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Relevant bibliographies by topics / Cell cycle protein

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Academic literature on the topic 'Cell cycle protein'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Cell cycle protein"

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Farley, John, Laurent Ozbun, Goli Samimi, and Michael J. Birrer. "Cell Cycle and Related Protein." Disease Markers 23, no. 5-6 (2007): 433–43. http://dx.doi.org/10.1155/2007/464712.

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Vázquez-Ramos, Jorge M., and María de la Paz Sánchez. "The cell cycle and seed germination." Seed Science Research 13, no. 2 (June 2003): 113–30. http://dx.doi.org/10.1079/ssr2003130.

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AbstractThe cell cycle is the series of molecular events that allows cells to duplicate and segregate their chromosomes to form new cells. The finding that a protein kinase, the product of the yeastcdc2gene, was fundamental in the regulation of the G2/M and G1/S transitions, associated with unstable proteins named cyclins, opened a very exciting and dynamic research area. The number of gene products that participate in the development and regulation of the cell cycle may be in the hundreds, and there is a high degree of conservation in protein sequences and regulatory pathways among eukaryotes. Although there are clear differences between plants and animals in cell structure, organization, growth, development and differentiation, the same types of proteins and very similar regulatory pathways seem to exist. Seed germination appears to be an excellent model system for studying the cell cycle in plants. Imbibition will reactivate meristematic cells – most initially with a G1DNA content – into the cell cycle in preparation for seedling establishment. Early events include a thorough survey of DNA status, since the drying process and seed storage conditions reduce chromosomal integrity. The initiation of cell cycle events leading to G1and S phases, and of the germination process itself, may depend on a G1checkpoint control. Most, if not all, cell cycle proteins appear to be already present in unimbibed embryos, although there is evidence of protein turnover in the early hours, suggesting the need forde novoprotein synthesis. Regulation also may occur at the level of protein modification, because existing G1, S and G2cell cycle proteins appear to be activated at precise times during germination. Thus, cell cycle control during seed germination may be exerted at multiple levels; however, knowledge of cell cycle events and their importance for germination is still scarce and fragmentary, and different species may have developed unique control mechanisms, more suited to specific germination characteristics and habitat.

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Evanko, Daniel. "Protein suicide highlights the cell cycle." Nature Methods 5, no. 4 (April 2008): 283. http://dx.doi.org/10.1038/nmeth0408-283.

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Wong, W. "Not Just a Cell Cycle Protein." Science Signaling 3, no. 106 (January 26, 2010): ec27-ec27. http://dx.doi.org/10.1126/scisignal.3106ec27.

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Hollingsworth, Robert E., Carmel E. Hensey, and Wen-Hwa Lee. "Retinoblastoma protein and the cell cycle." Current Opinion in Genetics & Development 3, no. 1 (February 1993): 55–62. http://dx.doi.org/10.1016/s0959-437x(05)80341-7.

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Wirth, Anna J., and Martin Gruebele. "Protein Folding across the Cell Cycle." Biophysical Journal 104, no. 2 (January 2013): 573a. http://dx.doi.org/10.1016/j.bpj.2012.11.3182.

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Pines, Jonathon. "Protein kinases and cell cycle control." Seminars in Cell Biology 5, no. 6 (December 1994): 399–408. http://dx.doi.org/10.1006/scel.1994.1047.

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Westwood, J. Tim, Robert B. Church, and Emile B. Wagenaar. "Patterns of protein synthesis during the cell cycle of Chinese hamster ovary cells." Biochemistry and Cell Biology 65, no. 3 (March 1, 1987): 219–29. http://dx.doi.org/10.1139/o87-028.

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The protein synthesis patterns at various stages of the cell cycle of Chinese hamster ovary cells were examined by labelling cells with [35S]methionine and then separating the proteins by isoelectric focussing and two-dimensional, nonequilibrium pH gradient gel electrophoresis. We have observed a number of proteins which display quantitative differences in synthesis at specific cell cycle stages and of these the α- and β-tubulins have been identified. A few proteins appear to be uniquely synthesized at specific times during the cell cycle. These include the histones and a modified version of them, which are synthesized only in S phase, and a pair of 21 kilodalton (kDa), pI 5.5 proteins, which appear only in late G2 and mitosis. We have also identified a 58-kDa, pI 7.5 protein which is present at all cell cycle stages except during late G2. This protein appears to have the same temporal properties as a 57-kDa protein called "cyclin" originally described in sea urchin embryos.

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Murphy, Eain A., Daniel N. Streblow, Jay A. Nelson, and Mark F. Stinski. "The Human Cytomegalovirus IE86 Protein Can Block Cell Cycle Progression after Inducing Transition into the S Phase of Permissive Cells." Journal of Virology 74, no. 15 (August 1, 2000): 7108–18. http://dx.doi.org/10.1128/jvi.74.15.7108-7118.2000.

