>農博第1808号<br>新制||農||979(附属図書館)<br>学位論文||H22||N4522(農学部図書室)<br>27901<br>京都大学大学院農学研究科応用生命科学専攻<br>(主査)教授 喜多 恵子, 教授 植田 和光, 教授 阪井 康能<br>学位規則第4条第1項該当
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Seifert, Jason Paul Harden T. Kendall. "Regulation of phospholipase C-epsilon by Rho and Ras family proteins." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2007. http://dc.lib.unc.edu/u?/etd,1008.
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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2007.<br>Title from electronic title page (viewed Dec. 18, 2007). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Pharmacology." Discipline: Pharmacology; Department/School: Medicine.
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Rasonabe, Zinna Marie [Verfasser]. "Intra- and Intermolecular Control of Phospholipase C-gamma / Zinna Marie Rasonabe." Ulm : Universität Ulm, 2016. http://d-nb.info/1104840235/34.
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Arastoo, Mohammed. "Characterisation of phospholipase C-η enzymes and their relevance to disease". Thesis, University of St Andrews, 2016. http://hdl.handle.net/10023/15698.
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Phospholipase C enzymes are a class of enzymes that catalyse the cleavage of the membrane phospholipid, phosphatidylinositol bisphosphate (PtdIns(4,5)P₂) into the second messengers, inositol trisphosphate (Ins(4,5)P₃) and diacylglycerol (DAG). Six classes of PLC enzymes have been identified based on their structure and mechanism of activation. PLCηs are the most recently identified family and consist of two isozymes, PLCη1 and PLCη2. The aim of this thesis is to further understand the mechanisms of PLCη activation, the role of PLCη2 in relation to neuritogenesis and their roles in certain disease states. Both isoforms were found to be activated by physiological concentrations of intracellular Ca²⁺. Activation of PLCη2 by Gß₁γ₂ was confirmed using a bacterial 2A co-expression system to allow expression of PLCη2, Gß₁ and Gγ₂ with a single plasmid. Localisation studies show a nuclear distribution for PLCη2, but a cytoplasmic distribution for PLCη1 in a neuroblastoma cells line (Neuro2A). PLCη2 has been implicated in brain development and neurite formation. Building on this, a neuronal differentiation model using RA-treated Neuro2A cells stably expressing mutant forms of PLCη2 was utilised, revealing that PLCη2 activity is essential for neuritogenesis but that this process is independent of the enzymes high sensitivity towards Ca²⁺. Furthermore, the direct interaction of PLCη2 and LIMK-1, a previously identified PLCη2 associated protein, is confirmed in the aforementioned neuronal model. Due to the high sensitivity of PLCη enzymes to Ca²⁺ and because of their presence within neurons, they may be involved in Ca²⁺ dysregulation that occurs in certain diseases such as Alzheimer's disease (AD). The role of PLCη2 was assessed in amyloid-ß (Aß) treated differentiated Neuro2A cells, a cellular model for AD pathogenesis. Also a developmental role for PLCη1 was investigated due to a recently identified PLCη1 polymorphism in patients with holoprosencephaly, an embryonic midline defect.
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Luo, Ding. "Localisation and function of phosphoinositide-specific phospholipase C in Sacchromyces cerevisiae." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/680/.
