Relevant bibliographies by topics / Yeast apoptosis

Academic literature on the topic 'Yeast apoptosis'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Yeast apoptosis"

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Reiter, Jochen, Eva Herker, Frank Madeo, and Manfred J. Schmitt. "Viral killer toxins induce caspase-mediated apoptosis in yeast." Journal of Cell Biology 168, no. 3 (January 24, 2005): 353–58. http://dx.doi.org/10.1083/jcb.200408071.

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In yeast, apoptotic cell death can be triggered by various factors such as H2O2, cell aging, or acetic acid. Yeast caspase (Yca1p) and cellular reactive oxygen species (ROS) are key regulators of this process. Here, we show that moderate doses of three virally encoded killer toxins (K1, K28, and zygocin) induce an apoptotic yeast cell response, although all three toxins differ significantly in their primary killing mechanisms. In contrast, high toxin concentrations prevent the occurrence of an apoptotic cell response and rather cause necrotic, toxin-specific cell killing. Studies with Δyca1 and Δgsh1 deletion mutants indicate that ROS accumulation as well as the presence of yeast caspase 1 is needed for apoptosis in toxin-treated yeast cells. We conclude that in the natural environment of toxin-secreting killer yeasts, where toxin concentration is usually low, induction of apoptosis might play an important role in efficient toxin-mediated cell killing.
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Wissing, Silke, Paula Ludovico, Eva Herker, Sabrina Büttner, Silvia M. Engelhardt, Thorsten Decker, Alexander Link, et al. "An AIF orthologue regulates apoptosis in yeast." Journal of Cell Biology 166, no. 7 (September 20, 2004): 969–74. http://dx.doi.org/10.1083/jcb.200404138.

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Apoptosis-inducing factor (AIF), a key regulator of cell death, is essential for normal mammalian development and participates in pathological apoptosis. The proapoptotic nature of AIF and its mode of action are controversial. Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis. Similar to mammalian AIF, Ynr074cp is located in mitochondria and translocates to the nucleus of yeast cells in response to apoptotic stimuli. Purified Ynr074cp degrades yeast nuclei and plasmid DNA. YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis. Conversely, overexpression of Ynr074cp strongly stimulates apoptotic cell death induced by hydrogen peroxide and this effect is attenuated by disruption of cyclophilin A or the yeast caspase YCA1. We conclude that Ynr074cp is a cell death effector in yeast and rename it AIF-1 (Aif1p, gene AIF1).
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Madeo, Frank, Eleonore Fröhlich, Martin Ligr, Martin Grey, Stephan J. Sigrist, Dieter H. Wolf, and Kai-Uwe Fröhlich. "Oxygen Stress: A Regulator of Apoptosis in Yeast." Journal of Cell Biology 145, no. 4 (May 17, 1999): 757–67. http://dx.doi.org/10.1083/jcb.145.4.757.

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Oxygen radicals are important components of metazoan apoptosis. We have found that apoptosis can be induced in the yeast Saccharomyces cerevisiae by depletion of glutathione or by low external doses of H2O2. Cycloheximide prevents apoptotic death revealing active participation of the cell. Yeast can also be triggered into apoptosis by a mutation in CDC48 or by expression of mammalian bax. In both cases, we show oxygen radicals to accumulate in the cell, whereas radical depletion or hypoxia prevents apoptosis. These results suggest that the generation of oxygen radicals is a key event in the ancestral apoptotic pathway and offer an explanation for the mechanism of bax-induced apoptosis in the absence of any established apoptotic gene in yeast.
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Jin, Can, and John C. Reed. "Yeast and apoptosis." Nature Reviews Molecular Cell Biology 3, no. 6 (June 2002): 453–59. http://dx.doi.org/10.1038/nrm832.

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Madeo, Frank, Eva Herker, Silke Wissing, Helmut Jungwirth, Tobias Eisenberg, and Kai-Uwe Fröhlich. "Apoptosis in yeast." Current Opinion in Microbiology 7, no. 6 (December 2004): 655–60. http://dx.doi.org/10.1016/j.mib.2004.10.012.

