Дисертації з теми "Cell biology, n.e.c"
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Lumngwena, Evelyn Ngwa. "The impact of HIV-1 subtype C Envelope N-glycosylation on DC-SIGN meditated modulation of DC function to facilitate transmission or enhance viral pathogenesis." Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/27096.
Повний текст джерелаSmith, Abigail O. "Defining the Role of c-Jun N-terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1141.
Повний текст джерелаAmin, Shahreen. "Regulation of the tyrosine phosphatase SHP-1 expression by C-jun-N-terminal kinase and RFX-1 and AP-4 transcription factors in insulin-like growth factor-1 (IGF-1) stimulated breast adenocarcinoma MCF-7 cells." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26837.
Повний текст джерелаSouyri-Caporale, Michèle. "Etude du pouvoir tumorigene de l'oncogene n-ras." Paris 7, 1987. http://www.theses.fr/1987PA077083.
Повний текст джерелаGavériaux, Claire. "Etude de l'interaction entre l'immunoglobuline e et son recepteur de forte affinite : mise au point d'un nouvel essai immunoenzymatique sur cellules, le celisa, importance de la n-glycosylation et de l'activation de la proteine kinase c dans l'expresion fonctionnelle de ce recepteur." Université Louis Pasteur (Strasbourg) (1971-2008), 1988. http://www.theses.fr/1988STR13014.
Повний текст джерелаBaalbaki, Zein El-A. "Vibrational relaxation of N₄O, C₄H₄, and C₄H₄-Ar mixtures." Thesis, University of Ottawa (Canada), 1986. http://hdl.handle.net/10393/4666.
Повний текст джерелаLloyd-Evans, Emyr. "Cell biology of Niemann-Pick type C disease." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437185.
Повний текст джерелаCo, Carl. "N-WASP at the membrane-actin interface." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2007. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3251943.
Повний текст джерелаAngers-Loustau, Alexandre. "Roles of c-Src and hDRR1 in glioma cell invasion." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85118.
Повний текст джерелаMcLachlan, Ian Gordon. "Genetic control of dendrite morphogenesis in C. elegans." Thesis, Harvard University, 2016. http://nrs.harvard.edu/urn-3:HUL.InstRepos:33493511.
Повний текст джерелаMedical Sciences
Dearth, Lawrence. "Characterization of C/EBPs in Mammary Epithelial Cell Biology." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1038840268.
Повний текст джерелаDearth, Lawrence R. "Characterization of C/EBPs in mammary epithelial cell biology /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486463803601699.
Повний текст джерелаMarais, Saberi. "XvVHA-c``1- a novel stress responsive V-ATPase subunit c`` homologue isolated from the resurrection plant Xerophyta viscosa Baker." Master's thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/4291.
Повний текст джерелаDriscoll, Kaitlin B. (Kaitlin Bridget). "Genetic and molecular studies of cell-autonomous execution during programmed cell death in C. elegans." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104177.
Повний текст джерелаCataloged from PDF version of thesis.
Includes bibliographical references.
Apoptosis or programmed cell death was originally defined by evolutionarily conserved morphological characteristics that include shrinkage of cell volume and chromatin condensation. Apoptosis functions as a highly controlled mechanism for the elimination of unwanted or damaged cells and is essential for disease prevention. Apoptotic cell death is a cell-autonomous process driven by the caspase family of cysteine proteases. The discovery of the CED-3 caspase in C. elegans led to the paradigm that caspase cleavage of substrates drives cell death and promotes engulfment. While many caspase substrates have been identified, it is not well understood how caspase substrates act to promote cell death and engulfment. The control of caspase activation in C. elegans is conserved among metazoans and involves the interplay of pro and anti-apoptotic BCL-2 and BH3-only family proteins. In C. elegans an increase in apoptotic cell refractility observed by Nomarski optics is one of the hallmark morphological characteristics of apoptosis. We found that the presumptive TRP channel CED-1 1 acts downstream of caspase activation in apoptotic cells to drive the increase in refractility. We discovered that CED-1 1 is also required for a decrease in cell volume and increase in nuclear permeability of apoptotic cells. We showed that CED-1 1 is required for efficient degradation of apoptotic cells and facilitates the death process, suggesting that the decrease in cell volume and/or increase in nuclear permeability could promote the death and degradation of the cell. We conclude that CED-1 1 acts downstream of caspase activation to effect multiple observed changes to apoptotic cells and to facilitate death and degradation. In addition we investigated the anti-apoptotic function of the generally pro-apoptotic BCL-2 homolog CED-9.
by Kaitlin B. Driscoll.
