Dissertations / Theses on the topic 'Biochemistry and Cell Biology'
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Camacho, Diogo Mayo. "In silico cell biology and biochemistry: a systems biology approach." Diss., Virginia Tech, 2007. http://hdl.handle.net/10919/27960.
Full textPh. D.
Agüera-González, Sonia. "Cell biology on NKG2D ligands and NK cell recognition." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609348.
Full textChambers, Jeremy W. "Studies in the biochemistry and cell biology of Trypanosoma brucei hexokinases." Connect to this title online, 2007. http://etd.lib.clemson.edu/documents/1202500780/.
Full textTrotman, Jackson B. "New Insights into the Biochemistry and Cell Biology of RNA Recapping." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523896565730483.
Full textDelorme, Marilyne. "Downregulation of ATRX disrupts cell proliferation and cell cycle progression." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27627.
Full textHussey, P. J. "Studies on the molecular and cell biology of plant tubulin." Thesis, University of Kent, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376791.
Full textYe, Qing. "LIPASE-KINASE ASSOCIATIONS INVOLVING PLD2, JAK3 AND FES THAT UNDERLIE CANCER CELL PROLIFERATION AND INVASION." Wright State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=wright1421939242.
Full textChu, Wei. "Mouse Mast Cell Proteases: Induction, Molecular Cloning, and Characterization." Digital Commons @ East Tennessee State University, 1991. https://dc.etsu.edu/etd/2656.
Full textPetosa, Adamo. "Isolation of human scFv expressing cells from a yeast library using magnetic and fluorescence activated cell sorting." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=101733.
Full textThe reduced size of the scFv relative to the intact IgG allows it to penetrate tissue with greater ease and therefore reach epitopes within both tissue and cells that would otherwise remain inaccessible. As a result, one possible scFv application is the study of cartilage destruction by proteases that occurs in both normal joint development and arthritis. Antibody fragments would allow for cartilage degradative processes to be studied in vivo . Fluorescently tagged scFvs could penetrate intact cartilage tissue, bind to epitopes and then be localized using techniques such as dual photon confocal microscopy. This would not be possible using IgG molecules.
The yeast library developed by Feldhaus et al. was obtained for the potential isolation of cells expressing scFvs to cartilage neoepitopes. While found to possess an inherent Candida parapsilosis contamination, the surface display library was screened using three peptide-ovalbumin-biotin complexes. Peptides corresponding to observed cartilage neoepitopes were bound to biotinylated ovalbumin and added to the library for screening. Excess unlabelled ovalbumin was also added to the library to prevent the isolation of ovalbumin binding cells.
In all, two rounds of MCS and two rounds of FACS with all three antigens were used to screen the library for binders. A portion of the remaining library cells was then screened by MCS with a single antigen and eight individual clones were isolated. The affinity of these clones was determined and the scFv region of one clone was sequenced. Despite preventative measures, all eight clones isolated and analyzed were found to have an affinity to undetermined ovalbumin complex regions other than the peptides of interest. Still, cells expressing scFvs binding to a portion of the antigen complexes presented to the library were clearly enriched and subsequently isolated using MCS and FACS.
Bainor, Anthony J. "Elucidating the Role of SIN3B as a Regulator of Cell Cycle Exit." Thesis, New York University, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10604607.
Full textProgression through the mammalian cell cycle is a tightly regulated process that allows cells to replicate their genomes and divide properly. In growth factor-deprived conditions or in response to stress, the cell will exit the cell cycle either reversibly through quiescence, or permanently via senescence. Studies have shown that the SIN3 family of proteins plays a crucial role in these cell cycle exit processes. SIN3 proteins are highly conserved, and exist in mammals as two family members: SIN3A and SIN3B, which function as flexible scaffolding proteins to assemble co-repressor complexes. Our laboratory has recently implicated SIN3B as a critical mediator of each of these cell cycle exit processes. However, its mechanism of action and the consequences of its disruption pertaining to cancer progression have not been comprehensively elucidated. Here we demonstrate that SIN3B is required for the induction of senescence in a mouse model of prostate cancer, and thus prevents the progression to aggressive and invasive carcinoma. In addition, through interaction analysis, we uncovered a novel and robust association between SIN3B and the DREAM complex. The DREAM complex, comprised of p107/p130, E2F4/5, DP1 and the MuvB core complex, is responsible for the repression of hundreds of cell cycle-related transcripts during quiescence. We determined that the deletion of SIN3B resulted in the derepression of DREAM target genes during quiescence, but was not sufficient to allow quiescent cells to resume proliferation. However, the ectopic expression of APC/CCDH1 inhibitor EMI1 was sufficient for SIN3B deleted cells, but not wild-type cells, to reenter the cell cycle. These studies demonstrate a critical role for SIN3B in the senescence and quiescence programs, and provide important mechanistic insight into the molecular pathways that exquisitely regulate cell cycle exit.
