Gotowe bibliografie tematyczne / Programmed cell death

Gotowa bibliografia na temat „Programmed cell death”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 10 marca 2023

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Artykuły w czasopismach na temat "Programmed cell death"

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Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro i Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells". Cancer Medicine Journal 1, nr 1 (31.08.2018): 12–23. http://dx.doi.org/10.46619/cmj.2018.1-1003.

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Programmed cell death is an essential physiological and biological process for the proper development and functioning of the organism. Apoptosis is the term that describes the most frequent form of programmed cell death and derives from the morphological characteristics of this type of death caused by cellular suicide. Apoptosis is highly regulated to maintain homeostasis in the body, since its imbalances by increasing and decreasing lead to different types of diseases. In this review, we aim to describe the mechanisms of cell death and the pathways through apoptosis is initiated, transmitted, regulated, and executed.
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Roy, Jean-Michel. "Is programmed cell death a programmed death?" Biofutur 1998, nr 178 (maj 1998): 12. http://dx.doi.org/10.1016/s0294-3506(98)80078-1.

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Lockshin, Richard A., i Zahra Zakeri. "Cell Death (Apoptosis, Programmed Cell Death)". Directions in Science 1 (27.02.2002): 41–44. http://dx.doi.org/10.1100/tsw.2002.161.

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Fulton, Alice B. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.b.

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Novak, Jan. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.a.

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Novak, J., A. B. Fulton i J. C. Ameisen. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 17–21. http://dx.doi.org/10.1126/science.274.5284.17c.

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Novak, J. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 20. http://dx.doi.org/10.1126/science.274.5284.20.

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Fulton, A. B. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 20. http://dx.doi.org/10.1126/science.274.5284.20-a.

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Novak, J. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 20a. http://dx.doi.org/10.1126/science.274.5284.20a.

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Fulton, A. B. "Programmed Cell Death". Science 274, nr 5284 (4.10.1996): 20b. http://dx.doi.org/10.1126/science.274.5284.20b.

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Rozprawy doktorskie na temat "Programmed cell death"

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Courtois-Moreau, Charleen Laetitia. "Programmed Cell Death in Xylem Development". Doctoral thesis, Umeå universitet, Umeå Plant Science Centre, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1831.