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ABSTRACT Human cytomegalovirus (HCMV) infection of permissive cells has been reported to induce a cell cycle halt. One or more viral proteins may be involved in halting progression at different stages of the cell cycle. We investigated how HCMV infection, and specifically IE86 protein expression, affects the cell cycles of permissive and nonpermissive cells. We used a recombinant virus that expresses the green fluorescent protein (GFP) to determine the effects of HCMV on the cell cycle of permissive cells. Fluorescence by GFP allowed us to select for only productively infected cells. Replication-defective adenovirus vectors expressing the IE72 or IE86 protein were also used to efficiently transduce 95% or more of the cells. The adenovirus-expressed IE86 protein was determined to be functional by demonstrating negative autoregulation of the major immediate-early promoter and activation of an early viral promoter in the context of the viral genome. To eliminate adenovirus protein effects, plasmids expressing GFP for fluorescent selection of only transfected cells and wild-type IE86 protein or a mutant IE86 protein were tested in permissive and nonpermissive cells. HCMV infection induced the entry of U373 cells into the S phase. All permissive cells infected with HCMV were blocked in cell cycle progression and could not divide. After either transduction or transfection and IE86 protein expression, the number of all permissive or nonpermissive cell types in the S phase increased significantly, but the cells could no longer divide. The IE72 protein did not have a significant effect on the S phase. Since IE86 protein inhibits cell cycle progression, the IE2 gene in a human fibroblast IE86 protein-expressing cell line was sequenced. The IE86 protein in these retrovirus-transduced cells has mutations in a critical region of the viral protein. The locations of the mutations and the function of the IE86 protein in controlling cell cycle progression are discussed.

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Gookin, Sara, Mingwei Min, Harsha Phadke, Mingyu Chung, Justin Moser, Iain Miller, Dylan Carter, and Sabrina L. Spencer. "A map of protein dynamics during cell-cycle progression and cell-cycle exit." PLOS Biology 15, no. 9 (September 11, 2017): e2003268. http://dx.doi.org/10.1371/journal.pbio.2003268.

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Dissertations / Theses on the topic "Cell cycle protein"

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Schymkowitz, Joost Wilhelm Hendrik. "Protein engineering studies on cell-cycle regulatory proteins." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.621312.

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Gad, Annica. "Cell cycle control by components of cell anchorage /." Stockholm : Division of Pathology, Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-359-0/.

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Dibble, Taylor Raymond. "Cell Cycle Regulation of the Centriolar Protein Ana2." Thesis, The University of Arizona, 2015. http://hdl.handle.net/10150/579244.

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The centrosome functions to nucleate microtubule growth and organize the mitotic spindle during cell division. The centrosome normally duplicates once per cell cycle, ensuring a bipolar spindle that divides sister chromatids equally between two daughter cells during mitosis. However, improper duplication or over-duplication of centrosomes can lead to chromosomal instability, a hallmark of cancer. Two barrel-shaped structures called centrioles function as the duplication factors for centrosomes. Mutations in important centriole structural proteins can cause either down-regulation or amplification of centriole duplication. One of these proteins, Ana2, is required for duplication and mutations in its human orthologue, STIL, can cause disorders in neurological development. Normally, Ana2 localizes to an existing ‘mother' centriole during S-phase and plays an essential role in the assembly of the procentriole that will become a mature ‘daughter' during G2. In this study, we identified changes in total cellular levels of Ana2 by arresting S2 Drosophila cells in different phases of the cell cycle and immunoblotting for Ana2. We found that levels of both endogenous Ana2 and transiently overexpressed Ana2 are low during G1 and increase during S-phase. Endogenous Ana2 levels were highest in G2, consistent with centriole maturation during this phase of the cell cycle.

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Ashford, Anne Louise. "The role of the protein kinase DYRK1B in cancer cell survival and cell cycle control." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648671.

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Gilker, Eva Adeline Gilker. "INTERACTIONS AND LOCALIZATION OF PROTEIN PHOSPHATASES, YWHA PROTEINS AND CELL CYCLE CONTROL PROTEINS IN MEIOSIS." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent1532699317257539.

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Chan, Ho Man. "Molecular basis of cell cycle control : p300 and pRb." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326430.

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Vaillant, Remi. "The role of adenoviral capsid protein VI in cell cycle modulation." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0297/document.