Upcher, William R. "Biochemical studies of the cohesin complex." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:e9a77a9c-40a5-466d-a894-c7fefeddef52.
Full textFernández, Lola. "Studies on the biochemistry and cell biology of the glycosyl-phosphatidylinositol (GPI)-anchored NKG2D-ligands." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609534.
Full textSipe, Conor W. "Cloning and Functional Characterization of Hypoxia-Inducible Factor 1alpha Upstream Regions in Xenopus laevis." W&M ScholarWorks, 2003. https://scholarworks.wm.edu/etd/1539626407.
Full textReimer, Michael. "Characterization of IQGAP1 Protein in Areas of Cell Retraction." Thesis, Southern Illinois University at Edwardsville, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=1582876.
Full textIQGAP1 interacts with numerous binding partners through a calponin homology domain (CHD), a WW motif, IQ repeats, a Ras GAP related domain (GRD), and a conserved C-terminal (CT) domain. Among various biological and cellular functions, IQGAP1 plays a role in cell-matrix interactions and actin cytoskeleton dynamics in membrane ruffling and lamellipodium protrusion. Phosphorylation in the CT domain regulates intramolecular interaction and IQGAP1 cellular activity. In a recent study, we discovered that IQGAP1 surprisingly localizes to actively retracting edges, instead of protruding areas, in B16F10 mouse melanoma cells and some other cells types. In these current studies we examined localization of IQGAP1 mutants to retracting versus protruding areas in phorbol ester-stimulated B16F10 cells. Cells were co-transfected with GFP-IQGAP1 full length (GFP-IQGAP1-FL), as an internal control, and one of five Myc-tagged IQGAP1 constructs (FL, CA, ΔCHD, ΔGRD or ΔCT). The cotransfected cells were plated onto laminin for 30 minutes, stained with anti-Myc and anti-WAVE2 antibodies, and normalized fluorescence measurements were made in retracting and protruding areas. Retracting cell areas were defined as GFP-IQGAP1-FL positive and WAVE2 negative, while protruding cell areas were defined as GFP-IQGAP1-FL negative and WAVE2 positive. In retracting areas there were large decreases in both ΔGRD and ΔCT localization, a slight decrease in ΔCHD localization, and normal localization of the CA mutant. In areas of cell protrusion there were large increases in both ΔGRD and ΔCT localization, and normal localization of ΔCHD and CA mutants. These results indicate that two domains, GRD and CT, are essential for normal localization of IQGAP1 to retracting cell areas. Furthermore, our results suggest a model in which IQGAP1 in the areas of cell retraction is in the open, phosphorylated, conformation. Additionally we investigated the knockdown of IQGAP1 in B16F10 cells by means of actin images. Cells were exposed to the lentil virus which contained short hairpin Ribonucleic acid (shRNA) that would silence IQGAP1. Two controls were used in the experiment, untransfected B16F10 cells and B16F10 cells which were exposed to the lentil virus without any shRNA. We found that the knockdown cells were in general much more compact and that they did not polarize. Surface stiffness was investigated in the effect it would have on B16F10 cells. Polyacrylamide gels were made and cross-linked using sulfo-SANPAH. Laminin was added to the cross-linked gels and B16F10 cells were placed on top of the laminin coated hydrogels. Investigation of the cells by means of actin images revealed that surface stiffness had an effect on cell morphology. The 1 kPa surfaces did not allow for spreading of the cells, while the surfaces greater than 100 kPa exhibited normal cell behavior.
Poole, Charla N. "Cardiovascular therapeutics derived from the paracrine biology of adult human progenitor cells." Thesis, Tulane University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3628932.