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Herker, Eva, Helmut Jungwirth, Katharina A. Lehmann, Corinna Maldener, Kai-Uwe Fröhlich, Silke Wissing, Sabrina Büttner, Markus Fehr, Stephan Sigrist, and Frank Madeo. "Chronological aging leads to apoptosis in yeast." Journal of Cell Biology 164, no. 4 (February 16, 2004): 501–7. http://dx.doi.org/10.1083/jcb.200310014.

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During the past years, yeast has been successfully established as a model to study mechanisms of apoptotic regulation. However, the beneficial effects of such a cell suicide program for a unicellular organism remained obscure. Here, we demonstrate that chronologically aged yeast cultures die exhibiting typical markers of apoptosis, accumulate oxygen radicals, and show caspase activation. Age-induced cell death is strongly delayed by overexpressing YAP1, a key transcriptional regulator in oxygen stress response. Disruption of apoptosis through deletion of yeast caspase YCA1 initially results in better survival of aged cultures. However, surviving cells lose the ability of regrowth, indicating that predamaged cells accumulate in the absence of apoptotic cell removal. Moreover, wild-type cells outlast yca1 disruptants in direct competition assays during long-term aging. We suggest that apoptosis in yeast confers a selective advantage for this unicellular organism, and demonstrate that old yeast cells release substances into the medium that stimulate survival of the clone.
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Liang, Qiuli, and Bing Zhou. "Copper and Manganese Induce Yeast Apoptosis via Different Pathways." Molecular Biology of the Cell 18, no. 12 (December 2007): 4741–49. http://dx.doi.org/10.1091/mbc.e07-05-0431.

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Metal ions are essential as well as toxic to the cell. The mechanism of metal-induced toxicity is not well established. Here, for the first time we studied two essential nutritional elements, copper and manganese, for their apoptotic effects in yeast Saccharomyces cerevisiae. Although beneficial at subtoxic levels, we demonstrated that at moderately toxic levels, both metals induce extensive apoptosis in yeast cells. At even higher concentrations, necrosis takes over. Furthermore, we investigated the molecular pathways mediating Cu- and Mn-mediated apoptotic action. Mitochondria-defective yeast exhibit a much reduced apoptotic marker expression and better survival under Cu and Mn stress, indicating mitochondria are involved in both Cu- and Mn-induced apoptosis. Reactive oxygen species (ROS) are generated in high amounts in Cu- but not in Mn-induced cell death, and Cu toxicity can be alleviated by overexpression of superoxide dismutase 2, suggesting ROS mediate Cu but not Mn toxicity. Yeast metacaspase Yca1p is not involved in Cu-induced apoptosis, although it plays an important role in the Mn-induced process. A genetic screen identified Cpr3p, a yeast cyclophilin D homologue, as mediating the Cu-induced apoptotic program. Cpr3p mutant seems to eliminate Cu-induced apoptosis without affecting ROS production, while leaving necrosis intact. These results may provide important insight into a detailed understanding at the molecular and cellular level of metal toxicity and metal accumulation diseases.
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LeBrasseur, Nicole. "Yeast apoptosis debate continues." Journal of Cell Biology 166, no. 7 (September 27, 2004): 938. http://dx.doi.org/10.1083/jcb1667iti1.

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Schmitt, Manfred J., and Jochen Reiter. "Viral induced yeast apoptosis." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1783, no. 7 (July 2008): 1413–17. http://dx.doi.org/10.1016/j.bbamcr.2008.01.017.

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Sousa, Maria João, Flávìa Azevedo, Ana Pedras, Carolina Marques, Olga P. Coutinho, Ana Preto, Hernâni Gerós, Susana R. Chaves, and Manuela Côrte-Real. "Vacuole–mitochondrial cross-talk during apoptosis in yeast: a model for understanding lysosome–mitochondria-mediated apoptosis in mammals." Biochemical Society Transactions 39, no. 5 (September 21, 2011): 1533–37. http://dx.doi.org/10.1042/bst0391533.