Ph. D.
Higuera, Urbano M��nica. "Regulaci��n de las v��as MAPK y Akt-FoxO1 en el mecanismo molecular de acci��n del Minerval contra el c��ncer de pulm��n y glioma." Doctoral thesis, Universitat de les Illes Balears, 2012. http://hdl.handle.net/10803/84084.
Повний текст джерелаGhilamicael, Amanuel Menghs. "Isolation and characterization of n-alkane utilizing bacteria, which produce biomulsifiers." Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/4265.
Повний текст джерелаBacterial strains were isolated by enrichment cultures from oil-contaminated soil samples. In the present study, several strains, capable of growing on crude oil, were isolated. Isolates were screened for their inherent abilities to produce bioemulsifiers when they were grown on hydrocarbon substrates.
Ouellet, Jimmy. "Control of cell division and quiescence during «C. elegans» developement." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18654.
Повний текст джерелаPuisque son développement ne varie pas, le nématode C. elegans est un organisme pouvant servir de modèle génétique pour identifier des gènes requis dans bon nombre de processus. De ce fait, le laboratoire du Dr Roy utilise cet organisme pour identifier des gènes qui régulent la division cellulaire durant son développement. L'isolement de 5 mutants, qui influencent la division cellulaire de l'intestin, m'a permis de caractériser le rôle de ces gènes dans la transition de la mitose vers la karyokinèse, puis vers l'endoréplication. Cette transition est spécifique aux cellules intestinales à la fin du premier stade larvaire du développement post-embryonnaire. Ces cinq mutants ont été groupés soit dans la classe de mutants avec plus de noyaux intestinaux que la souche sauvage (rr33 et rr45), soit dans celle en contenant moins (rr42, rr43 et rr44). Le clonage des mutants contenant plus de noyaux intestinaux m'a permis d'observer l'influence de la mutation rr33 sur le gène lin-35, l'homologue du gène du rétinoblastome chez l'humain, et de rr45 sur le gène nol-10. Je démontre que lin-35 interagit avec les composantes de la voie RNAi afin de permettre la répression des gènes requis pour la transition du cycle cellulaire des cellules intestinales. Mes résultats permettent également d'observer le rôle de met-2, un homologue de la méthyltransférase Suv39h et de deux protéines hétérochromatiques hpl-1 et hpl-2, dans le maintien de cette répression. De plus, j'ai pu constater que, durant ma caractérisation de l'arrêt du cycle cellulaire propre au stade dauer, le ligand Notch lag-2 est spécifiquement exprimé au début et durant tout ce stade dans 6 neurones Inter Labial 2 (IL2). J'ai pu démontrer que l'expression de ce ligand correspond au besoin de la voie de signalement canonique Notch pour maintenir ce stade de développement et aussi que l'expression du récepteur Notch glp-1 dans les neurones empêche le défaut de maintien$
Galvin, Brendan D. (Brendan Daniel). "The regulation of programmed and pathological cell death in C. elegans." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/38633.
Повний текст джерелаIncludes bibliographical references.
Programmed cell death, or apoptosis, is important in the development and homeostasis of metazoans. In the nematode C. elegans, four genes, egl-1, ced-9, ced-4, and ced-3, constitute the core pathway acting in all somatic programmed cell deaths. This pathway is evolutionarily conserved in humans. The BH3-only protein EGL-1 is transcriptionally upregulated in cells fated to undergo programmed cell death, and EGL-1 blocks cell-death inhibition by the cell-death regulator CED-9, a Bcl-2 family member. The binding of EGL- 1 to CED-9 releases the Apaf- 1-like adaptor protein CED-4 from CED-9, so that CED-4 can activate the caspase CED-3, a protease that is the effector of programmed cell death. In this thesis, I describe three projects, each of which examines one aspect of C. elegans cell death. From. screens for mutations that increase cell death in a sensitized genetic background, I identified a gene that protects cells from programmed cell death.