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Les Adénovirus humains sont des virus non enveloppés se répliquant dans le noyau des cellules hôtes.Durant l’infection et après leur entrée par endocytose, les Adénovirus sont transportés au noyau pourinitier l’expression du génome viral. Dans l’endosome, les capsides virales subissent un désassemblagepartiel et libèrent le facteur viral lytique, la protéine VI (pVI). Au niveau de la membrane de l’endosome,cette protéine va alors induire sa rupture permettant ainsi le relargage des virions au sein du cytoplasmegrâce à son hélice amphipatique N-terminale. Par la suite, pVI est transportée vers des structuresnucléaires appelées PML nuclear bodies (PML-NB), associée une ubiquitine ligase cytoplasmique, laNedd4.2. Les PML-NB sont des complexes nucléaires multi-protéiques qui ont des propriétésantivirales. Celles-ci impliquent le recrutement de facteurs de transcription répressifs comme parexemple la protéine anti apoptotique Daxx ou encore le suppresseur de tumeur p53, impliqué dans larégulation du cycle cellulaire. Il a été montré que la protéine pVI en complexe avec Nedd4.2 induit larelocalisation de Daxx des PML-NB dans le cytoplasme, ce qui permet une expression efficace dugénome viral. Ainsi, l’inhibition fonctionnelle de Daxx par pVI suggère que cette protéine virale puisseaussi être impliquée dans la restriction de p53.Dans cette étude, nous avons montré que le nombre des modifications post-traductionnelles (PTM) dep53 augmentent en présence de pVI dans la cellule. De plus, les données obtenues montrent quel’expression de pVI affecte la transcription dépendante de p53 et que l’interaction avec Nedd4.2 n’estpas nécessaire pour inhiber les fonctions de p53. Pour étudier l’implication de pVI dans la modulationdu cycle cellulaire, nous avons créé une lignée cellulaire humaine exprimant cette protéine virale defaçon stable. La caractérisation de cette lignée a permis de mettre en évidence une prolifération cellulaireaccrue. Nos observations ont aussi montré une perte importante des PML-NB et une réduction desprotéines clés du cycle cellulaire p53 et pRb, un autre suppresseur de tumeur. Par des techniques demicro-injection et l’utilisation de l’inhibiteur MG132, nous avons observé que ces deux facteurscellulaires sont ciblés vers le protéasome et dégradés lors de la surexpression de pVI. L’étude desfonctions de cette protéine virale laisse penser que la protéine pVI présente un potentiel oncogéniquecar en effet, sa surexpression induit la dérégulation de l’homéostasie cellulaire et l’inhibition desuppresseurs de tumeur, comme p53 et pRb
Human Adenovirus are non-enveloped viruses which replicate inside the host cell nucleus. Uponinfection and after receptor-mediated entry, they are transported towards the nucleus to initiate the viralgene expression. Viral capsids deliver from the endosome into the cytoplasm by partial disassembly andrelease inside the endosome mediated by viral lytic factor protein VI (pVI). pVI is targeted to themembrane via an amphipathic helix structure in the N-terminus of the viral protein. After membranerupture and capsid release, pVI is transported to sub-nuclear structures, so-called PML nuclear bodies(PML-NBs), together with the cytoplasmic ubiquitin ligase Nedd4.2. PML-NBs represent multiproteinaggregates in the host-cell nucleus with an antiviral capacity, as to several PML-associated repressivetranscription factors, such as the anti-apoptotic Daxx protein and the tumor suppressor p53 were reportedto localize at these foci. In addition, pVI-mediated displacement of Daxx from PML-NBs was shown tooccur in dependency of Nedd4.2 to support efficient viral gene expression. Therefore, we postulate thatbesides Daxx functional inhibition, pVI might also be involved in p53 restriction.Here, we show that p53 posttranslational modification (PTM) is increased when pVI protein is presentin the host-cell. Moreover, we obtained data that pVI expression severely impacts p53 inducedtransactivation of cellular transcription. Biochemical approaches indicate that pVI binding of theubiquitin ligase Nedd4.2 is no prerequisite for the capacity to inhibit p53 functions. In a next step toelucidate the role of pVI on cell cycle regulation, we generated a human cell line stably expressing theviral pVI protein. Our characterization analyses show significantly that these cells benefit from thepresence of pVI as we proved increased cell proliferation rates. We also observed an intense loss ofPML-NBs and reduced protein concentrations of cycle key regulators p53 and pRb. Usingmicroinjection and the inhibitor MG132 we were able to show that both cellular restriction factors weresequestered into the proteasomal degradation pathway of the cell. Evaluation of pVI functions temptedus to speculate, whether pVI might execute oncogenic potential upon overexpression, due toderegulation of host-cell homeostasis and inhibition of tumor suppressive determinants
Humane Adenoviren (HAdV) sind unbehüllte Doppelstrang-DNA-Viren mit einem Proteinkapsid, diesich im Wirtzellkern replizieren. Der lytische Infektionsverlauf beginnt mit dem rezeptor-vermitteltenEintritt des Viruspartikels und dem gerichteten Transport des viralen Genoms zum Wirszellkern. Dasvirale Protein VI (pVI) ist nötig um den effizienten Austritt des bereits disassemblierten Viruspartikelsaus dem zellulären Endosom zu gewährleisten. Durch eine amphipathische Helix im N-terminalenProteinbereich interkaliert dieser lytische Faktor in die endosomale Membran und führt zum Aufbruchdes zellulären Organells. pVI wird anschließend an zelluläre Kernstrukturen, sogenannte PML nuclearbodies (PML-NBs) lokalisiert und komplexiert dort mit der zytoplasmatischen Ubiquitinligase Nedd4.2.PML-NBs stellen nukleäre Multiproteinkomplexe dar, die mittlerweile aufgrund ihrer antiviralenEigenschaften in den Mittelpunkt der virologischen Forschung gerückt sind. Diese zellulären Aggregatebestehen hauptsächlich aus repressiven Transkriptionsfaktoren, wie dem anti-apoptotischen DaxxProtein sowie dem Tumosupressor p53. In diesem Zusammenhang konnte bereits eine pVI-vermittelteRelokalisation des Daxx Proteins aus den PML-NBs gezeigt und als Vorraussetzung zur effizientenVirusgenexpression bestätigt werden. Es stellte sich im Rahmen der vorliegenden Arbeit die Frage, obneben der pVI-abhängigen Daxx Inhibition, auch p53 ein Zielprotein des viralen Capsidproteinsdarstellt.Unsere Arbeiten zeigen erstmals, dass nach der pVI Expression vermehrt posttranslationaleModifikationen am p53 Protein beobachtet werden. Weitere Befunde konnten außerdem einen Einflussvon pVI auf die p53-abhängige Transaktivierung zellulärer Promotoren beweisen. Mittelsbiochemischer Analysemethoden konnten wir zeigen, dass die Kooperation zwischen pVI und Nedd4.2keine Rolle bei der p53 Inhibition zu spielen scheint. Um im nächsten Schritt die Rolle von pVI imZellzyklus genau zu beleuchten, wurde zunächst ein zell-basiertes Modelsystem mit stabilerÜberexpression des viralen Faktors generiert, Anschließende phenotypische Analysen konnten zeigen,dass die Anwesenheit von pVI zur Steigerung der Zellproliferationsrate führt. Im Rahmen unsererUntersuchungen konnten wir auch einen signifikanten Verlust zellulärer PML-NBs beobachten sowieeine Reduktion der p53 und pRb Proteinkonzentration nachweisen. Mittels unter Verwendung vonMikroinjektion und dem Inhibitor MG132 war es uns möglich zu zeigen, dass pVI den proteasomalenProteinabbau der beiden Wirtszelldeterminaten p53 und pRb induziert. Deswegen kann man basierendauf den erhobenen Befunden zur pVI vermittelten Dysregulierung des zellulären Wachstums einonkogenens Potenzial des viralen Faktors annehmen