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The yeast apoptosis field emerged with the finding that key components of the apoptotic machinery are conserved in these simple eukaryotes. Thus it became possible to exploit these genetically tractable organisms to improve our understanding of the intricate mechanisms of cell death in higher eukaryotes and of severe human diseases associated with apoptosis dysfunctions. Early on, it was recognized that a mitochondria-mediated apoptotic pathway showing similarities to the mammalian intrinsic pathway was conserved in yeast. Recently, lysosomes have also emerged as central players in mammalian apoptosis. Following LMP (lysosomal membrane permeabilization), lysosomal proteases such as cathepsins B, D and L are released into the cytosol and can trigger a mitochondrial apoptotic cascade. CatD (cathepsin D) can also have anti-apoptotic effects in some cellular types and specific contexts. Nonetheless, the mechanisms underlying LMP and the specific role of cathepsins after their release into the cytosol remain poorly understood. We have recently shown that yeast vacuoles, membrane-bound acidic organelles, which share many similarities to plant vacuoles and mammalian lysosomes, are also involved in the regulation of apoptosis and that the vacuolar protease Pep4p, orthologue of the human CatD, is released from the vacuole into the cytosol in response to acetic acid. Here, we discuss how the conservation of cell-death regulation mechanisms in yeast by the lysosome-like organelle and mitochondria may provide new insights into the understanding of the complex interplay between the mitochondria and lysosome-mediated signalling routes during mammalian apoptosis.
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Dissertations / Theses on the topic "Yeast apoptosis"

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Ilina, Yulia. "Functions of the yeast protein Stm1 and its involvement in apoptotic cell death." [S.l. : s.n.], 2005.

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Nargund, Amrita Mohan. "Mechanism (S) of Metal-Induced Apoptosis in Saccharomyces Cerevisiae." Digital Archive @ GSU, 2010. http://digitalarchive.gsu.edu/biology_diss/80.

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Heavy metals, such as copper and cadmium have been linked to a number of cellular dysfunctions in single and multicellular organisms that are associated with apoptosis. The yeast, Saccharomyces cerevisiae, provides a valuable model for elucidating apoptosis mechanisms, and this study extends that capability to Cu and Cd-induced apoptosis. We demonstrate that S. cerevisiae undergoes a glucose-dependent, programmed cell death in response to low cadmium concentrations, which is initiated within the first hour of Cd exposure. The response was associated with induction of the yeast caspase, Yca1p, and was abolished in YCA1∆ mutant. Other apoptotic markers, including sub-G1 DNA fragmentation and hyper-polarization of mitochondrial membranes, were also evident among Cd-exposed cells. We also show that low levels of copper can induce a similar apoptotic response in yeast within the first hour of exposure. Such cellular responses were verified by analyzing mitochondrial perturbation, generation of superoxide ions, activation of the yeast caspase1, and the eventual fragmentation of nuclear DNA (through TUNEL). In analyzing the response of yeast to the different metals, we also demonstrated that the metal-induced PCD is instigated through the sequential activity of at least two caspase-like proteins (i.e., Yca1 and Atg4), both of which appear to be in involved in the process of inducing mitochondrial stress. The additional caspase-like activity is shown to be derived from an enzyme involved in the latter stages of autophagy (Atg4), and provides an intriguing association of apoptosis with autophagy. Here we also demonstrate that metals such as copper and cadmium causes oxidative damage to mitochondrial proteins. Such oxidative attack is targeted and we show that oxidation of certain crucial proteins is required for apoptosis upon metal exposure. By showing that such targeted protein oxidation is dependent on YCA1 and ATG, we also confirm the finding that in yeast that have been exposed to a heavy metal, YCA1 and ATG are essential for damaging mitochondria and to initiate apoptosis. These novel findings highlight several new perspectives about the mechanism of metal-dependent apoptosis, while opening up future analyses to the power of the yeast model system.
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Costa, Ana Margarida Pinto e. ""The Role Of Ceramide Pathway In Yeast Apoptosis Induced By Acetic Acid"." Master's thesis, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/26276.

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Costa, Ana Margarida Pinto e. ""The Role Of Ceramide Pathway In Yeast Apoptosis Induced By Acetic Acid"." Dissertação, Instituto de Ciências Biomédicas Abel Salazar, 2009. http://hdl.handle.net/10216/26276.