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Phosphoinositide-specific phospholipase C enzymes (PLCs) cleave the plasma membrane phospholipid PtdIns(4,5)P\(_2\) to generate two messengers, inositol (1,4,5) trisphosphate [Ins(1,4,5)P\(_3\)] and diacylglycerol (DAG). Ins(1,4,5)P\(_3\) is an important second messenger in animal cells. It releases calcium from intracellular stores by opening Ins(1,4,5)P\(_3\) receptors (InsP\(_3\)Rs) and is formed in response to activation of cell surface hormone and growth factor receptors. It is also important for its immediate phosphorylation to form higher phosphorylated inositol phosphates (InsPs), which are critical for various cell signaling functions. Sub-families of PLC enzymes exist in cells and the regulation of the \(\beta\) and \(\gamma\) type PLCs via G-protein coupled receptors and receptor tyrosine kinases respectively, is well understood. In contrast, the regulation of PLC-\(\delta\)s is still a mystery. This is particularly frustrating because these enzymes are the only isoforms of PLC found in fungi and plants, as well as animals, and thus are likely to perform an ancient and important function. Plc1p is the single PLC of the \(\delta\) family in the budding yeast Sacchromyces cerevisiae. It plays a key role in generating Ins(1,4,5)P\(_3\) in this fungi in response to stress and yet the yeast genome encodes no Ins(1,4,5)P\(_3\) receptor. This suggests that the functions of PLC-\(\delta\)s are mediated in a novel fashion, probably occurs via the higher inositol phosphates that derived upon rapid phosphorylation of Ins(1,4,5)P\(_3\) by a series of kinases (Arg82p, Ipk1p, Kcs1p and Vip1p). This study focuses on the localisation of GFP-Plc1p in order to gain insight into its function. Plc1p is present in both cytoplasm and nucleus. Plc1p is too large to diffuse through the nuclear pore complex, and thus relies on nuclear export signals (NES) and nuclear localisation signals (NLS) to facilitate its passage through the nuclear envelope. By creating mutants of Plc1p that are restricted to one of these compartments: GFP-Plc1p\(^{CAAX}\) for plasma membrane localisation, GFP-Plc1p\(^{NES}\) for nucleus and GFP-Plc1p\(^{PKI}\) for cytoplasm, I investigated which defects persist in yeast expressing these mutants as their sole Plc1p. My data suggest that these mutants do appear to display distinct subsets of phenotypes consistent with the idea of separate pools of inositol phosphates. I showed that both cytoplasmic and nuclear pools of Plc1p are important for function as neither PLC1\(^{NES}\) nor PLC1\(^{PKI}\) rescue the stress sensitivity of plc1\(\Delta\) mutants. Therefore, Plc1p are likely to shuttle in between different compartments to exert its diverse functions. It will be instructive to characterise inositol phosphate metabolism in these mutants to determine in which compartments basal and stimulated rises in inositol phosphates occur in yeast cells. In addition, I report the novel finding that Plc1p interacts with one (or more than one) of its metabolites. Plc1p appears to associate tightly with the plasma membrane in the absence of the inositol phosphate kinase Arg82p, most likely due to the absence of Arg82p-derived inositol polyphosphates, and such association is required for intact PH, X-Y and C2 domain – disruption in any of these domains would result in failure of such association. Hence, higher phosphorylated inositol phosphates seem to influence Plc1p’s localisation, and a physiological feedback cycle of regulation probably exists where Plc1p may be regulated by the products of its own catalytic activity. Future studies will seek to understand the role of this feedback cycle in stress signalling and physiology in yeast cells.
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Phillips, Sally Victoria. "Expression of phospholipase c zeta (PLCzeta) in a mammalian cell line." Thesis, Cardiff University, 2009. http://orca.cf.ac.uk/55886/.
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Phospholipase C zeta (PLCzeta) is a sperm specific isoform of phospholipase C. It has been shown to produce a long lasting series of calcium oscillations and triggers the activation of development when introduced into mammalian eggs. It is not known how PLCzeta is regulated or if its effects are specific to eggs. Here Chinese Hamster Ovary (CHO) cells were transfected with cDNA encoding PLCzeta tagged with enhanced yellow fluorescent protein (eYFP) or luciferase (LUC). Comparisons were made between these cells and cells transfected with the catalytically inactive PLCzeta, the corresponding reporter gene, or nontransfected cells. PLCzeta exhibited variable levels of nuclear localisation in a manner that depended upon time after transfection. Analysis of resting intracellular calcium levels in transfected CHO cells produced no evidence that PLCzeta expression has a significant effect upon calcium homeostasis. The calcium response to ATP receptor stimulation also remained unchanged after PLCzeta expression. A lack of any clear effect on cell viability enabled the generation of a stably transfected PLCzeta cell line. Individual cells were estimated to be expressing PLCzeta within and above the range required to initiate calcium transients in eggs, and are therefore considered to be expressing at levels comparable with that of sperm. Despite the lack of effect on calcium in CHO cells, the injection of either cytosolic extracts, or whole cells, from the PLCzeta transfected cell line were able to cause calcium oscillations in mouse eggs. Such an effect was not seen with control CHO cells. These data suggest that PLCzeta is inactive when expressed in CHO cells and yet active when subsequently introduced into an egg. The results imply that the enzymatic activity of PLCzeta may be reversibly inhibited in somatic cells, or else specifically stimulated by factors in the egg cytoplasm.