(cont.) This gene, spk-1, encodes a homolog of SR protein kinases, which regulate alternative splicing. Previous work has shown that ced-4 pre-mRNA is alternatively spliced to generate two transcripts that function oppositely in cell death. I found that spk-1 regulates ced-4 transcript splicing, thereby influencing the amount of programmed cell death that occurs. From a screen for genes that promote programmed cell death, I isolated a mutation in a conserved non-coding element in the transcriptionally regulated cell-death activator gene egl-1. This element regulates the deaths of specific cells in the C. elegans ventral nervous system. I found a novel C. elegans transcription factor, Y38C9A. 1, that binds this element and might function to regulate egl-1 transcription and programmed cell death in the ventral nervous system. In addition to the programmed cell deaths that occur in C. elegans, pathological death of specific cells can be caused by mutations in some genes. I characterized two genes, lin-24 and lin-33, that can mutate to cause the inappropriate death of specific hypodermal blast cells. One of these genes, lin-24, contains a domain similar to that found in some bacterial toxins.
(cont.) By morphological and genetic criteria, I show that the lin-24- and lin-33-mediated deaths are unlike previously characterized necrotic and apoptotic cell deaths in C. elegans. These deaths require some of the genes responsible for engulfing the corpses generated by programmed cell death, even though the deaths do not require the core genes of the genetic pathway of programmed cell death.
by Brendan D. Galvin.
Ph.D.
Chen, Xiulian. "The negative impact of copper deficiency upon cardiac and C₂C₁₂ cell mitochondria biology /." Search for this dissertation online, 2004. http://wwwlib.umi.com/cr/ksu/main.
Повний текст джерелаRico, Vargas Sergio Arturo. "Regulation and dysregulation of B lymphopoiesis in mouse bone marrow: in vivo role of macrophage activation (pristane-treatment and malaria-infection), c-myc, c-kit, and immunoglobulin genes." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41340.
Повний текст джерелаLee, Kyung-Joo 1977. "Identification of proteins interacting with the N-termini of USP2 deubiquitinating enzyme isoforms." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81352.
Повний текст джерелаTo identify substrates or interacting proteins that may serve to localize these enzymes, a bacterial two-hybrid assay was performed using a mouse testis cDNA library and the N-termini of the enzymes as baits. Kpna6, an isoform of Karyopherin alpha (also known as importin alpha) and SKD3, the suppressor of K + transport defect protein were found to be possible interacting proteins of USP2a and USP2b respectively.
Corral, Marisol. "Caracterisation de genes cellulaires dont l'expression est associee a la cancerisation hepatique." Paris 6, 1987. http://www.theses.fr/1987PA066124.
Повний текст джерелаKim, Saechin. "Two C. elegans genes that can mutate to cause degenerative cell death." Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/11945.
Повний текст джерелаChihara, Daisuke. "An E-cadherin-mediated hitchhiking mechanism for C. elegans germ cell internalization during gastrulation." Thesis, New York University, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=3556984.
Повний текст джерелаWe have used the C. elegans primordial gonad to understand how stem cells assemble into a niche during development. The C. elegans primordial gonad contains two somatic gonad precursor cells (SGPs) and two primordial germ cells (PGCs). The primordial gonad assembles during embryogenesis when PGCs and SGPs come together adjacent the intestine.