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Concerns about climate changes and scarcity of fossil fuels are rising. Hence wood is becoming an attractive source of renewable energy and raw material and these new dimensions have prompted increasing interest in wood formation in trees, in both the scientific community and wider public. In this thesis, the focus is on a key process in wood development: programmed cell death (PCD) in the development of xylem elements. Since secondary cell wall formation is dependent, inter alia, upon the life time of xylem elements, the qualitative features of wood will be affected by PCD in xylem, about which there is little information. This thesis focuses on the anatomical, morphological and transcriptional features of PCD during xylem development in both the stem of hybrid aspen, Populus tremula (L.) x tremuloides (Michx.) and the hypocotyl of the herbaceous model system Arabidopsis thaliana (L. Heynh.). In Populus, the progressive removal of organelles from the cytoplasm before the time of death (vacuolar bursts) and the slowness of the cell death process, illustrated by DNA fragmentation assays (such as TUNEL and Comet assays), have been ascertained in the xylem fibres by microscopic analyses. Furthermore, candidate genes for the regulation of fibre cell death were identified either from a Populus EST library obtained from woody tissues undergoing fibre cell death or from microarray experiments in Populus stem, and further assessed in an in silico comparative transcriptomic analysis of Arabidopsis thaliana. These candidate genes were either putative novel regulators of fibre cell death or members of previously described families of cell death-related genes, such as autophagy-related genes. The induction of the latter and the previous microscopic observations suggest the importance of autophagy in the degradation of the cytoplasmic contents specifically in the xylem fibres. Vacuolar bursts in the vessels were the only previously described triggers of PCD in the xylem, which induce the very rapid degradation of the nuclei and surrounding cytoplasmic contents, therefore unravelling a unique previously unrecorded type of PCD in the xylem fibres, principally involving autophagy. Arabidopsis is an attractive alternative model plant for exploring some aspects of wood formation, such as the characterisation of negative regulators of PCD. Therefore, the anatomy of Arabidopsis hypocotyls was also investigated and the ACAULIS5 (ACL5) gene, encoding an enzyme involved in polyamine biosynthesis, was identified as a key regulator of xylem specification, specifically in the vessel elements, though its negative effect on the cell death process. Taken together, PCD in xylem development seems to be a highly specific process, involving unique cell death morphology and molecular machinery. In addition, the technical challenges posed by the complexity of the woody tissues examined highlighted the need for specific methods for assessing PCD and related phenomena in wood.
Oron för klimatförändringar och brist på fossila bränslen har ökat påtagligt under de senaste åren. De enorma möjligheter som skogsråvaran erbjuder som alternativ källa för förnyelsebar energi och råmaterial har väckt ett stort intresse också för den biologiska processen bakom vedbildning i träd. Denna avhandling fokuserar på en viktig process i vedbildning: programmerad celldöd (PCD) i xylemet. Xylemcellernas livstid påverkar bildningen av sekundära cellväggar, vilket i sin tur påverkar vedens kvalitativa egenskaperna, så som veddensitet. Trots dess betydelse för viktiga egenskaper hos vedråvaran existerar fortfarande väldigt lite information om xylem PCD på cellulär eller molekylär nivå. I den här avhandlingen belyses de anatomiska, morfologiska och genetiska aspekterna av PCD i xylemutveckling i både stam av hybridasp, Populus tremula (L.) x tremuloides (Michx.) och hypokotyl av det örtartade modellsystemet Arabidopsis thaliana (L. Heynh.). Xylemet i både Populus och Arabidopsis består av två olika celltyper; de vattentransporterade kärlen och de stödjande fibrerna. Det är känt att celldöd i kärlen pågår mycket snabbt efter att den centrala vakuolen brister och de hydrolytiska enzymer släpps in i cytoplasman. I den här avhandlingen ligger fokus på fibrerna i Populus xylemet. Med hjälp av mikroskopianalyser av cellmorfologin (elektronmikroskopi) och DNA-fragmentering i cellkärnan (TUNEL- och Comet-analyser) kunde vi konstatera att till skillnad från kärlen så uppvisar fibrerna en långsam och progressiv nedbrytning av organellerna och cellkärnans DNA före vakuolbristning. Dessutom har kandidatgener för reglering av fibercelldöd identifierats antingen från ett Populus EST bibliotek från vedartade vävnader som genomgår fibercelldöd eller från mikroarray experiment i Populus stam. Dessa kandidatgener är antingen potentiella nya regulatorer av fibercelldöd eller medlemmar av tidigare beskrivna familjer av celldödsrelaterade gener. Bland de sistnämnda finns autofagi-relaterade gener, vilket stöder funktionen av autofagi i samband med autolys av cellinnehållet i xylemfibrerna. Dessa studier pekar därför på en typ av PCD som har inte tidigare beskrivits för xylemet. Arabidopsis är ett alternativt växtmodellsystem för studier av vissa aspekter av vedbildningen, såsom karakteriseringen av negativa regulatorer av PCD. Därför har också hypokotylanatomin analyserats, och ACAULIS5 (ACL5) genen, som kodar för ett enzym i biosyntesen av polyaminer, har visats vara en viktig regulator av xylemspecifikation genom dess negativa effekt på kärlens celldöd. Sammantaget visar denna avhandling att PCD i xylemutvecklingen verkar involvera unika morfologiska och molekylära mekanismer. Vi visar dessutom att komplexiteten hos de vedartade vävnaderna leder till ett behov av bättre anpassade verktyg för att djupare kunna bedöma PCD och liknande fenomen i veden.
Även med namnet Moreau-Courtois, Charleen L. samt Moreau, Charleen.
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Świdziński, Jodi A. "Programmed cell death in Arabidopsis thaliana". Thesis, University of Oxford, 2003. http://ora.ox.ac.uk/objects/uuid:6e2580fc-8873-4722-89f7-b206d4be2a5f.

