Relevant bibliographies by topics / Cell death pathways

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Cell death pathways'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Cell death pathways"

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Fernández-Lázaro, Diego, César Ignacio Fernández-Lázaro, and Martínez Alfredo Córdova. "Cell Death: Mechanisms and Pathways in Cancer Cells." Cancer Medicine Journal 1, no. 1 (August 31, 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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Stekovic, Slaven, and Frank Madeo. "Cell death pathways." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1833, no. 12 (December 2013): 3447. http://dx.doi.org/10.1016/j.bbamcr.2013.09.016.

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Fulda, Simone. "Alternative Cell Death Pathways and Cell Metabolism." International Journal of Cell Biology 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/463637.

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While necroptosis has for long been viewed as an accidental mode of cell death triggered by physical or chemical damage, it has become clear over the last years that necroptosis can also represent a programmed form of cell death in mammalian cells. Key discoveries in the field of cell death research, including the identification of critical components of the necroptotic machinery, led to a revised concept of cell death signaling programs. Several regulatory check and balances are in place in order to ensure that necroptosis is tightly controlled according to environmental cues and cellular needs. This network of regulatory mechanisms includes metabolic pathways, especially those linked to mitochondrial signaling events. A better understanding of these signal transduction mechanisms will likely contribute to open new avenues to exploit our knowledge on the regulation of necroptosis signaling for therapeutic application in the treatment of human diseases.
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Choi, Soo Youn, Whaseon Lee-Kwon, Hwan Hee Lee, Jun Ho Lee, Satoru Sanada, and Hyug Moo Kwon. "Multiple cell death pathways are independently activated by lethal hypertonicity in renal epithelial cells." American Journal of Physiology-Cell Physiology 305, no. 10 (November 15, 2013): C1011—C1020. http://dx.doi.org/10.1152/ajpcell.00384.2012.

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When hypertonicity is imposed with sufficient intensity and acuteness, cells die. Here we investigated the cellular pathways involved in death using a cell line derived from renal epithelium. We found that hypertonicity rapidly induced activation of an intrinsic cell death pathway—release of cytochrome c and activation of caspase-3 and caspase-9—and an extrinsic pathway—activation of caspase-8. Likewise, a lysosomal pathway of cell death characterized by partial lysosomal rupture and release of cathepsin B from lysosomes to the cytosol was also activated. Relationships among the pathways were examined using specific inhibitors. Caspase inhibitors did not affect cathepsin B release into the cytosol by hypertonicity. In addition, cathepsin B inhibitors and caspase inhibitors did not affect hypertonicity-induced cytochrome c release, suggesting that the three pathways were independently activated. Combined inhibition of caspases and cathepsin B conferred significantly more protection from hypertonicity-induced cell death than inhibition of caspase or cathepsin B alone, indicating that all the three pathways contributed to the hypertonicity-induced cell death. Similar pattern of sensitivity to the inhibitors was observed in two other cell lines derived from renal epithelia. We conclude that multiple cell death pathways are independently activated early in response to lethal hypertonic stress in renal epithelial cells.
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Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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Wong, Brian, and Yongwon Choi. "Pathways leading to cell death in T cells." Current Opinion in Immunology 9, no. 3 (June 1997): 358–64. http://dx.doi.org/10.1016/s0952-7915(97)80082-9.

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Mansilla, Sylvia, Laia Llovera, and Jose Portugal. "Chemotherapeutic Targeting of Cell Death Pathways." Anti-Cancer Agents in Medicinal Chemistry 12, no. 3 (March 1, 2012): 226–38. http://dx.doi.org/10.2174/187152012800228805.

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Jin, Zhaoyu, and Wafik S. El-Deiry. "Overview of cell death signaling pathways." Cancer Biology & Therapy 4, no. 2 (February 2, 2005): 147–71. http://dx.doi.org/10.4161/cbt.4.2.1508.

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Horowitz, Stuart. "Pathways to Cell Death in Hyperoxia." Chest 116 (July 1999): 64S—67S. http://dx.doi.org/10.1378/chest.116.suppl_1.64s.

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MacFarlane, M. "Cell death pathways – potential therapeutic targets." Xenobiotica 39, no. 8 (July 21, 2009): 616–24. http://dx.doi.org/10.1080/00498250903137990.

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Dissertations / Theses on the topic "Cell death pathways"

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McComb, Scott. "The Paradoxical Roles of Cell Death Pathways in Immune Cells." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24331.