As a first step in understanding niche assembly, we investigated how PGCs move to the site where the primordial gonad forms. PGCs and somatic cells move into the interior during gastrulation. Because somatic cells require transcription to ingress whereas PGCs are transcriptionally quiescent, we hypothesized that somatic cells might push or pull the PGCs into the embryo. We used videomicroscopy to identify cells that contact the PGCs, and used laser killing to determine if the contacting cells are required for PGC ingression. The PGCs are surrounding by adjacent mesodermal cells and internal endodermal cells. We found that the only contacting cells necessary for PGC ingression were the endodermal cells, which ingress into the embryo an hour before the PGCs. Killing or altering the fate of the endodermal cells prevented PGC ingression but not ingression of other somatic cells. Using fluorescent membrane markers and live imaging, we showed that PGCs and endodermal cells maintain contact throughout gastrulation, and that endodermal cells move dorsally as PGCs ingress form the ventral surface. PGCs express high levels of E-cadherin/HMR-1, and knocking down E-cadherin/HMR-1 caused PGCs to detach from endodermal cells and remain on the surface of the embryo. Finally, we show that the enrichment of HMR-1 protein in the PGCs is not due to transcriptional upregulation, but is instead due to an increase in protein expression mediated by the hmr-1 3' UTR. We propose that PGCs upregulate E-cadherin/HMR-1 to maintain tight adhesion with endodermal cells, which pull the PGCs into the embryo and position them at the site of primordial gonad assembly. Our results highlight the importance of germ cell - gut interactions during development and of E-cadherin-mediated adhesion in niche formation.
Lu, Yu. "Cell cycle uncoupling, elimination, and functional modification of centrioles during C. elegans development." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116920.
Повний текст джерелаLa duplication des centrosomes est couplé à la division cellulaire afin qu'elle n'ait lieu qu'une seule fois par cycle cellulaire. Cependant, lors de certains contextes développementaux, ce couplage n'a pas lieu et ceci reste mal compris à ce jour. Chez C. elegans, alors que les cellules hypodermales et intestinales font de l'endo-replication, les cellules souches germinales sortent de la mitose pour entrer en méiose. L'utilisation de ces différents modèles cellulaires, nous permet de mieux comprendre comment la duplication des centrosomes est dans la plupart des cas intimement couplée au cycle cellulaire, et d'étudier les mécanismes où la duplication des centrioles est indépendante à la division cellulaire au cours de contextes développementaux particuliers.SPD-2 est une protéine essentielle à la duplication des centrioles chez C.elegans. En observant ses niveaux d'expression, nous avons pu montré qu'alors que les centrioles sont correctement dupliqués lors de la division des cellules intestinales, ils ne se re-dupliquent pas au cours du 1er-cycle d'endo-replication. En effet, SPD-2 diffuse dans le noyau, avant d'être éliminé. Cette dynamique semble être activement régulée, car elle n'est pas observée dans des situations où l'ADN est très anormalement répliqué. Afin d'étudier l'importance des régulateurs du cycle cellulaire dans ce découplage centrosome/cycle cellulaire, nous avons généré des variants SPD-2, phosphomimétiques ou non-phosphorylables. De manière très intéressante, la modification de la serine 545, site très conservé pour la phosphorylation par CDK, entraine le découplage de la duplication du centriole par rapport au cycle cellulaire. Au contraire, en mimant la phosphorylation par PLK ou en diminuant l'activité de la voie de l'ubiquitylation, par ARNi, la protéine SPD-2 s'accumule dans le noyau. Cette accumulation est probablement due à la stabilisation de la protéine, mais elle n'affecte pas la duplication du centrosome. Notre étude révèle donc l'importance des phosphorylations de SPD-2 par différentes kinases clés du cycle cellulaire dans la régulation son activité. En effet, celles ci pourraient réguler le découplage de la duplication des centrosomes du cycle cellulaire et affecter leur élimination au cours du développement chez C. elegans.Parallèlement, nous nous sommes aussi intéressé au rôle de RNF-1, une protéine contenant des domaines RING qui interagit avec CKI-2, un membre de la famille Cip/Kip. Nous avons démontré que RNF-1 joue un rôle crucial dans l'ubiquitylation de CKI-2, qui est alors dégradé par la voie du protéasome. Ainsi, l'expression de RNF-1 réduit la létalité embryonnaire causée lors d'une mauvais expression de CKI-2. RNF-1 se localise à la périphérie du noyau, toutefois la fonction associée à cette localisation nécessite une étude plus approfondie.Finalement, nous avons etudié le rôle de la γ-tubuline au cours de la progression des cellules germinales. Nous avons trouvé que la γ-tubuline est redistribuée depuis sa localisation centriolaire vers la membrane cytoplasmique des cellules germinales pendant la méiose. Cette redistribution inhibe les capacités du centriole à générer la nucléation des microtubules, ceci résultant probablement de signaux transmis lors de la transition entre la mitose et la méiose. Nous continuons notre travail afin de comprendre le rôle et les mécanismes impliqués dans cette redistribution.