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Kritsiligkou, Paraskevi. "Peroxiredoxins : yeast redox switches that regulate multiple cellular pathways." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/peroxiredoxins-yeast-redox-switches-that-regulate-multiple-cellular-pathways(fbb44664-5021-4dbc-88c7-64aef8a6c045).html.

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Peroxiredoxins are small ubiquitous cysteine-containing proteins that exhibit high reactivity to hydrogen peroxide. Apart from their role as antioxidants, detoxifying hydrogen peroxide to water, peroxiredoxins have been implicated in other cellular processes, such as protein folding and signalling. Using S. cerevisiae as a model organism, we utilised a variety of techniques to examine previously unexplored links between peroxiredoxins and mitochondrial function. Firstly, we characterised the role of Gpx3 in yeast mitochondria. Proteomic work revealed the presence of Gpx3 in the mitochondrial intermembrane space (IMS) and we characterised when, how and why Gpx3 can be found within the mitochondria. We showed that cells lacking Gpx3 have aberrant mitochondrial morphology and defective protein import capacity and inner membrane potential upon H2O2 stress. Gpx3 translocates to the IMS via a targeting sequence encoded from a non-AUG codon. This provides a novel and unique molecular mechanism that protects mitochondria from the exceptional oxidative stress which their activity imposes. Secondly, we focused on the role of Tsa1 upon protein aggregation-induced stress. Previous studies using the proline analogue AZC to cause protein misfolding revealed that protein aggregates are localised adjacent to mitochondria and mitochondrial ROS are generated in response. We questioned what effect this might have on mitochondrial function and we showed that upon AZC treatment there is a drop in respiratory rate, dependent on Tsa1. We questioned whether Tsa1, like other peroxiredoxins, is involved in regulating signalling cascades and we showed that cells that are lacking Tsa1 have alterations in the activity of the cAMP/PKA pathway. In parallel, we looked for differences both in the proteome and the transcriptome to understand what is the cause of the lethality of a tsa1 strain upon protein aggregation stress. We propose a mechanism where Tsa1 mediates a transcriptional response to protein misfolding stress via the activity of the heat shock transcription factor, Hsf1. Finally, we focused on the role of the mitochondrial peroxiredoxin Prx1. Under conditions where the mitochondrial matrix is oxidised, either genetically or by chemical addition, we showed than an apoptotic pathway is activated, dependent on the redox state of thioredoxin, Trx3. We showed that Trx3 can interact with Prx1 and loss of Prx1 also stops the induction of cell death. Analysis of the interactome of Trx3 unraveled the involvement of Bxl1/Ybh3, the yeast BH3 domain-containing protein and Aim9, a previously uncharacterised protein with kinase-like motifs, in the progression of cell death. The data presented in this thesis widens our understanding of the function of peroxiredoxins and their involvement in the regulation of cellular cascades that ensure correct mitochondrial function and responses to stress.
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Yang, Hui. "Chromosome dynamics and chromosomal proteins in relation to apoptotic cell death in yeast." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1594496261&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.

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Koduru, Rupa. "Study of Cellular Activities in Response to Metal-Induced Apoptosis in Saccharomyces Cerevisiae using FTIR." Digital Archive @ GSU, 2011. http://digitalarchive.gsu.edu/biology_theses/30.

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Saccharomyces cerevisiae exhibits an apoptotic response upon exposure to toxic metals such as cadmium (Cd) and copper (Cu). Preliminary findings indicate that this response is dependent –to some extent- on the presence of a fermentable carbon source, glucose. To investigate this dependency we monitored the apoptotic response to both metals in the presence and absence of glucose and have shown that glucose is absolutely necessary in order to induce apoptosis in yeast at least during the exposure to metal. We have also looked at the biochemical changes that are taking place in yeast when treated with Cd using Fourier Transform Infra-Red (FTIR) Spectroscopy. Our results suggest that there are definitive changes in cellular activities that are discernable at 1660-1640cm-1 (amide I), 1540-1510cm-1 (amide II) and 1140-1080cm-1(DNA absorption bands).
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Brezniceanu-Mehedinti, Marie-Luise Ligia. "Identification of mammalian proteins inhibiting apoptosis downstream of cytochrome c release in a yeast survival screen." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969077343.