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Programmed Cell Death (PCD) describes an orderly cellular breakdown that occurs in both plants and animals throughout development and in response to biotic and abiotic stresses. The molecular machinery that functions in the induction and execution of animal PCD has been characterised in great detail. Conversely, few genes and proteins involved in plant PCD have been identified. While certain features of animal PCD may be conserved, the induction and execution of plant PCD is also likely to involve novel proteins and mechanisms. The aim of the work presented in this thesis was to investigate experimental approaches for studying plant PCD and to gain an understanding of the molecular mechanisms involved. To this end, an Arabidopsis thaliana cell suspension system was developed in which PCD could be induced by both a heat treatment (55°C, 10 min) and senescence (13 to 14 days-old). This system allowed for the molecular responses related to programmed cell death to be distinguished from those that were a specific response to the inducing stimulus. The Arabidopsis cell suspension system was utilised for an analysis of transcriptomic and proteomic changes that occur following the induction of PCD. A custom cDNA microarray analysis of ~100 putative cell death-related genes was used to measure the abundance of transcripts of these genes during PCD, and this work was extended to a whole-genome transcriptomic analysis of PCD. A number of candidate genes that may play a role in plant PCD were identified. These included those encoding antioxidant enzymes, cytosolic heat shock proteins, the mitochondrial adenine nucleotide translocase, ion transporters, a two-component response regulator (ARR4), several pathogenesis-related proteins, phospholipases and proteases, extracellular glycoproteins and enzymes (including a subtilisin-like protease, chitinases, and glucanases), and transcriptional regulators such as a homeobox leucine zipper and NAC-domain proteins. The induction and execution of plant PCD is also likely to involve mechanisms that are not transcriptionally regulated. A proteomic analysis of changes in the total cellular protein profile during heat- and senescence-induced PCD was therefore used to identify 12 proteins that are modulated in both systems and may play a PCD-specific role. These included the mitochondrial voltage-dependent anion channel (Athsr2), catalase, mitochondrial superoxide dismutase, an extracellular glycoprotein, and aconitase. Selected genes and proteins identified in the transcriptomic and proteomic analyses were further investigated in an attempt to define their role in plant PCD. Since PCD is difficult to quantitatively analyse at the whole-plant level, initially a strategy of transient expression of genes of interest in Arabidopsis protoplasts was adopted. However, it proved to be technically difficult to accurately quantify the number of dead cells in this system. As an alternative, Arabidopsis T-DNA insertional mutants within genes of interest were investigated for PCD-related phenotypes. Mutants in Senescence-Related Gene 3, the mitochondrial voltage-dependent anion channel (Athsr2), and cytosolic Heat shock protein 70-3 were isolated. The mutant lines were not visibly affected in their development, formation of xylem, onset and progression of senescence, or responses to abiotic and biotic stresses. This indicated that these genes are either not involved in the PCD pathway or that their functional role can be fulfilled by other gene products.
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Sharma, Pundrique Radheyshyam. "Programmed cell death during heart development". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272255.

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Palazzo, Francesco Fausto. "Programmed cell death in autoimmune thyroid disease". Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270709.

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Wilkinson, Derek. "Proteases and programmed cell death in fungi". Thesis, University of Exeter, 2011. http://hdl.handle.net/10036/3629.