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Cell death plays a vital role throughout the immune response, from the onset of inflammation to the elimination of primed T cells. Understanding the regulation of cell death within immune cells is of vital importance to understanding the immune system and developing therapies against various immune-disorders. In this thesis I have investigated the regulation of cell death and its functional role in of the innate and adaptive arms of the immune system. The mechanisms that govern expansion and contraction of antigen stimulated CD8+ T cells are not well understood. In the first section of this thesis, I show that caspase-3 becomes activated in proliferating CD8+ proliferation, yet this does not result in cell death. I used both in vivo and in vitro models to demonstrate that caspase-3 activation is specifically driven by antigen presentation and not inflammation, and that it likely plays a role in promoting T cell proliferation. Next, I present novel data regarding the regulation of a newly identified form of programmed cell death via necrosis, known as necroptosis. I show that the cellular inhibitor of apoptosis (cIAP) proteins act to limit activation of key necroptosis proteins in macrophage cells. Furthermore, I show that necroptosis can be exploited by intracellular bacterial pathogens to escape removal by the immune system. I also demonstrate that necroptosis is highly intertwined with the pathway of inflammation, and the autocrine production of type-I interferon constitutes a vital positive feedback loop in the induction of inflammatory cell death. In the final section of my thesis work, I delve into the specific regulation of Rip1 kinase and demonstrate that in addition to previously demonstrated regulation by caspase-8, cathepsins are also able to cleave Rip1 kinase and limit necroptosis. This thesis presents a wide variety of novel data regarding the regulation of cell death within immune cells. In total, the results reveal a picture of two divergent forms of programmed cell death, apoptosis and necroptosis. Through improving the understanding of the cross-regulation of these two key cell death pathways this work aims to improve the understanding of the immune function.
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Yung, Hong Wa. "Regulation of astrocyte cell death by kinase signalling pathways." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620576.

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Mässenhausen, Anne von, Wulf Tonnus, and Andreas Linkermann. "Cell Death Pathways Drive Necroinflammation during Acute Kidney Injury." Karger, 2018. https://tud.qucosa.de/id/qucosa%3A71624.

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Renal tubules represent an intercellular unit and function as a syncytium. When acute tubular necrosis was first visualized to occur through a process of synchronized regulated necrosis (SRN) in handpicked primary renal tubules, it became obvious that SRN actually promotes nephron loss. This realization adds to our current understanding of acute kidney injury (AKI)-chronic kidney disease (CKD) transition and argues for the prevention of AKI episodes to prevent CKD progression. Because SRN is triggered by necroptosis and executed by ferroptosis, 2 recently identified signaling pathways of regulated necrosis, a combination therapy employing necrostatins and ferrostatins may be beneficial for protection against nephron loss. Clinical trials in AKI and during the process of kidney transplantation are now required to prevent SRN. Additionally, necrotic cell death drives autoimmunity and necroinflammation and therefore represents a therapeutic target even for the prevention of antibody-mediated rejection of allografts years after the transplantation process.
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Guo, Jing. "Studying the signaling pathways in ROS-induced neuronal cell death /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BIOL%202005%20GUO.

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Benford, Helena L. "Molecular pathways of bisphosphonate-induced apoptosis." Thesis, University of Aberdeen, 2000. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602025.