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Benzing, Jörg. "Identifikation intrazellulärer Interaktionspartner der Rezeptortyrosinkinasen UFO und MET im Two-Hybrid-System." Ulm : Universität Ulm, Medizinische Fakultät, 2001. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB9394024.

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Ligr, Martin. "Apoptosis in the yeast Saccharomyces cerevisiae a novel cell death process regulated by the Ubiquitin-Proteasome system /." [S.l. : s.n.], 2001. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB9203728.

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Books on the topic "Yeast apoptosis"

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Hammond, Ester Mary. Apoptosis specific protein: A link between yeast autophagy and eukaryotic intermediate filament collapse. Birmingham: University of Birmingham, 1997.

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Sharan, Niki. Cloning of the marine apoptosis inducer, interleukin-1B converting enzyme (ICE), into a yeast expression vector. Sudbury, Ont: Laurentian University, 1996.

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Laun, Peter, Michael Breitenbach, and S. Michal Jazwinski. Aging Research in Yeast. Springer Netherlands, 2014.

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Aging Research In Yeast. Springer, 2011.

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Laun, Peter, Michael Breitenbach, and S. Michal Jazwinski. Aging Research in Yeast. Springer London, Limited, 2011.

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Book chapters on the topic "Yeast apoptosis"

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Mittler, Ron, and Vladimir Shulaev. "Apoptosis in Plants, Yeast, and Bacteria." In Essentials of Apoptosis, 125–33. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-361-3_8.

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Chen, Kun, Nailong Liang, Jing Yang, and Hua Zhao. "UV-B Irradiation Regulates Apoptosis in Yeast." In Proceedings of the 2012 International Conference on Applied Biotechnology (ICAB 2012), 1869–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37925-3_201.

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Breitenbach, Michael, Frank Madeo, Peter Laun, Gino Heeren, Stefanie Jarolim, Kai-Uwe Fröhlich, Silke Wissing, and Alena Pichova. "Yeast as a model for ageing and apoptosis research." In Model Systems in Aging, 61–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-540-37005-5_4.

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Bloomer, David T., Tanja Kitevska, Ingo L. Brand, Anissa M. Jabbour, Hang Nguyen, and Christine J. Hawkins. "Modeling Metazoan Apoptotic Pathways in Yeast." In Methods in Molecular Biology, 161–83. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3581-9_13.

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Zhang, Hong, and John C. Reed. "Chapter 20 Studies of apoptosis proteins in yeast." In Apoptosis, 453–68. Elsevier, 2001. http://dx.doi.org/10.1016/s0091-679x(01)66021-7.

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"Regulators and applications of yeast apoptosis." In Genetics of Apoptosis, 153–54. Garland Science, 2003. http://dx.doi.org/10.1201/9780203427538-23.

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"-Regulators and applications of yeast apoptosis 137." In Genetics of Apoptosis, 155–62. Garland Science, 2003. http://dx.doi.org/10.1201/9780203427538-24.

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Libby Sherr, Goldie, and Chang-Hui Shen. "The Interplay of Key Phospholipid Biosynthetic Enzymes and the Yeast V-ATPase Pump and their Role in Programmed Cell Death." In Regulation and Dysfunction of Apoptosis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97886.