Full textAdult multipotent stromal cells (MSCs) may repair tissue through the action of secreted factors on endogenous stem/progenitor cells. We determined the effects of MSC-secreted factors on adult cardiac progenitor cells (CPCs). Serum-free conditioned medium (CdM) was collected from MSCs isolated by plastic adherence (MSCs) and by magnetic sorting against the p75 nerve-growth factor receptor (p75MSCs). Compared to serum-free medium (α-MEM), CdM significantly increased adult rat CPC proliferation in a concentration-dependent manner, led to phosphorylation (Tyr705) and nuclear localization of signal transducer and activator of transcription 3 (STAT3) and was blocked by both AG490, a Janus kinase 2 (Jak2)/STAT3 inhibitor, and Stattic, a specific STAT3 (Tyr705) inhibitor. Also signaling through Jak2/STAT3, MSC CdM cytoprotective factors significantly increased survival of hypoxic CPCs compared to α-MEM. Intra-arterial infusion of p75MSC CdM 24 hours after myocardial infarction (MI) in mice significantly reduced myocardial necrosis at 48 hours after MI compared to α-MEM (vehicle). Echocardiography at 1 week after MI demonstrated significantly better cardiac function in p75MSC CdM-treated mice compared to controls. Thus in vivo benefits of MSCs may be derived in part by the action of their secreted factors on CPCs.
Epicardial-derived cells are required for cardiac development, support myogenesis through secreted factors and participate in repair and remodeling after injury. We tested whether factors secreted by epicardial-derived precursor cells (EPDCs) would protect jeopardized ischemic myocardium after myocardial infarction and reperfusion (MI-I4R). Human epicardial progenitor cells, isolated from right atrial appendages removed during cardiac bypass surgery, were keratin-positive, epithelial in morphology and expressed TFs associated with pro-epicardium, epicardium and cardiac development. Upon progenitor cell epithelial-mesenchymal transition (EMT) into EPDCs, concentrated conditioned medium (EPI CdM) was generated. When compared to á-MEM (vehicle), intra-arterial infusion of human EPI CdM led to a reduction in infarct size of 50% in both immunodeficient and immunocompetent MI-I4R mice and improved cardiac function. These in vivo results were evident as early as 24 hours after MI, sustained for at least 1 month, and may derive in part through paracrine protection of jeopardized coronary microvasculature. Our results indicate that EPI CdM or a combination of its ligands may provide an effective treatment for MI.
Ng, Shyh Chang. "Regulation of Stem Cell Metabolism by the Lin28/let-7 Axis." Thesis, Harvard University, 2013. http://dissertations.umi.com/gsas.harvard:11217.
Full textSakanovic, Alenko. "EphrinB2 reverse signaling in endothelial cell migration and actin remodeling." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/27030.
Full textIbarra-Sánchez, Maria. "Biochemical and cellular function of t-cell protein tyrosine phosphatase." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82895.
Full textIn the second part of this thesis, I studied the putative role of TC-PTP in response to DNA damage. I demonstrated that mice and cells lacking TC-PTP have a high sensitivity to genotoxic stress, which seems to be associated with an increased stability and elevated phosphorylation of serine-15 of the tumor suppressor p53. We found that the p53 inhibitor, Mdm2 is highly tyrosine phosphorylated in TC-PTP-/- cells. High tyrosine phosphorylation levels on Mdm2 are associated with more stability of p53. Although, it was not possible to show that Mdm2 is a direct substrate for TC-PTP, this seems to be the most likely mechanism used by TC-PTP to control p53. Interestingly, I also showed that double deficient mice for both TC-PTP and p53 live longer and display a normal spleen compared with the TC-PTP single knockout. However, another phenotype like the anemia is not rescued in the double knockout mice. Murine embryonic fibroblasts from TC-PTP-/- p53-/- embryos also have a better survival after genotoxic stress when compared with the TC-PTP-/- cells. Thus, we propose that TC-PTP plays a role in response to DNA damage by affecting the tyrosine phosphorylation levels of Mdm2, and its associated increased stability of the tumor suppressor p53
In the last part of my thesis, I tested the genetic interaction between the protein kinase c-Abl and the protein tyrosine phosphatase TC-PTP. Taking in account the knockout phenotypes of both enzymes, we generated double deficient mice for both TC-PTP and cAbl. TC-PTP-/- c-Abl-/- mice are viable, but there was no difference in the time of survival of these animals when compared with the single knockouts. However, data obtained with primary fibroblasts indicated that indeed there is a genetic interaction between TC-PTP and c-Abl. Double deficient primary fibroblasts proliferate better than TC-PTP-/- cells, and also present a better survival in response to genotoxic stress. The induction of p53 is also reduced in comparison with TC-PTP-/- cells. These results indicate that a genetic interaction between both enzymes exists and that this phenomenon is likely to be resulting from the existence of at least one common substrate.
Buchanan, 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.