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Gellatly, Steven Alexander. "Cloning and characterisation of phospholipase C X-domain containing proteins (PLCXDs)." Thesis, University of St Andrews, 2015. http://hdl.handle.net/10023/7033.
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Members of the phosphoinositide-specific phospholipase C (PI-PLC) enzyme family play a fundamental role in cell signalling pathways by regulating cytosolic calcium and/or the activity of several protein kinases. This thesis reports the identification, molecular cloning and characterisation of a potential seventh sub-class of the PI-PLC enzyme family, the phospholipase C X-domain containing proteins (PLCXDs), which contain only an X domain in their structure. Comparative sequence analysis has identified at least three PLCXD isoforms in the human and mouse genomes (PLCXDs 1, 2 and 3), and at least four isoforms in the European eel (PLCXDs 1-4). Key amino acid residues responsible for the catalytic properties of PI-PLCs were found to be conserved in human, mouse and eel PLCXDs 1, 2 and 3, but were absent in the sequence of eel PLCXD4. PLCXD isoforms displayed unique tissue-specific expression profiles and some similarities between species. Interestingly, in mouse PLCXD1-3 mRNA were found to be predominantly expressed in the brain, however this is yet to be confirmed in humans. Analysis of in situ hybridisation data in mice revealed each PLCXD to be localised in neurons within different brain regions, highly suggestive of unique roles in brain function. Furthermore, the levels of PLCXD3 protein were reduced by more than 99% in cerebella samples from a mouse model of neurodegeneration (Harlequin mouse) compared to control mice. Human PLCXD1, 2 and 3 were found to increase phosphoinositide turnover when overexpressed in the HeLa cell line, and recombinant PLCXD3, purified to homogeneity from E. coli, was found to interact with various phosphoinositides including PI(4,5)P₂. ³¹P-NMR analysis of PI(4,5)P₂ and PI before and after the addition of PLCXD3 purified from HeLa cells and E. coli revealed no difference in the ³¹P spectra whereas expected chemical shifts were seen following the addition of purified bacterial PI-PLC. Significant formation of inclusion bodies was noted when human PLCXDs 1, 2 and 3 were expressed as recombinant proteins in E. coli. Different strategies aimed at optimising the expression of recombinant PLCXD1, 2 and 3, including the use of different fusion proteins and screening expression in E. coli, mammalian and insect cells had limited success, with the best soluble expression only seen with PLCXD3 in insect cells. Attempts to scale-up the purification of PLCXD3 from insect cells to provide sufficient protein for enzyme assays and crystal screens were unsuccessful. The results presented herein suggest that these novel proteins possess distinct and as yet uncharacterised tissue-specific roles in cell physiology.
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Grebert, Chloé. "Rôle des phospholipases C dans la régulation de la sécrétion d'ions chlorure et de l'homéostasie calcique dans les cellules épithéliales bronchiques : intérêt dans la mucoviscidose." Thesis, Poitiers, 2019. http://www.theses.fr/2019POIT2301.