Mathopa, Byatlela Abel. "Isolation of bacterial strains capable of efficient conversion of n-alkanes into value added products." Master's thesis, University of Cape Town, 2004. http://hdl.handle.net/11427/4294.
Повний текст джерелаBacteria that are capable of degrading alkane fractions, C12-C13 and C14-C17, were isolated from oil-contaminated soil collected from the petrochemical company, CALTEX Refineries, South Africa. A total of twenty-three environmental strains were isolated. A preliminary procedure, Nile Blue A straining suggested that twelve of the twenty-three environmental strains might accumulate polyhydroxyalkanoates (PHAs) in their cytoplasm, which is a good candidate for biodegradable plastics. The gene that catalyzes PHA polymerization, phaC, was detected using PCR in some of the environmental strains. The strains of interest were identified and characterized biochemically using various techniques and later sequenced by 16S rONA PCR. The environmental isolate 2 showed a 99 % identity to Pseudomonas aeruginosa BHP7 -6 and was for that reason given a name, Pseudomonas aeruginosa MB2SA. P. aeruginosa MB2SA was shown to possess a 0.5 kb internal fragment corresponding to the phaC gene and capable of degrading the alkane fractions, Cn-CI3 and CI4-CI7, effectively. P. aeruginosa MB2SA was shown to grow optimally in the long alkane fraction, Cw C17, and was further grown in pure alkanes, n-dodecane, n-tetradecane, and hexadecane for comparison. In addition, the strain, P. aeruginosa MB2SA, was grown in an appropriate medium for PHA synthesis and high yields of PHA were observed when both the long alkane fraction, Cw CI7, and pure alkane, hexadecane, were employed as sole carbon sources respectively.
Learmont, Jessica. "Prion-like properties of the N-terminal domains of the rat and human FoxG1 transcription factors." Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/4285.
Повний текст джерелаIncludes bibliographical references (leaves 82-90).
The purpose of this study was to investigate the possible prion-like properties of the N-terminal domains of the winged-helix transcription factor FoxG1.
Stanfield, Gillian Marie 1970. "Genetic analysis of timing, morphology and degradation of cell corpses in C. elegans." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85286.
Повний текст джерелаZhao, Xi. "Cell cycle regulation : the role of the c-mos oncoprotein and the cytoskeleton /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487677267731537.
Повний текст джерелаTiensuu, Teresa. "Cell fate specification by Ras-mediated cell signalling in C. elegans." Doctoral thesis, Umeå : Univ, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-120.
Повний текст джерелаBuchanan, Fritz G. "Endogenous Alkylglycerol Functions As a Mediator of Protein Kinase C Activity and Cell Proliferation." Digital Commons @ East Tennessee State University, 1997. https://dc.etsu.edu/etd/2885.
Повний текст джерелаSiam, Rania. "Mechanisms of C. crescentus regulation of chromosome replication by a cell cycle regulator protein." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37838.
Повний текст джерелаThis cooperative CtrA binding at [a] and [b] is independent from the upstream binding sites [c-e] (Chapter 2). CtrA∼P binding in the origin is altered in the presence of the histone-like protein (IHF) that also binds and overlaps CtrA binding site [c] (Chapter 5). In-fact, IHF binds and overlaps binding site [c] (Chapter 5). We propose a replication model in the stalked cell were IHF binding hinders active CtrA binding in the replication origin and regulates cooperative transcription that coincides with replication initiation.
Halsey, Richard James. "Construction and characterization of chimaeric human immunodefiency virus type 1 subtype C Gag virus-like particles." Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/4269.