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Exposure of the yeast Saccharomyces cerevisiae to environmental stress can influence cell growth, physiology and differentiation, and thus result in a cell’s adaptive response. During the course of an adaptive response, the yeast vacuoles play an important role in protecting cells from stress. Vacuoles are dynamic organelles that are similar to lysosomes in mammalian cells. The defect of a lysosome’s function may cause various genetic and neurodegenerative diseases. The multi-subunit V-ATPase is the main regulator for vacuolar function and its activity plays a significant role in maintaining pH homeostasis. The V-ATPase is an ATP-driven proton pump which is required for vacuolar acidification. It has also been demonstrated that phospholipid biosynthetic genes might influence vacuolar morphology and function. However, the mechanistic link between phospholipid biosynthetic genes and vacuolar function has not been established. Recent studies have demonstrated that there is a regulatory role of Pah1p, a phospholipid biosynthetic gene, in V-ATPase disassembly and activity. Therefore, in this chapter we will use Saccharomyces cerevisiae as a model to discuss how Pah1p affects V-ATPase disassembly and activity and how Pah1p negatively affect vacuolar function. Furthermore, we propose a hypothesis to describe how Pah1p influences vacuolar function and programmed cell death through the regulation of V-ATPase.
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Kareem, Ozaifa, Ghulam Nabi Bader, Faheem Hyder Pottoo, Mohd Amir, Md Abul Barkat, and Mukesh Pandey. "Beclin 1 Complex and Neurodegenerative Disorders." In Quality Control of Cellular Protein in Neurodegenerative Disorders, 236–60. IGI Global, 2020. http://dx.doi.org/10.4018/978-1-7998-1317-0.ch009.

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Beclin1 is the mammalian orthologue of yeast Atg6/vacuolar protein sorting-30 (VPS30). Beclin1 interacts with various biological macromolecules like ATG14, BIF-1, NRBF2, RUBICON, UVRAG, AMBRA1, HMGB1, PINK1, and PARKIN. Such interactions promote Beclin1-PI3KC3 complex formation. Autophagy is blocked in apoptosis owing to the breakdown of Beclin1 by caspase whereas autophagy induction inhibits effector caspase degradation, therefore, blocks apoptosis. Thus, the Beclin1 is an essential biomolecular species for cross-regulation between autophagy and apoptosis. Various studies carried out in neurodegenerative animal models associated with aggregated proteins have confirmed that multifunctional Beclin1 protein is necessary for neuronal integrity. The role of Beclin1 protein has been investigated and was reported in various human neurodegeneration disorders. This chapter aims to provide an insight into the role of Beclin1 in the development of neurodegenerative disorders.
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Anbu, Ananth, and Umadevi Ananth. "Biological Activity of Defence-Related Plant Secondary Metabolites." In Secondary Metabolites [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101379.

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The message that everyone needs to know is that secondary metabolites in plants and natural products are involved in various activities. The phenolics, quinones, terpenes, flavonoids, and other thousands of low molecular weight metabolites activity is unknown. Well-understood secondary metabolites have been implicated in the defense against pathogens; the operating system of some of these has been established. In particular, to date, a relatively small number of processes have been shown to be targets of plant metabolism, including electron transport chains, mitochondrial function, and membrane integration. However, it is now emerging that other specific enzymes and processes may also be targets of specific metabolites. There is a general belief that modern genetic approaches will identify new targets and mechanisms of plant metabolism. Molecules that trigger apoptosis or autoimmunity in tumor cells, especially triterpenoids, are of particular interest in this regard. Before proceeding to specific studies in plant or human cells, we discuss whether there is a case for conducting preliminary studies on the mechanism of action in the genetic pathway system, such as yeast Saccharomyces cerevisiae, considering the approaches taken so far in botany and strategies that have led to success in the biomedical field.
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Conference papers on the topic "Yeast apoptosis"

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Tamura, Kenji, and Yasushi Minamitani. "Investigation of frequency response of apoptosis induction to budding yeast by burst pulse electric field for cancer treatment." In 2013 IEEE 40th International Conference on Plasma Sciences (ICOPS). IEEE, 2013. http://dx.doi.org/10.1109/plasma.2013.6634804.

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"Antioxidant Activity of Ethanol Extract from Guazuma ulmifolia Lamk. Leaves in Modulating Apoptosis of Yeast Cells (Saccharomyces cerevisiae)." In August 8-10, 2018 Pnom Penh (Cambodia). Dignified Researchers Publication, 2018. http://dx.doi.org/10.17758/dirpub4.dir0818208.

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Tamura, K., R. Kageyama, and Y. Minamitani. "Investigation of frequency response of apoptosis induction to budding yeast by burst pulse electric field for cancer treatment." In 2013 IEEE Pulsed Power and Plasma Science Conference (PPPS 2013). IEEE, 2013. http://dx.doi.org/10.1109/ppc.2013.6627552.

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