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Thomas, Elizabeth Baby. "Analysis of protein kinases regulating the Trypanosoma brucei cell cycle." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6229/.

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Trypanosoma brucei spp. are protozoan parasites that cause Human African Trypanosomiasis in humans, and Nagana in cattle. These diseases are mostly fatal if left untreated and there is an urgent need for safe, effective drugs that can be easily administered. T. brucei has a complex cell cycle, the regulation of which appears to be divergent compared to other model eukaryotes. This implies that the regulators of the T. brucei cell cycle could be exploited as a source of novel drug targets. One such cell cycle regulator of interest is T. brucei polo-like kinase (TbPLK), a serine/threonine protein kinase thought to diverge from its canonical functions in eukaryotic mitosis and be mainly involved in the duplication of the parasite’s cytoskeletal structures. This study sought to investigate how the activity and localisation of TbPLK is regulated in procyclic form (PCF) and bloodstream form (BSF) parasites. A second aim of this study was to identify novel protein kinases (PKs) which regulate the T. brucei cell cycle by screening part of a kinome-wide RNA interference (RNAi) library of BSF cell lines, that has recently been established (Jones et al. 2014). The cell lines had already been assessed for proliferation defects upon RNAi induction by using an Alamar blue viability assay. In this study, the cell lines which displayed proliferation defects were further screened for cell cycle defects using growth curves and DAPI staining, to identify as yet uncharacterised protein kinases required for T. brucei cell cycle regulation. 50 PKs had been shown to be required for viability in vitro and were screened for potential cell cycle roles. Of these, 25 were identified as potential cell cycle regulators, 15 of which were detected for the first time. The majority of the hits were deemed to be involved in either just cytokinesis, or cytokinesis in combination with kinetoplast duplication or mitosis, with surprisingly few in G1/S. Knockdown of a number of these putative cell cycle PKs induced cell death signifying their potential as drug targets. Indeed, one of the hits, CLK1, was genetically validated as a potential drug target in a mouse model. The identification of these putative cell cycle kinases has also provided valuable starting points by which the signalling pathways that regulate the cell division cycle of these parasitic organisms can be elucidated.