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Les phospholipases C (PLC) sont des enzymes indispensables dans la transmission des signaux cellulaires via l’hydrolyse des phospholipides membranaires et régulent, par exemple, l’activité de protéines et de canaux ioniques. Les PLC génèrent des seconds messagers tels que le DAG et l’IP3 qui vont respectivement activer la protéine kinase C et augmenter le Ca2+ intracellulaire, deux mécanismes impliquées dans l’activité du canal chlorure CFTR (Cystic Fibrosis Transmembrane conductance Regulator), dont la mutation du gène dans la mucoviscidose est liée à la perte de l’expression et/ou de fonction du canal. L’objectif du projet est d’étudier dans quelle mesure les PLC peuvent jouer un rôle dans l’activité du canal CFTR. Nous avons mis en évidence une implication des phospholipase C dans la sécrétion d’ions chlorures dépendante de l’activité du canal CFTR WT et CFTR F508del corrigé à la membrane par la température. Ainsi nous avons montré que les PLC participent au maintien de la sécrétion chlorure dans le temps via l’activation d’un canal chlorure autre que CFTR. Par ailleurs nous avons identifié la PLCγ1 et la PLCβ3 comme étant nécessaires à l’activation maximale du courant CFTR dépendant, possiblement via des interactions avec les protéines NHERF et SHANK 2, deux protéines qui régulent l’activité de CFTR. Nous avons aussi montré que la PLCβ3 intervient dans la sécrétion d’ions chlorure par les canaux chlorures activés par le calcium (CaCC). Enfin, les PLC régulent l’homéostasie calcique dans les cellules bronchiques et nous avons mis en évidence des différences de régulation du canal calcique TRPV6 entre les cellules qui expriment le CFTR WT et celles qui expriment le CFTR F508del par un mécanisme impliquant les PLC. En résumé nous avons montré que les phospholipases C, et notamment la PLCβ3, jouent un rôle dans l’activité de trois conductances chlorure mais aussi dans la régulation de l’homéostasie calcique dans les cellules épithéliales bronchiques, résultats qui pourraient être exploités dans les recherches visant à améliorer la sécrétion de fluide dans le contexte de la mucoviscidose<br>Phospholipases C (PLC) are key enzymes involved in cellular transmission signals by membrane phospholipids hydrolysis and control, for instance, activities of proteins and ion channels. By producing DAG and IP3, PLC respectively activate protein kinase C and increase intracellular Ca2+ concentration, two pathways involved in the chloride channel CFTR (Cystic Fibrosis Transmembrane conductance Regulator) activity. Mutations on CFTR gene leads to the cystic fibrosis disease related to a loss of function and/or activity of CFTR. The aim of the thesis project is to study the extent to which PLC play a role in CFTR activity. Our results revealed an involvement of PLC in chloride secretion in bronchial epithelial cells depending on WT CFTR or temperature corrected F508del CFTR activity. In this way, we showed that PLC take part in maintaining chloride secretion over time via the activation of a non CFTR chloride channel. In addition, we identified PLCγ1 and PLCβ3 as two PLC required for maximal CFTR dependent chloride secretion, possibly by interacting with NHERF and SHANK2, both proteins involved in CFTR regulation. We also showed that PLCβ3 take part in calcium activated chloride channels (CaCC) activity. At last we showed a difference in the regulation of the TRPV6 calcium channel between bronchial epithelial cells expressing WT CFTR or F508del CFTR by a pathway involving PLC. To sum up, we showed that PLC take part in chloride secretion in bronchial epithelial cells. PLCβ3 in particular plays a role in different chloride channels including CFTR, CaCC and possibly a non CFTR chloride channel. These results could be managed in the future research to improve fluid secretion in context of cystic fibrosis
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Marc, Sylvie. "Étude de la régulation du système de transduction phospholipase C - inositol phosphates dans le muscle utérin : caractérisation pharmacologique de sous-classes fonctionnelles distinctes de récepteurs muscariniques." Paris 11, 1989. http://www.theses.fr/1989PA112038.