Повний текст джерелаIn this study I explored the possibility of making HIV-1 subtype C Pr55gag-based chimaeric virus-like particles (VLPs) as a boost to the HIV-IC multigene DNA vaccine pTHr.grttnC, which encodes a modified Gag-RT-Tat-Nef fusion protein (GRTTN). Furthermore, an attempt was made to produce VLP analogues to the HIV-IA polyepitope DNA vaccine pTHr.HIVA. A range of in-frame fusions with the C-termini of myristylation-competent p6-truncated Gag and native Pr55gag were made to test how the length of polypeptide and its sequence might affect VLP formation and structure.
Jackson, Andrew R. 1972. "Estrogenic regulation of N-cadherin in the rat testis : an examination using agonists and antagonists of estradiol." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27349.
Повний текст джерелаI have examined the estrogen effects on N-cadherin protein levels in the testes of 21-day-old rats. The rats were injected with either 17$ beta$-estradiol, the anti-estrogens Tamoxifen and ICI 182,780, or estradiol in combination with ICI 182,780. Immunoblotting analysis of testicular proteins shows that N-cadherin levels in the 21-day-old rat are stimulated by estrogen. Treatment with anti-estrogens decrease N-cadherin levels. Administration of estrogen was able to overcome the inhibitory effects of anti-estrogen treatment. The results obtained from these studies indicate that the effect of estrogen on testicular N-cadherin levels is mediated through the estrogen receptor. Estrogen receptor levels within the testis are not altered by exogenous estrogen, but can be affected by treatment with anti-estrogen.
These experiments support the hypothesis that estrogens play an important role in spermatogenesis. In addition, the results provide insight into how disruption of testicular estrogen responsiveness can reduce fertility and why chronic anti-estrogen treatment results in disorganization of the seminiferous epithelium.
Finney, Michael. "The genetics and molecular biology of unc.-86, a C. elegans cell lineage gene." Thesis, Massachusetts Institute of Technology, 1987. http://hdl.handle.net/1721.1/14628.
Повний текст джерелаBabbar, Naveen. "Regulation and function of spermidine/spermine N¹ acetyl transferase (SSAT) in colon carcinogenesis." Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/289966.
Повний текст джерелаCarson, Christine. "Characterization of lamins A and C expression during differentiation of HL-60 cells towards monocytes/macrophages in vitro." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/9718.
Повний текст джерелаHocevar, Barbara Ann. "Characterization of nuclear protein kinase C." Case Western Reserve University School of Graduate Studies / OhioLINK, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=case1057177248.
Повний текст джерелаVandermeer, Lisa Anne. "Evaluation of c-KIT in ovarian surface epithelial cells and ovarian tumours." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/27067.
Повний текст джерелаAl-Mazidi, Hayfa A. "Unique localization of protein kinase C isozymes in T51B rat liver cells and their role in proliferation and apoptosis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq20987.pdf.
Повний текст джерелаIlbay, Orkan. "Robustness Mechanisms of Temporal Cell-Fate Progression in C. Elegans." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1057.
Повний текст джерелаTebo, Julie M. "Characterization of the C-reactive protein receptor on the human monocytic cell line U-937 /." The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487681788253375.
Повний текст джерелаGrönberg, Naima. "Induction of pathogenesis-related genes, PR-17a and N-methyltransferase, in barley infested by the aphid Rhopalosiphum padi." Thesis, Södertörn University College, School of Life Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:sh:diva-656.
Повний текст джерелаPlants produce a large diverse array of organic compounds that may function in protection against pathogens. Diverse antifungal compounds were reported to exist in barley (Hordeum vulgare L.); the indole alkaloid, gramine, and the pathogenesis-related proteins are some of them. Both the N-methyltransferase that is involved in gramine biosynthesis and PR-17a were studied in barley upon infestation by the bird cherry-oat aphid (Rhopalosiphum padi).
The effect of infestation by R. padi on induction of PR-17a and N-methyltransferase was investigated in different barley lines, susceptible and resistant.
The gene expression of PR-17a was down-regulated in the susceptible cv. Golf and to some extent up-regulated at the first days in var. Lina and then down-regulated. The PR-17a was induced by the aphid infestation in the resistant line CI16145; the gene expression was stronger in the infested plants than in the controls. The different responses in resistant and susceptible lines indicate that the induced PR-17a may play a role in the resistance against aphid infestation. PR-17a was up-regulated systemically in the base in barley after infestation by R. padi.