Full textArojo, Omotooke Ajoke. "The Role of Sin 1-mTORC2 in the Regulation of T Cell Homeostasis." Thesis, Yale University, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10783434.
Full textIn healthy individuals, T cells generally exist in a state of equilibrium or homeostasis. This homeostasis is achieved by a tight and dynamic regulation of signaling cascades that control T cell numbers, localization, metabolism, and differentiation at any given time. Dysregulation of T cell homeostasis underlies several immunopathologic conditions including autoimmune diseases and cancer, hence the need to better understand molecular mechanisms that control T cell homeostasis. The mechanistic target of rapamycin (mTOR) is a critical hub within several important signaling cascades that are operational throughout the life of a T cell from thymic development to antigen encounter and beyond. While significant progress has been made in uncovering the roles of mTOR in various aspects of T cell immunity, the molecular mechanisms that dynamically regulate the threshold of mTOR signaling at various stages of the T cell life cycle and how this contributes to T cell homeostasis are poorly understood. mTOR functions as the enzymatic nucleus of two multiprotein complexes designated mTOR complex 1 (mTORC1) and mTORC2. We investigated the role of mTORC2 in naïve T cell homeostasis and the dynamic biochemical regulation of mTORC2 signaling by Sin1 and its isoforms. This led us to uncover a previously unappreciated but fundamental aspect of T cell biology; active mTORC2 signaling in naïve T cells suppresses bone marrow homing and in this manner allows T cells recirculate more efficiently through secondary lymphoid organs for better immune-surveillance. Furthermore, our exploration of the dynamic biochemical regulation of mTORC2 in naïve versus activated T cells revealed a potential mechanism through which dynamic mTORC2 signaling is achieved. We found that the overall strength of mTOR signaling is controlled at the level of transcriptional expression of mTOR and its adaptors by TCR stimulation. More broadly, we also investigated the biochemical regulation of mTORC2 by Sin1 isoforms, taking advantage of their domains to understand how various upstream signals might control mTORC2 activity. Through these investigations, we established that Sin1 isoforms differentially regulate mTORC2 response to Pi3K and non-Pi3K signals as well as mTORC2 target substrate specificity.
Miller, Christina Roshek 1969. "Photosensitive liposome-cell interaction in vitro." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/288913.
Full textRodrigues, Sonia Patricia. "The function of the Crk adapter proteins in cell migration and invasion /." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80866.
Full textLi, Ge. "Cell physiology, biochemistry, and molecular biology of 5-aminolevulinic acid-induced protoporphyrin IX in normal, immortalized, transfected, and malignant cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0005/NQ27837.pdf.
Full textNiedowicz, Dana M. "The mechanisms of hyperglycemia-induced oxidative stress in human erythrocytes." [Bloomington, Ind.] : Indiana University, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3204307.
Full textSource: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0043. Adviser: David L. Daleke. "Title from dissertation home page (viewed Feb. 21, 2007)."
Abrol, Meena. "The role of Sir2alpha in myogenesis." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26434.
Full textGangaraju, Sandhya. "Role of mitofusin2 in the regulation of mitochondrial dynamics." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/26483.
Full textTaylor, Rebecca Ann C. "VSV infection of resting and activated T lymphocytes." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26782.
Full textDunkley, Rosamund. "Ubiquitous over-expression of human X-linked inhibitor apoptosis (XIAP) in a transgenic mouse and implications for tumorigenesis." Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/26895.
Full textCzechura, Pawel. "Saturated neoglycopolymers for tissue engineering." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27121.
Full textDykstra, Natalie. "The investigation of microbial-intestinal epithelial cell interactions in the gut and their effects on inhibitor of apoptotic proteins (IAPs)." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27978.
Full textEwing, Robyn. "Analysis of the subcellular trafficking of the glucocorticoid receptor and properties of the ligand binding domain." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27979.
Full textGuzzo, Rosa M. "Sarcolemmal membrane associated proteins: Structure-function analyses and localization studies." Thesis, University of Ottawa (Canada), 2003. http://hdl.handle.net/10393/29048.
Full textBou, Khalil Maroun. "Biophysical and biochemical properties of the mammalian male germ cell specific sulfogalactosylglycerolipid (SGG): Contribution to the structure and zona pellucida affinity of pig sperm raft membranes." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/29079.
Full textStewart, Nicolas Andre Stirling. "In vacuo chemical modifications of proteins and peptides." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/29170.
Full textKorley, Robert E. C. "Characterization of a major protein of the mouse perinuclear theca." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0035/MQ64383.pdf.