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La première partie de ce travail est une analyse du système de transduction phospholipase C-inositol phosphates dans le muscle utérin de cobaye : a) Dans le myomètre prémarqué au [3H] inositol, la stimulation par le carbachol, l'ocytocine et les prostaglandines conduit à la dégradation de PIP2 avec apparition séquentielle des inositol phosphates dans l'ordre IP3, IP2, IP. B) Une corrélation entre l'efficacité des différents effecteurs pour induire la contraction utérine et l'effet phosphoinositide permet d'impliquer l'inositol triphosphate dans leur action contracturante. C) L'utilisation de NaF plus AICI3 a permis la mise en évidence d'une protéine régulatrice G dans l'activation de la phospholipase C. Cette proteine G qui couple les récepteurs muscariniques et ceux de l'ocytocine à la phopholipase C est insensible à la pertussis toxine et à la choléra toxine; elle est donc différente de Gi et Gs impliquées dans la régulation du système adénylate cyclase. Une analyse pharmacologique du fonctionnement du récepteur muscarinique par l'utilisation de divers agonistes (carbachol, oxotrémorine, pilocarpine) et antagonistes (pirenzépine, AF-DX116, 4-DAMP) permet de caractériser deux sous-classes distinctes de récepteurs muscariniques couplées via des protéines G distinctes : a) à l'inhibition du système adénylate cyclase (sous-classes M2) et b) à l'activation de la phospholipase C et à la contraction Ca²+ -dépendante qui l'accompagne (sous-classe M3).
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Parre, Elodie. "La signalisation lipidique et le métabolisme de la proline en réponse à des contraintes hydriques : rôles des phospholipases C et D chez Arabidopsis thaliana." Paris 6, 2008. http://www.theses.fr/2008PA066213.
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Parmi les stratégies adaptatives que les plantes ont développées pour faire face aux contraintes hydriques, l’accumulation de proline est une réponse physiologique fréquemment observée chez un grand nombre d’espèces. Alors que le métabolisme de ce soluté compatible a été relativement bien caractérisé, les voies de signalisation impliquées dans sa régulation restent en grande partie inconnues. Par une approche pharmacologique, nous avons mis en évidence l’existence d’un contrôle positif de la biosynthèse de la proline par les phospholipases C – et la synthèse d’ IP3 – en réponse au NaCl et non au mannitol. D’autre part, nos données montrent l’importance du niveau de calcium intracellulaire et non de la signature calcique lors de la réponse prolinique. Au cours de ces dernières années, nous avons montré que la biosynthèse de la proline était régulée négativement par une activité PLD en conditions de croissance favorable. À la lumière de ces résultats, nous avons concentré nos efforts sur les PLD1 et PLD2 qui, parmi les douze isoformes de PLD végétales, sont les seules présentant une activité calcium-indépendante. Par une approche de génétique inverse, nous avons obtenu et caractérisé des mutants d’insertion pour les gènes PLD1 et PLD2. Bien que les niveaux de proline chez ces mutants ne soient pas affectés, ils présentent néanmoins des phénotypes très intéressants au niveau de la capacité de germination et de croissance racinaire en conditions de stress hydrique. Enfin, ce travail nous a permis de montrer que les plantes sont capables de discerner un stress salin d’un stress hyperosmotique par des voies de signalisation spécifiques.
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Chen, Wei. "Understanding the kinetic profile of phosphatidylinositol-specific phospholipase C from Listeria monocytogenes." Thesis, Boston College, 2008. http://hdl.handle.net/2345/966.