In the susceptible varieties Lina and Golf, the accumulation of N-methyltransferase did not increase with time from 1 day to 7 days after infestation, as determined by western blots with antibody raised against NMT from barley. The NMT-gene was down-regulated after 7 days infestation in both variety Lina and Golf both locally in the first leaf and in the base. Barley line CI16145 had no accumulation of NMT as was seen by western blotting. There was no induction of NMT in barley upon aphid infestation.
Bandawe, Gama. "Expression of HIV-1 subtype C nef in E. coli and Nicotiana benthamiana : development of plant-based vaccines for HIV." Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/4242.
Повний текст джерелаExpression of the nefgene from HIV-1 subtype C in Nicotiana benthamiana was carried out using a TMV -based vector with the aim of developing a plant-based candidate vaccine for HIV-1. The nef gene of the DU151 isolate of mV-l subtype C taken from a recently seroconverted individual was amplified by PCR with a deletion of 59 amino acids from the cytotoxic N-terminal. The amplified gene was inserted into a bacterial expression vector pProEXHTb for rapid expression of Nef protein, which was used as a diagnostic tool in the development of an indirect ELISA assay for detection of Nef in Nicotiana benthamiana. An indirect ELISA assay was developed using a commercially available polyclonal anti Nef antiserum raised in sheep. The role of codon optimization in expression of Nef in benthamiana was investigated. A synthetic nef gene was constructed based on the codon usage of benthamiana. The plant codon optimized gene and the wild type nef genes were inserted into the TMV -based vector pBSG1057. RNA transcripts from both constructs were used to infect young benthamiana plants. Expression of nefmRNA was confirmed by RT -PCR analysis of total RNA extracted from plants inoculated with respective constructs. The Nef protein was expressed at low levels which were detectable by ELISA. Nef was detectable by Western blot after concentration of plant extract using a membrane filter device. Quantitative analysis of Nef expression in plants was done by western blot on concentrated plant extract from three separate infections. Codon optimization of the nef gene improved the expression of Nef by a factor of about two.
Keszthelyi, Eniko Judith. "The effects of hormones, growth factors and cyclic AMP on ovarian carcinoma cell proliferation and expression of c-kit and Kit ligand." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0001/MQ36707.pdf.
Повний текст джерелаYuan, Libin. "A stretch of 17 amino acids in the prosaposin C-terminus is critical for its binding to sortilin and targeting to lysosomes." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=92262.
Повний текст джерелаTo identify the sequences and amino acids involved in the interaction of prosaposin to sortilin and its transport to the lysosomes, we generated six prosaposin deletion constructs and examined the effect of truncation by co-immunoprecipitation and confocal microscopy. The experiments revealed that a 17 amino acid stretch in the first half of the C-terminus (aa524-540) was necessary for the binding of prosaposin to sortilin and essential for its transport to the lysosomes.
Since the pH is able to induce conformational changes in the four saposin domains, we performed a pH-dependent binding assay to test whether or not the binding of prosaposin to sortilin was affected by different pHs. The experiments demonstrated that binding of prosaposin to sortilin occurred at 6.0 or higher. A substantial decrease in binding was detected at pH 5.5, and at pH 5.0 both proteins did not form complexes. This result indicated that the binding of prosaposin to sortilin is pH-dependent.
Since hydrophilic residues usually modulate pH-dependent protein interactions we introduced six site-directed point mutations in hydrophilic residues within the first half of the C-terminus. The results showed that the mutation of single hydrophilic amino acids did not affect the binding of prosaposin to sortilin.
Considering that tryptophan, cysteine and proline residues are important in protein structure and function, we also introduced eight site-directed point mutations to these residues within the 17 amino acid stretch in the C-terminus. The experiments revealed that two tryptophans (W530 and W535), and two cysteines (C528 and C536) were essential for the transport of prosaposin to the lysosomes. In addition, one proline residue (P532) was critical for the proper folding of prosaposin during its synthesis, which was demonstrated by the MG132 Proteasome Inhibition Assay.