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Programmed cell death in animals, plants and protists is in part regulated by a variety of proteases, including cysteine aspartyl proteases, (caspases, paracaspases and metacaspases), cathepsins, subtilisin-like serine proteases, vacuolar processing enzymes and the proteasome. The role of different proteases in the cell death responses of the fungi is however largely unknown. A greater understanding of the fungal cell death machinery may provide new insights into the mechanisms and evolution of PCD and potentially reveal novel targets for a new generation of antifungal drugs. The role of a metacaspase encoding gene, MCA1, in the cell death response of the human pathogen Candida albicans pathogen has been investigated by functional analysis. MCA1 deletion not only alters the sensitivity of cells to a number of cell death stimuli, it also enhances virulence in an insect model. C. albicans shows altered cell and colony morphology on Lee’s medium. Evidence is presented to suggest that these functions appear to be dependent upon active mitochondria. In this study it has also been shown that key caspase substrates may be conserved between humans and the yeasts Saccharomyces cerevisiae and Candida albicans. Many substrates, particularly those which are essential, have retained their caspase cleavage motifs. 14 protease mutants displayed altered activity against caspase 1, 3, 6 or 8 substrates during acetic acid-induced PCD and caspase 1-like activity appeared to be particularly associated with PCD. Using a novel bioinformatic analysis of experimental LC-MS/MS data, changes in the degradation patterns of the proteome (destructome) following acetic acid-induced cell death have been investigated in wild-type yeast. In addition, potential native substrates of the yeast Mca1 have also been identified. The future challenge is to characterise the destructome of different proteases under a range of cell death conditions. In this way it may be possible to identify key components of the cell death machinery and their substrates and so reveal the most promising targets for future therapeutics.
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Jagasia, Ravi. "Mitochondrial dynamics in Caenorhabditis elegans programmed cell death". Diss., [S.l.] : [s.n.], 2005. http://edoc.ub.uni-muenchen.de/archive/00004281.

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Cowling, Victoria Haigh. "Regulation of capase activation during programmed cell death". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397249.

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Drury, Georgina E. "UVC-induced programmed cell death in Arabidopsis thaliana". Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.678199.

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Cameron, Angus Crawford. "The control of physiological programmed cell death : apoptosis". Thesis, The University of Sydney, 1991. http://hdl.handle.net/2123/4751.

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Nelson, Charles J. "MicroRNA Regulation of Autophagy during Programmed Cell Death: A Dissertation". eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/756.

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Autophagy delivers cytoplasmic material to the lysosome for degradation, and has been implicated in many cellular processes, including stress, infection, survival, and death. Although the regulation and role that autophagy plays in stress, infection, and survival is apparent, its involvement during cell death remains relatively unclear. In this thesis I summarize what is known about the roles autophagy can play in cell death, and the differences between the utilization of autophagy during nutrient deprivation and cell death. Utilizing Drosophila melanogaster as a model system, the roles autophagy plays in both of these contexts can be studied. The goal of this thesis is to provide a better understanding of the regulatory mechanisms that distinguish between autophagy as a survival mechanism and autophagy as a cell death mechanism. From my studies I was able to determine that microRNAs can regulate autophagy in vivo, and that the microRNA miR-14 controls autophagy specifically during the destruction of the larval salivary glands of Drosophila melanogaster. I found that miR-14 regulates autophagy through modulation of IP3 and calcium signaling, and this miR-14 control of IP3 and calcium signaling does not influence the induction of autophagy during nutrient deprivation. Therefore, this knowledge demonstrates how autophagy can be regulated to distinguish its use during cell survival and death providing insight into how autophagy can used to treat diseases.
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Książki na temat "Programmed cell death"

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Puthalakath, Hamsa, i Christine J. Hawkins, red. Programmed Cell Death. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3581-9.

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Shi, Yun-Bo, Yufang Shi, Yonghua Xu i David W. Scott, red. Programmed Cell Death. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2.

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Paul, Mattson Mark, Estus Steven i Rangnekar Vivek, red. Programmed cell death. Amsterdam: Elsevier, 2001.

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Yun-Bo, Shi, i International Symposium on Programmed Cell Death (1996 : Shanghai, China), red. Programmed cell death. New York: Plenum Press, 1997.

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Gunawardena, Arunika N., i Paul F. McCabe, red. Plant Programmed Cell Death. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-21033-9.

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De Gara, Laura, i Vittoria Locato, red. Plant Programmed Cell Death. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7668-3.