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Tait, Xavier Alastair Claude. "Investigation of human Pix protein regulation during cell cycle progression." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/10853.

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Proteomic analyses of centrosomes from diverse species are helping to identify conserved components of these organelles. Amongst these studies, a group of novel proteins has been identified and postulated as candidate core centriolar components, dubbed Poc proteins, for proteome of centriole. Meanwhile, studies on the Xenopus germ plasm protein, Xpat, led to the identification of an interacting protein, named Pix for protein that interacts with Xpat. Later sequence comparison revealed that Poc1 and Pix are the same protein and will here be referred to as Pix. Pix proteins localize to centrosomes and spindle poles in human cells and the basal bodies of Chlamydomonas and Tetrahymena. It has been suggested that Pix proteins are required for centriole duplication and length control, as well as potentially ciliogenesis. Pix proteins have also been localized to mitochondria in human cells where they might act as molecular adaptors to anchor microtubules to mitochondria. Human cells encode two Pix proteins and the aim of this thesis was to investigate the cell cycle-dependent regulation of Pix1 and Pix2 in human cells. For this purpose, we first generated polyclonal rabbit antibodies that were specific for either Pix1 or Pix2. We then showed for the first time that both Pix isoforms localize to centrosomes throughout the cell cycle and independently from one another. Using the antibodies, we also confirmed that Pix1, but not obviously Pix2, is not an intrinsic mitochondrial protein but localizes to the surface of mitochondria. Through a proteomic approach, we identified two molecular chaperons that potentially interact with Pix proteins, HSP90 and TCP1, and demonstrated that Pix proteins can form dimers. In addition, we produced the first experimental evidence that human Pix proteins are alternatively spliced, suggesting that additional, undiscovered Pix isoforms might be expressed in human cells. Finally, we found that Pix1 is phosphorylated in a mitosis-specific manner, and that this is potentially regulated by Cdk1. Thus, we propose that Pix proteins have a specific and previously unidentified role in human mitotic cell division.

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Helt, Anna-Marija. "Multiple biological activities of the human papillomavirus type 16 E7 oncoprotein contribute to the abrogation of human epithelial cell cycle control /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/11514.

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Books on the topic "Cell cycle protein"

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Pontus, Aspenstrøm, ed. The pombe Cdc 15 homology proteins. Austin, Tex: Landes Bioscience, 2009.

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L, Chen K., ed. Progress in cell cycle control research. New York: Nova Science Publishers, 2008.

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1949-, Lee R. C., Despa Florin, Hamann Kimm Jon, and New York Academy of Sciences., eds. Cell injury: Mechanisms, responses, and repair. New York, N.Y: New York Academy of Sciences, 2005.

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H, Leroy Nathan, and Fournier Noah T, eds. Cell cycle control: New research. New York: Nova Science Publishers, 2008.

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Calcium, cell cycles, and cancer. Boca Raton, Fla: CRC Press, 1990.

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Whitfield, James F. Calcium in cell cycles and cancer. 2nd ed. Boca Raton, Fla: CRC Press, 1995.

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Siddik, Zahid H. Checkpoint controls and targets in cancer therapy. Totowa, N.J: Humana Press, 2010.

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Bradshaw, Ralph A. Regulation of organelle and cell compartment signaling. Amsterdam: Elsevier/Academic Press, 2011.

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1950-, Karmazyn M., Avkiran M, and Fliegel Larry 1956-, eds. The sodium-hydrogen exchanger: From molecule to its role in disease. Boston: Kluwer Academic Publishers, 2003.

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Checkpoint controls and targets in cancer therapy. Totowa, N.J: Humana Press, 2010.

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Book chapters on the topic "Cell cycle protein"

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Brautigan, David L., Jian Chen, Fran Pinault, Jeremy Somers, and Richard Zimmerman. "Phosphorylation in the Regulation of Protein Phosphatases." In The Cell Cycle, 25–32. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_3.

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Robbins, David J., Erzhen Zhen, Mangeng Cheng, Colleen A. Vanderbilt, Douglas Ebert, Clark Garcia, Alphonsus Dang, and Melanie H. Cobb. "Extracellular Signal-Regulated Protein Kinases (ERKS) 1, 2, and 3." In The Cell Cycle, 61–66. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_7.

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Joubès, Jérôme, Christian Chevalier, Denes Dudits, Erwin Heberle-Bors, Dirk Inzé, Masaaki Umeda, and Jean-Pierre Renaudin. "CDK-related protein kinases in plants." In The Plant Cell Cycle, 63–76. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-010-0936-2_6.