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Thesis advisor: Mary F. Roberts<br>The phosphatidylinositol-specific phospholipase C (PI-PLC) from Listeria monocytogenes (a monomer in solution) shows unusual kinetic properties compared to other well-studied phospholipases: (i) increased specific activity with decreasing protein concentration, (ii) activation of the phosphotransferase step by salts, and (iii) activation of both the interfacial phosphotransferase and water-soluble phosphodiesterase steps by zwitterionic and neutral amphiphiles. A variety of biophysical studies (fluorescence, NMR, monolayer, vesicle binding) of enzyme/lipid complexes coupled with kinetics have allowed us to propose a model that accounts for these features. The enzyme binds tightly to anionic surfaces and much more weakly to a zwitterionic interface. The tight binding can be reduced by adding KCl at concentrations that activate the enzyme. In the crystal structure of the enzyme, many basic residues are clustered on the sides and bottom of TIM-barrel far away from the opening to the active site. These cause the enzyme to adopt a non-productive orientation on negatively charged membranes that leads to a reversible clustering of anionic lipids and vesicle aggregation. An increased surface concentration of zwitterionic / neutral amphiphiles along with the salt disperses the anionic substrate, shields charges on the protein, and enhances productive encounters of the protein with substrate molecules. This model has been tested by examining the behavior of enzyme with citraconylated lysines and mutants of neutral surface residues at the rim of the active site. The unusual kinetic behavior of this PI-PLC also appears to contribute to the escape of L. monocytogenes from vacuoles during infection<br>Thesis (PhD) — Boston College, 2008<br>Submitted to: Boston College. Graduate School of Arts and Sciences<br>Discipline: Chemistry
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Zhao, Li. "Mechanistic Studies on Phosphatidylinositol-specific Phospholitase C." The Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=osu1047485476.
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Savopoulos, John William. "Functional characterisation of the pleckstrin homology domain of phospholipase C-#delta#1." Thesis, Institute of Cancer Research (University Of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243307.
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Owen, Helen Jane. "Characterisation of a phospholipase C-δ from sea urchin eggs and embryos." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411314.
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Cai, Jingfei. "Probing the Membrane Association Mechanisms for Pulmonary Collectins and Mammalian Phospholipase C." Thesis, Boston College, 2013. http://hdl.handle.net/2345/3872.
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Thesis advisor: Mary F. Roberts<br>Thesis advisor: Eranthie Weerapana<br>Peripheral proteins from mammals often exhibit multi-domain structures and require metal ions such as calcium as co-factors. This dissertation investigates two types of such proteins -- pulmonary collectins (surfactant proteins A and D) and phosphatidylinositol-specific phospholipase C (PLC) delta1 -- and their interactions with model membranes. One approach to work around the complexity brought upon by such multi-domain protein structure is to use a truncated construct or an isolated single domain. For pulmonary collectins, homotrimers consisting of the neck domain and the carbohydrate recognition domain were used in a novel NMR assay for better understanding of their lipid-specific interactions with the membranes. For PLC delta1, we were particularly interested in the role of the EF-hand domain. The isolated EF-hand domain of PLC delta1 was first used to characterize its interactions with membranes and identify key residues responsible for such interactions. These key residues in the N terminal lobe of the EF-hand domain, either cationic or hydrophobic, were then found to affect the hydrolysis activity of the full-length enzyme. A common role for this region of the PLC in facilitating proper membrane association was thus proposed<br>Thesis (PhD) — Boston College, 2013<br>Submitted to: Boston College. Graduate School of Arts and Sciences<br>Discipline: Chemistry
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Yilmaz, Umut [Verfasser]. "Calcium-abhängige Translokation der Phospholipase C-β1a aus der Plasmamembran / Umut Yilmaz". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1025238826/34.
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Reynolds, Nicholas John. "Investigation of phospholipase C/protein kinase C signalling pathways in skin relevant to the pathogenesis of psoriasis." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307375.
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盛建中 and Jianzhong Sheng. "Phosphoinositol/Ca2+ pathway in the cardiac k-opioid receptor: physiological role and alternations upontolerance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31237654.
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Yu, Yan Mei. "Effector regulation domains on G[alpha]16 and their role in the activation of phospholipase C[Beta] and other effectors /." View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?BICH%202004%20YU.
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Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2004.<br>Includes bibliographical references (leaves 94-103). Also available in electronic version. Access restricted to campus users.