In conclusion, we have narrowed down the sortilin recognition site on the prosaposin molecule to a specific 17-residue stretch in the first half of the C-terminus and discovered the essential residues in this region for the lysosomal trafficking of prosaposin.
Les protéines lysosomiales solubles récemment identifiées et synthétisées sont transférées de l'appareil de Golgi des cellules vers les lysosomes par deux récepteurs, des mannoses 6-phosphates. Cependant l'activateur sphingolipidique de la prosaposine est ciblé sur la lysosomes par un récepteur alternatif, la sortiline. La prosaposine est le précurseur de quatre saposines lysosomiales requises pour l'hydrolyse des sphingolipides. Une étude récente a déjà démontré que l'élimination de la terminaison-C de la sphingolipide empêche le transport de la prosaposine vers les lysosomes.
Pour identifier les séquences d'acides aminés impliqués dans l'interaction de la prosaposine avec la sortiline et ainsi clarifier le mode de transport de ces séquences vers les lysosomes, nous avons procédé, par co-immunoprécipitation et immunomicroscopie confocale et à l'élimination de six séquences distinctes de la saposine. Ces expériences ont montré que la première moitié de la terminaison-C (aa524-540) la séquence des 17 résidus peptidiques est nécessaire pour permettre la liaison de la sortiline à la prosaposine et le transport de la prosaposine vers les lysosomes. fr
Le pH du milieu agit sur l'interaction d'un ligand à son récepteur. Nous avons donc analysé la liaison de la prosaposine à la sortiline à différents pH. Les résultats on montré que la liaison de la prosaposine à la sortiline se fait à un pH de 6.0 ou plus. Par contre la prosaposine ne forme pas de complexes avec la sortiline à des pH de 5.0 et 5.5. fr
Puisque les résidus hydrophiles modulent normalement l'interaction des protéines nous avons introduit des mutations focales (point mutations) sur six sites de tels résidus hydrophiles de la terminaison-C de la prosaposine. Les résultats ont montré que de telles mutations n'ont aucun effet sur la liaison de la sortiline à la prosaposine. fr
Considérant que le tryptophane, la cystéine et la proline forment des séquences importantes de la structure et de la fonction des protéines, nous avons inséré huit mutations focales additionnelles sur la séquence de 17 résidus de la terminaison-C de la prosaposine. Les résultats ont révélé que deux molécules de tryptophane (W530 etW535) et deux molécules de cystéine (C528 et C536) sont essentielles au transport de la prosaposine vers les lysosomes. Par ailleurs, une molécule de proline (P532) provoque la dégradation de la prosaposine par des protéosomes. fr
En conclusion nous avons circonscrit certains aspects moléculaires de la relation de la sortiline à la prosaposine. Nous avons montré en particulier que la liaison de la sortiline à la prosaposine se situe au niveau d'un site précis du segment de la terminaison-C de la prosaposine dont certains éléments jouent un rôle essentiel dans le transport de la prosaposine vers les lysosomes. fr
Wang, Haizhen. "The C-Phycocyanin/Beta Protein Inhibits Cancer Cell Proliferation." unrestricted, 2008. http://etd.gsu.edu/theses/available/etd-04212008-155113/.
Повний текст джерелаTitle from file title page. Zhi-Ren Liu, committee chair; Delon W. Barfuss, Jenny J. Yang, committee members. Electronic text (69 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed June 11, 2008. Includes bibliographical references (p. 61-67).
Fearon, Shelley Helen. "The Development of an African Horse Sickness Virus VP7 Quasi-Crystal Vaccine Candidate in N. benthamiana." Master's thesis, Faculty of Science, 2019. https://hdl.handle.net/11427/31671.
Повний текст джерелаJannie, Karry Marie. "Activated leukocyte cell adhesion molecule (ALCAM) regulation of tumor cell behavior and neuronal targeting." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/2901.
Повний текст джерелаPrevost, Manon. "The effects of stromal-derived factors and gonadotropins on rat ovarian surface epithelial cell proliferation and expression of c-Kit and Kit ligand." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6452.
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