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Xie, Han-qing, and Valerie W. Hu. "Evidence for M-Phase-Specific Modification of a Gap Junction Protein." In The Cell Cycle, 223–28. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_26.

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Alberts, Arthur S., and Axel Schönthal. "Positive and Negative Regulation of Cell Cycle Progression by Serine/Threonine Protein Phosphatases." In The Cell Cycle, 33–40. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_4.

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Lahti, Jill M., Jialing Xiang, and Vincent J. Kidd. "The PITSLRE protein kinase family." In Progress in Cell Cycle Research, 329–38. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1809-9_27.

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Davidson, Jean M., and Robert J. Duronio. "Using Drosophila S2 Cells to Measure S phase-Coupled Protein Destruction via Flow Cytometry." In Cell Cycle Checkpoints, 205–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-273-1_15.

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Maller, James L. "Protein Phosphorylation and the Regulation of Key Events in Oocyte and Egg Cell Cycles." In The Cell Cycle, 3–15. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_1.

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Warren, Stephen L., David B. Bregman, Yi Li, and Lei Du. "Cytostellin: A Nuclear Protein that Redistributes to Peripheral Cytoskeletal Locations During Mitosis and G1." In The Cell Cycle, 211–21. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_25.

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Lees, Emma. "Protein Mapping in Cell Cycle Studies." In Cell Cycle — Materials and Methods, 264–70. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-57783-3_23.

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Conference papers on the topic "Cell cycle protein"

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Wang, Haiying, Huiru Zheng, Fiona Browne, and Chaoyang Wang. "Minimum dominating sets in cell cycle specific protein interaction networks." In 2014 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2014. http://dx.doi.org/10.1109/bibm.2014.6999122.

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Hastings, RH, R. Quintana, E. Healy, LJ Deftos, Y. Rascon, and PR Montgrain. "Cell Cycle Actions of Parathyroid Hormone-Related Protein in Non-Small Cell Lung Carcinoma." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5010.

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Dai, Lingyun, Tianyun Zhao, Xavier Bisteau, Wendi Sun, Nayana Prabhu, Yan Ting Lim, Radoslaw Sobota, Philipp Kaldis, and Pär Nordlund. "Abstract 4303: Modulation of protein interaction states through the cell cycle." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4303.

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Azuma, Takehito, Masachika Kurata, Noriko Takahashi, and Shuichi Adachi. "Estimation and robustness analysis of protein networks for cell cycle systems." In Control (MSC). IEEE, 2010. http://dx.doi.org/10.1109/cca.2010.5611122.

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SHA, YOBAO, Lavannya M. Pandit, shenyan zeng, Li-Yuan Yu-Lee, and Tony N. Eissa. "CHIP Is A Novel Centrosomal Protein Involved In Cell Cycle Progression." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4933.

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Barszcz, M., A. Tuśnio, E. Święch, M. Taciak, and J. Skomiał. "Effect of pea and yellow lupine on colonic epithelial cell cycle and apoptosis in piglets." In 6th EAAP International Symposium on Energy and Protein Metabolism and Nutrition. The Netherlands: Wageningen Academic Publishers, 2019. http://dx.doi.org/10.3920/978-90-8686-891-9_97.

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Sobol, Anna, Paola Galluzzo, Shuang Liang, Brittany Rambo, Sylvia Skucha, Megan Weber, and Maurizio Bocchetta. "Abstract C40: Amyloid precursor protein (APP) synchronizes cell cycle progression and the rate of global protein synthesis in dividing cells." In Abstracts: Third AACR International Conference on Frontiers in Basic Cancer Research - September 18-22, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.fbcr13-c40.

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Parrilla, A., B. Majem, M. Barber, M. Olivan, G. Tamayo, J. Castellví, A. Pérez, A. Gil-Moreno, and A. Santamaria. "PO-048 Therapeutic relevance of the cell cycle protein BORA in cancer." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.92.

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Buck, T. E., A. Rao, L. P. Coelho, M. H. Fuhrman, J. W. Jarvik, P. B. Berget, and R. F. Murphy. "Cell cycle dependence of protein subcellular location inferred from static, asynchronous images." In 2009 Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2009. http://dx.doi.org/10.1109/iembs.2009.5332888.

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Holcomb, Ilona, Gajalakshmi Dakshinamoorthy, Benjamin Liu, Marc Unger, Ramesh Ramakrishnan, and Haibiao Gong. "Abstract B20: Single-cell profiling of EGFR-regulated protein changes involved in cell cycle, cell proliferation and apoptosis." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-b20.

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Reports on the topic "Cell cycle protein"

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Dovichi, Norman J. The Single Cell Proteome Project - Cell-Cycle Dependent Protein Expression in Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, January 2005. http://dx.doi.org/10.21236/ada433000.