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service), ScienceDirect (Online, red. Programmed cell death: General principles for studying cell death. San Diego, Calif: Academic Press, 2008.

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Pérez Martín, José Manuel. Programmed Cell Death in Protozoa. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-76717-8.

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Programmed cell death in protozoa. Austin, Tex: Landes Bioscience, 2008.

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1965-, Gray John, red. Programmed cell death in plants. Oxford: Blackwell, 2004.

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Części książek na temat "Programmed cell death"

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McAllister-Williams, R. Hamish, Daniel Bertrand, Hans Rollema, Raymond S. Hurst, Linda P. Spear, Tim C. Kirkham, Thomas Steckler i in. "Programmed Cell Death". W Encyclopedia of Psychopharmacology, 1074. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3497.

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Shen, Jie. "Programmed Cell Death". W Encyclopedia of Gerontology and Population Aging, 1–6. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_430-1.

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Mehlhorn, Heinz. "Programmed Cell Death". W Encyclopedia of Parasitology, 2255. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4209.

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Mehlhorn, Heinz. "Programmed cell death". W Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4209-1.

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Baker, Julien S., Fergal Grace, Lon Kilgore, David J. Smith, Stephen R. Norris, Andrew W. Gardner, Robert Ringseis i in. "Programmed Cell Death". W Encyclopedia of Exercise Medicine in Health and Disease, 727. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4473.

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Shen, Jie. "Programmed Cell Death". W Encyclopedia of Gerontology and Population Aging, 3996–4002. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_430.

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Tata, Jamshed R. "How Hormones Regulate Programmed Cell Death during Amphibian Metamorphosis". W Programmed Cell Death, 1–11. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_1.

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Scott, David W., Tommy Brunner, Dubravka Donjerković, Sergei Ezhevsky, Terri Grdina, Douglas Green, Yufang Shi i Xiao-rui Yao. "Murder and Suicide". W Programmed Cell Death, 91–103. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_10.

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Zheng, Dexian, Yanxin Liu, Yong Zheng, Ying Liu, Shilian Liu, Baoping Wang, Markus Metzger, Emiko Mizoguchi i Cox Terhorst. "Molecular Mechanisms of T Lymphocyte Apoptosis Mediated by CD3". W Programmed Cell Death, 105–12. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_11.

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Shi, Yufang, Gordon B. Mills i Ruoxiang Wang. "Mitogenic Cytokines Promote Apoptosis". W Programmed Cell Death, 113–24. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0072-2_12.

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Streszczenia konferencji na temat "Programmed cell death"

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He, Xiao-Yan, Robert A. Sikes, Sharon L. Thomsen, L. Chung i Steven L. Jacques. "Photodynamic therapy-induced programmed cell death in carcinoma cell lines". W OE/LASE'93: Optics, Electro-Optics, & Laser Applications in Science& Engineering, redaktor Thomas J. Dougherty. SPIE, 1993. http://dx.doi.org/10.1117/12.146321.

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Carotenuto, Luciano, Vincenza Pace, Dina Bellizzi i Giovanna De Benedictis. "Dynamical analysis of the programmed cell death pathway". W European Control Conference 2007 (ECC). IEEE, 2007. http://dx.doi.org/10.23919/ecc.2007.7068411.

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Song, Yongle, Zuojun Liu, Ling Qi i Huijie Wang. "Study of programmed cell death algorithm and its application". W 2015 IEEE International Conference on Information and Automation (ICIA). IEEE, 2015. http://dx.doi.org/10.1109/icinfa.2015.7279680.

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Subiros-Funosas, Ramon, Nicole Barth, Jesus Sot, Felix Goni, Lorena Mendive-Tapia, Rodolfo Lavilla, Rodger Duffin, Adriano Rossi, Ian Dransfield i Marc Vendrell. "Fluorogenic peptides for the detection of programmed cell death". W 35th European Peptide Symposium. Prompt Scientific Publishing, 2018. http://dx.doi.org/10.17952/35eps.2018.056.