Full textHarrouk, Wafa. "Mitogen-activated protein kinase during oocyte growth in the mouse." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55499.
Full textIn growing mouse oocytes, a group of partially competent oocytes are abundant. Such oocytes arrest at metaphase I where they assemble a morphologically normal spindle. Immunoblotting results of partially competent oocytes show that MAP kinase is present and becomes phosphorylated following culture as is indicated by the retarded mobility on the SDS gels.
Okadaic acid, an inhibitor of protein phospharases 1 and 2A, induces incompetent oocytes to enter metaphase. These oocytes contain the slow migrating phosphorylated forms of p42 and p44, indicating that okadaic acid causes the phosphorylation of MAP kinase. A time course study shows that the okadaic acid-induced phosphorylation of MAP kinase occurs coincidentally with entry into metaphase in incompetent oocytes. In fully competent oocytes, this phosphorylation occurs after entry into metaphase. In addition, these oocytes do not assemble a spindle, indicating that phosphorylation of MAP kinase, although it may be necessary, is not a sufficient event to induce spindle formation.
Schroeder, Hans R. "S-acylation and intracellular targeting of lipid-modified proteins and model lipopeptides." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36812.
Full textThe second study examined the intracellular S-acylation of lipopeptides which mimic the carboxy-terminus of N-ras. S-acylation of lipopeptides was again specific for cysteinyl residues as opposed to serinyl residues. The exact structure of the attached prenyl group, for example the farnesyl versus geranyl group, does not affect the ability of the lipopeptide to undergo S-acylation, however, an attached moiety with sufficient hydrophobicity to promote high affinity but rapidly reversible interactions with membranes is required for efficient S-acylation. Fluorescence microscopy suggests that S-acylation of these peptides and likely N-ras protein itself occurs at the plasma membrane of mammalian cells.
The third study examined the hypothesis that proteins of different sequences may be S-acylated by distinct S-acyltransferases. Lipopeptides bearing sequences mimicking the N-termini of src-like nonreceptor protein tyrosine kinases or heterotrimeric G-protein alpha-subunits, incorporate similar ratios of [3H]palmitate/[3H]stearate following incubation of lipopeptide with cells and equal activities of [3H]palmitate and [3H]stearate. In contrast, lipopeptides which mimic the C-terminus of N-ras exhibit ratios which are significantly different from the ratios for those lipopeptides described above. These results suggest that these two groups of structurally-different lipopeptides are S-acylated by distinct S-acyltransferases within the plasma membrane. Further, lipopeptides bearing nonphysiological sequences which are preferentially S-acylated in the Golgi, incorporate radiolabeled fatty acids in ratios which are significantly different from those determined for most lipopeptides S-acylated at the plasma membrane, suggesting that distinct S-acyltransferases may exist in the plasma membrane and Golgi apparatus of mammalian cells.
Lee, Menq-Jer. "Biochemical characterization of statin, a protein marker specific fofor nonproliferating cells, and identification of its associated proteins in cultured human diploid fibroblasts." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=41296.
Full textThe p45 statin-associated protein is a serine/threonine kinase. The specificity of the association of statin and p45 kinase is strongly supported by the fact that the kinase activity of p45 correlates both qualitatively and quantitatively with the amount of statin present in immunoprecipitates from cultured fibroblasts having different states of growth or from different subcellular fractions. In addition, the p45 kinase can phosphorylate statin in vitro, suggesting that statin may be one of the physiological substrates for the p45 kinase in vivo. The biochemical evidence indicates that p45 is not a member of the casein kinase II, cAMP-dependent kinase, calmodulin-dependent kinase, or protein kinase C families. The relationship of this kinase to other families is yet to be investigated.
The p110 statin-associated protein reacts with antibodies specific for the retinoblastoma susceptibility gene product, Rb. Also present in anti-Rb immunoprecipitates is 57 kDa protein which is recognized by anti-statin antibody (S44). Both p57 and p110 are co-precipitated from ($ sp{35}$S) -labelled quiescent cell extracts with either anti-Rb or anti-statin antibodies. However, in ($ sp{35}$S) -labelled extracts of growing cells, neither p110 nor p57 is present in S44-immunoprecipitates; and anti-Rb immunoprecipitates contain several protein species, the phosphorylated forms of Rb (112-116 kDa), but not p57. Comparisons of V8 digests indicate that p110 in S44-immunoprecipitates is Rb, and p57 in anti-Rb immunoprecipitates is statin. Confocal microscopical analysis shows that statin and Rb are colocalized within fibroblasts, predominantly in the nuclear envelope and matrix regions. These results strongly suggest that statin also associates with unphosphorylated species of Rb in the nuclei of nonproliferative cells.