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Rajabi, Hasan N. The Mechanism of Retinoblastoma Protein-Mediated Terminal Cell Cycle Arrest. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada421731.

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Shen, Zhiyuan. Regulation of Cell Cycle by BCCIP a BRCA2 and CDKN1(p21) Interacting Protein. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada425667.

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Grafi, Gideon, and Brian Larkins. Endoreduplication in Maize Endosperm: An Approach for Increasing Crop Productivity. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575285.bard.

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The focus of this research project is to investigate the role of endoreduplication in maize endosperm development and the extent to which this process contributes to high levels of starch and storage protein synthesis. Although endoreduplication has been widely observed in many cells and tissues, especially those with high levels of metabolic activity, the molecular mechanisms through which the cell cycle is altered to produce consecutive cycles of S-phase without an intervening M-phase are unknown. Our previous research has shown that changes in the expression of several cell cycle regulatory genes coincide with the onset of endoreduplication. During this process, there is a sharp reduction in the activity of the mitotic cyclin-dependent kinase (CDK) and activation of the S-phase CDK. It appears the M-phase CDK is stable, but its activity is blocked by a proteinaceous inhibitor. Coincidentally, the S-phase checkpoint protein, retinoblastoma (ZmRb), becomes phosphorylated, presumably releasing an E2F-type transcriptional regulator which promotes the expression of genes responsible for DNA synthesis. To investigate the role of these cell cycle proteins in endoreduplication, we have created transgenic maize plants that express various genes in an endosperm-specific manner using a storage protein (g-zein) promoter. During the first year of the grant, we constructed point mutations of the maize M-phase kinase, p34cdc2. One alteration replaced aspartic acid at position 146 with asparagine (p3630-CdcD146N), while another changed threonine 161 to alanine (p3630-CdcT161A). These mutations abolish the activity of the CDK. We hypothesized that expression of the mutant forms of p34cdc2 in endoreduplicating endosperm, compared to a control p34cdc2, would lead to extra cycles of DNA synthesis. We also fused the gene encoding the regulatory subunit of the M- phase kinase, cyclin B, under the g-zein promoter. Normally, cyclin B is expected to be destroyed prior to the onset of endoreduplication. By producing high levels of this protein in developing endosperm, we hypothesized that the M-phase would be extended, potentially reducing the number of cycles of endoreduplication. Finally, we genetically engineered the wheat dwarf virus RepA protein for endosperm-specific expression. RepA binds to the maize retinoblastoma protein and presumably releases E2F-like transcription factors that activate DNA synthesis. We anticipated that inactivation of ZmRb by RepA would lead to additional cycles of DNA synthesis.

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Sleadd, Isaac. CCAAT/Enhancer-Binding Protein Delta (C/EBP-delta) Expression in Antarctic Fishes: Implications for Cell Cycle and Apoptosis. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.994.

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Wang, Bin, and Stephan Elledge. Involvement of 53BP1, a p53 Binding Protein, in Chk2 Phosphorylation of p53 and DNA Damage Cell Cycle Checkpoints. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada426338.

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Wang, Bin, and Stephen J. Elledge. Involvement of 53BP1, a p43 Binding Protein, in Chk2 Phosphorylation of p53 and DNA Damage Cell Cycle Checkpoints. Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada417278.

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Gafni, Yedidya, and Vitaly Citovsky. Molecular interactions of TYLCV capsid protein during assembly of viral particles. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587233.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. The present proposal, a continuation of a BARD-funded project, expanded our understanding of the molecular mechanisms by which CP molecules, as well as its pre-coat partner V2, interact with each other (CP), with the viral genome, and with cellular proteins during assembly and movement of the infectious virions. Specifically, two major objectives were proposed: I. To study in detail the molecular interactions between CP molecules and between CP and ssDNA leading to assembly of infectious TYLCV virions. II. To study the roles of host cell factors in TYLCV assembly. Our research toward these goals has produced the following major achievements: • Characterization of the CP nuclear shuttling interactor, karyopherin alpha 1, its pattern of expression and the putative involvement of auxin in regulation of its expression. (#1 in our list of publication, Mizrachy, Dabush et al. 2004). • Identify a single amino acid in the capsid protein’s sequence that is critical for normal virus life-cycle. (#2 in our list of publications, Yaakov, Levy et al. in preparation). • Development of monoclonal antibodies with high specificity to the capsid protein of TYLCV. (#3 in our list of publications, Solmensky, Zrachya et al. in press). • Generation of Tomato plants resistant to TYLCV by expressing transgene coding for siRNA targeted at the TYLCV CP. (#4 in our list of publications, Zrachya, Kumar et al. in press). •These research findings provided significant insights into (i) the molecular interactions of TYLCV capsid protein with the host cell nuclear shuttling receptor, and (ii) the mechanism by which TYLCV V2 is involved in the silencing of PTGS and contributes to the virus pathogenicity effect. Furthermore, the obtained knowledge helped us to develop specific strategies to attenuate TYLCV infection, for example, by blocking viral entry into and/or exit out of the host cell nucleus via siRNA as we showed in our publication recently (# 4 in our list of publications). Finally, in addition to the study of TYLCV nuclear import and export, our research contributed to our understanding of general mechanisms for nucleocytoplasmic shuttling of proteins and nucleic acids in plant cells. Also integration for stable transformation of ssDNA mediated by our model pathogen Agrobacterium tumefaciens led to identification of plant specific proteins involved.