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Kovaleva, L. V., E. V. Zakharova i G. V. Timofeeva. "S-RNase-BASED SELF-INCOMPATIBILITY AND PROGRAMMED CELL DEATH". W The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-931-935.

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Onyundo, Megan, Matthew Sanborn, Victoria Timmel i Nicanor Austriaco. "Abstract 2333: Genetic characterization of programmed cell death in aneuploid yeast cells". W 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.am2018-2333.

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Wang, Gang, JunJie Wang, BaoYuan Li, YingDong Sun, ZhaoXing Ding i ChangLing Ding. "p53-Induced ROS-accumulation induces programmed cell death in C6 glioma cells". W 2014 International Conference on Information Science, Electronics and Electrical Engineering (ISEEE). IEEE, 2014. http://dx.doi.org/10.1109/infoseee.2014.6948063.

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Yamane, Hiromichi, Hideko Isozaki, Nobuaki Ochi, Kenichiro Kudo, Yoshihiro Honda, Tomoko Yamagishi, Toshio Kubo, Katsuyuki Kiura i Nagio Takigawa. "Abstract 1323: Both programmed cell death protein 1 and programmed death-ligand 1 molecules can be expressed on the cell surface of small-cell lung cancer". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1323.

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Liu Zuojun, Zhao Jing, Yang Peng i Zhang Yan. "Research of evolutionary algorithm based on programmed cell death theory". W 2008 Chinese Control and Decision Conference (CCDC). IEEE, 2008. http://dx.doi.org/10.1109/ccdc.2008.4598312.

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Bilyy, Rostyslav O., Alexander I. Bilyi, Vasyl B. Getman, Yuriy Ya Kit, Christina Ya Mayor, Volodmyr O. Antonyuk i Rostyslav S. Stoika. "Some new approaches to the detection of programmed cell death". W SPIE Proceedings, redaktor Valery V. Tuchin. SPIE, 2006. http://dx.doi.org/10.1117/12.696967.

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Raporty organizacyjne na temat "Programmed cell death"

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Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, sierpień 1995. http://dx.doi.org/10.21236/ada300581.

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Distelhorst, Clark W. Programmed Cell Death in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, październik 1997. http://dx.doi.org/10.21236/ada340671.

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Drews, Gary, N. Programmed Cell Death During Female Gametophyte Development. Office of Scientific and Technical Information (OSTI), wrzesień 2004. http://dx.doi.org/10.2172/1014978.

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Engelberg-Kulka, Hanna. Bacterial Programmed Cell Death as a Population Phenomenon. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2013. http://dx.doi.org/10.21236/ada587504.

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Cowburn, David. Rational Design of Regulators of Programmed Cell Death in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2000. http://dx.doi.org/10.21236/ada395357.

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Julie M. Stone. Role of a Transcriptional Regulator in Programmed Cell Death and Plant Development. Office of Scientific and Technical Information (OSTI), wrzesień 2008. http://dx.doi.org/10.2172/937080.

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Cowburn, David. Rational Design of Regulators of Programmed Cell Death in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2003. http://dx.doi.org/10.21236/ada460041.

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Xiao, Youchao, Jiaqi Hao, Xingguang Ren, Hubin Duan, Chunyan Hao, Huan Wang, Xin Yang i in. Programmed cell death ligand 1 is a prognostic factor for glioblastoma: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, lipiec 2020. http://dx.doi.org/10.37766/inplasy2020.7.0079.

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Granot, David, i Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, styczeń 2003. http://dx.doi.org/10.32747/2003.7585189.bard.

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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .
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Liu, Shu, Xin Zhang, Wenhan Yang i Shun Xu. Association of Patient Sex with Efficacy of Programmed Death-1/Ligand-1 Inhibitors in Advanced Non–small-cell Lung Cancer: A Systematic Review and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2021. http://dx.doi.org/10.37766/inplasy2021.1.0005.

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