Finally, the kinetics of statin expression in two states of cellular growth arrest, i.e. in young quiescent and in in vitro aged fibroblasts, was examined. I found that 95% of serum-starved cells express statin, independent of their in vitro age. After the addition of serum, the majority of senescent cells (CPDL $>$ 50) persistently express statin, whereas young cells (CPDL $<$ 20) lose statin after feeding. I also directly demonstrated that statin expression and DNA synthesis cannot occur simultaneously in the same cell. Furthermore, one additional nuclear protein possessing a common antigenic epitope to p57$ sp{ rm statin}$, with a molecular mass of 80 kDa, is detected only in senescent cells, but not in their young quiescent counterparts. Analysis of peptide maps indicates that this 80 kDa protein is different from p57$ sp{ rm statin}$. This finding implies that this unidentified 80 kDa protein may be a protein marker specific for senescent cells.
Brignole, Claudine. "The adenovirus E4orf4 protein induces G2 / M arrest and cell death by inhibiting PP2A phosphatase activity regulated by the B Alpha subunit /." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81604.
Full textRoudaia, Liya. "Characterization of RasGAP-SH3-binding protein's functions." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82418.
Full textCardillo, Marricco Nadia. "Characterization of casein kinase I-c2, as a serinethreonine protein kinase associated with the adaptor protein, Nck." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21603.
Full textPark, Minwoo. "2',3'-Cyclic nucleotide 3'-phosphodiesterase : investigation of interaction with Fyn tyrosine kinase during the development of nervous system, and mitochondrial import of CNP2 isoform." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81423.
Full textFirst, a possible interaction of CNP with Fyn tyrosine kinase during myelination is investigated. Fyn is an important factor known to be active during the process of myelination, and CNP contains a number of possible tyrosine phosphorylation sites. Furthermore, their presence in an isolated domain of cell membrane called lipid rafts, further strengthened the possibility of interaction. However, no evidence was found which could support the possibility, neither in new born mouse brain nor in in-vitro experiment using transfected cells expressing Fyn and CNP.
Secondly, the role of CNP2 isoform in mitochondria is investigated. CNP2 is found to be associated with mitochondria, and its 20 amino acid segment at the N-terminus possesses characteristics of a mitochondrial import signal. Furthermore, two known sites of serine phosphorylation in the N terminus of CNP2 show influence on mitochondrial localization of the protein. However, results collectively suggests that CNP2 is not imported into mitochondria, as pulse chase did not show the typical processing of what was suspected to be the N-terminal import signal sequence. Furthermore, CNP was degraded when partially purified mitochondria was subjected to protease action, showing that CNP is not enclosed by mitochondrial membranes. Two serine residues at positions 9 and 22 in the N-terminus of CNP2 are likely phosphorylated by both PKA and PKC, and is responsible for the decrease in mitochondrial localization of CNP2.
Minuk, Jeffrey. "Studies on the intracellular sorting of the two myelin-associated glycoprotein isoforms." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23414.
Full textCôté, Richard Gaston. "Characterization of the retinoblastoma binding protein 2 (RBP2)." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33388.
Full textTremblay, Gilles B. "Methylenetetrahydrofolate dehydrogenases in eucaryotic cells." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40012.
Full textAjdukovic, Boris. "Dystrophin expression during skeletal myogenesis." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56988.
Full textTaheri, Maryam. "Characterization of the structural determinants of two functions of human carcinoembryonic antigen (CEA) : intercellular adhesion and differentiation inhibition." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=36841.
Full textOliva, Rossella Norma. "Characterization of the isoform gamma 2 ([gamma] 2) of the serinethreonine protein kinase Casein Kinase I (CKI-[gamma] 2)." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=81369.
Full textTerrone, Donato Gerardo. "Ras protein targeting in mammalian cells." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98506.
Full textLi, Jing 1957. "Studies on iron-dependent regulation of transferrin receptor gene expression in chicken HD3 cells." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27368.
Full textWe found that treatment of the differentiating HD3 cell with Pyridoxal Isonicotinoyl Hydrazone (PIH) causes an increase in TfR mRNA accumulation as a result of increased TfR gene transcription. No evidence was obtained for stabilization of TfR mRNA. These data indicate that there may be another distinct iron-dependent regulatory mechanism for the TfR gene expression during erythroid cell differentiation.