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David A. Boothman. Role of Cell Cycle Regulation and MLH1, A Key DNA Mismatch Repair Protein, In Adaptive Survival Responses. Final Report. Office of Scientific and Technical Information (OSTI), August 1999. http://dx.doi.org/10.2172/767322.

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Epel, Bernard L., Roger N. Beachy, A. Katz, G. Kotlinzky, M. Erlanger, A. Yahalom, M. Erlanger, and J. Szecsi. Isolation and Characterization of Plasmodesmata Components by Association with Tobacco Mosaic Virus Movement Proteins Fused with the Green Fluorescent Protein from Aequorea victoria. United States Department of Agriculture, September 1999. http://dx.doi.org/10.32747/1999.7573996.bard.

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The coordination and regulation of growth and development in multicellular organisms is dependent, in part, on the controlled short and long-distance transport of signaling molecule: In plants, symplastic communication is provided by trans-wall co-axial membranous tunnels termed plasmodesmata (Pd). Plant viruses spread cell-to-cell by altering Pd. This movement scenario necessitates a targeting mechanism that delivers the virus to a Pd and a transport mechanism to move the virion or viral nucleic acid through the Pd channel. The identity of host proteins with which MP interacts, the mechanism of the targeting of the MP to the Pd and biochemical information on how Pd are alter are questions which have been dealt with during this BARD project. The research objectives of the two labs were to continue their biochemical, cellular and molecular studies of Pd composition and function by employing infectious modified clones of TMV in which MP is fused with GFP. We examined Pd composition, and studied the intra- and intercellular targeting mechanism of MP during the infection cycle. Most of the goals we set for ourselves were met. The Israeli PI and collaborators (Oparka et al., 1999) demonstrated that Pd permeability is under developmental control, that Pd in sink tissues indiscriminately traffic proteins of sizes of up to 50 kDa and that during the sink to source transition there is a substantial decrease in Pd permeability. It was shown that companion cells in source phloem tissue export proteins which traffic in phloem and which unload in sink tissue and move cell to cell. The TAU group employing MP:GFP as a fluorescence probe for optimized the procedure for Pd isolation. At least two proteins kinases found to be associated with Pd isolated from source leaves of N. benthamiana, one being a calcium dependent protein kinase. A number of proteins were microsequenced and identified. Polyclonal antibodies were generated against proteins in a purified Pd fraction. A T-7 phage display library was created and used to "biopan" for Pd genes using these antibodies. Selected isolates are being sequenced. The TAU group also examined whether the subcellular targeting of MP:GFP was dependent on processes that occurred only in the presence of the virus or whether targeting was a property indigenous to MP. Mutant non-functional movement proteins were also employed to study partial reactions. Subcellular targeting and movement were shown to be properties indigenous to MP and that these processes do not require other viral elements. The data also suggest post-translational modification of MP is required before the MP can move cell to cell. The USA group monitored the development of the infection and local movement of TMV in N. benthamiana, using viral constructs expressing GFP either fused to the MP of TMV or expressing GFP as a free protein. The fusion protein and/or the free GFP were expressed from either the movement protein subgenomic promoter or from the subgenomic promoter of the coat protein. Observations supported the hypothesis that expression from the cp sgp is regulated differently than expression from the mp sgp (Szecsi et al., 1999). Using immunocytochemistry and electron microscopy, it was determined that paired wall-appressed bodies behind the leading edge of the fluorescent ring induced by TMV-(mp)-MP:GFP contain MP:GFP and the viral replicase. These data suggest that viral spread may be a consequence of the replication process. Observation point out that expression of proteins from the mp sgp is temporary regulated, and degradation of the proteins occurs rapidly or more slowly, depending on protein stability. It is suggested that the MP contains an external degradation signal that contributes to rapid degradation of the protein even if expressed from the constitutive cp sgp. Experiments conducted to determine whether the degradation of GFP and MP:GFP was regulated at the protein or RNA level, indicated that regulation was at the protein level. RNA accumulation in infected protoplast was not always in correlation with protein accumulation, indicating that other mechanisms together with RNA production determine the final intensity and stability of the fluorescent proteins.

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