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Recent studies have proposed that non-nitrogen-containing and nitrogen- containing bisphosphonate drugs inhibit osteoclastic bone resorption by different molecular mechanisms. The aim of this thesis was to investigate the molecular mechanisms of action of bisphosphonates in macrophages and osteoclasts and, in particular, the activation of caspase proteases and their role in apoptotic cell death. Apoptosis of J774 macrophages induced by nitrogen-containing bisphosphonates was found to involve the activation of caspase-3. By contrast, non-nitrogen- containing bisphosphonates did not cause caspase activation or J774 apoptosis, indicating that these bisphosphonates have different cellular effects. Further studies demonstrated that nitrogen-containing bisphosphonates induced J774 macrophage apoptosis by inhibiting the mevalonate pathway and preventing protein farnesylation and/or geranylgeranylation, since these compounds inhibited incorporation of [14 C] mevalonate into isoprenylated proteins, and addition of cell-permeable intermediates of the mevalonate pathway (FPP and GGPP) prevented bisphosphonate-induced apoptosis. Apoptosis of J774 macrophages induced by nitrogen-containing bisphosphonates or mevastatin (another inhibitor of the mevalonate pathway) was dependent on protein synthesis, since cycloheximide effectively prevented the activation of caspase-3 and prevented J774 cell apoptosis. Both nitrogen-containing bisphosphonates and non-nitrogen-containing bisphosphonates caused caspase-3 activation and apoptosis of rabbit and human osteoclasts in vitro. The active form of caspase-3 was detected in apoptotic osteoclasts by immunofluorescence staining, whilst caspase-3 activity was visualised in osteoclasts using a cell-permeable, fluorogenic substrate and detected in cell lysates using caspase-specific substrates. Bisphosphonate-induced osteoclast apoptosis involved loss of mitochondrial membrane potential and could be prevented by a specific inhibitor of caspase-3/-7. The ability of bisphosphonates to activate caspase-3 and cause apoptosis was mimicked by GGTI-298, a specific inhibitor of protein geranylgeranylation, suggesting that caspase activation and apoptosis in osteoclasts induced by bisphosphonates is the consequence of loss of geranylgeranylated proteins. Bisphosphonate-induced osteoclast apoptosis and inhibition of bone resorption in vitro was suppressed by RANK ligand. This did notappear to involve changes in Akt phosphorylation or increased expression of cIAP-1 or cIAP-2. These studies have helped to identify the molecular mechanisms of action of bisphosphonate drugs and have provided new insights into the involvement of caspases in osteoclast apoptosis.
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Zhang, Tongli. "Mathematical Models of Some Signaling Pathways Regulating Cell Survival and Death." Diss., Virginia Tech, 2008. http://hdl.handle.net/10919/29443.

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In a multi-cellular organism, cells constantly receive signals on their internal condition and surrounding environment. In response to various signals, cells proliferate, move around or even undergo suicide. The signal-response is controlled by complex molecular machinery, understanding of which is an important goal of basic molecular biological research. Such understanding is also valuable for clinical application, since lethal diseases like cancer show maladaptive responses to growth-regulating signals. Because the multiple feedbacks in the molecular regulatory machinery obscure cause-effect relations, it is hard to understand these control systems by intuition alone. Here we translate the molecular interactions into differential equations and recapture the cellular physiological properties with the help of numerical simulations and non-linear dynamical tools. The models address the physiological features of programmed cell death, the cell fate decision by p53 and the dynamics of the NF-?B control system. These models identify key molecular interactions responsible for the observed physiological properties, and they generate experimentally testable predictions to validate the assumptions made in the models.
Ph. D.
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Yatim, Nader. "Coordinated activation of cell death and inflammatory pathways in dying cells regulate adaptive immunity." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC233.

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Les Cellules mourantes initient l'immunité adaptative en fournissant des stimuli inflammatoires et des antigènes pour les cellules dendritiques (CD), qui à leurs tour activent les cellules T CD8 + par un processus appelé la présentation-croisée. Pour définir comment les différentes formes programmées de la mort cellulaire influencent l'immunité, nous avions établi des modèles de nécroptose et apoptose, par l'activation spécifique de RIPK3 ou CASP8, que nous avons utilisé pour évaluer in vitro et in vivo la réponse immunitaire. Nous avons alors trouvé que les cellules nécroptotiques exprimant l'antigène ovalbumin (OVA) induisent une forte réponse T CD8+ anti-OVA. Elles étaient plus immunogènes que les cellules apoptotiques ou nécrotiques. Étonnamment, l'activation simultanée de RIPK1 lors de la nécroptose etait responsable de l'immunogencité. En effet, l'abolition du recrutement de RIPK1 aux oligomères RIPK3 diminue le cross-priming et l'immunité anti-tumorale, en dépit d'un relargage équivalent de DAMPs (ATP et HMGB1), d'activation similaires des CDs et de l'inflammation in vivo. Nous avons aussi démontré que RIPK1 active la voie NF-kB et l'expression d'un programme transcriptionnel inflammatoire au sein des cellules nécroptotiques, nécessaire au cross-priming. De même, l'axe RIPK1-NF-kB était requis dans un modèle d'apoptose immunogenique. Nos résultats montrent que RIPK1, par sa capacité à coordonner la mort cellulaire et l'inflammation, orchestre la réponse T CD8 + et fournissent de nouveaux éclairages sur les interconnexions complexes entre la mort cellulaire, l'immunité innée et l'immunité adaptative
Dying cells initiate adaptive immunity by providing both antigens and inflammatory stimuli for dendritic cells (DCs), which in turn activate CD8' T cells through a process called antigen cross-priming. To define how different forms of programmed cell death influence immunity, we established models of necroptosis and apoptosis, where dying cells are generated by RIPK3 and CASP8 dimerization, respectively. We found that release of inflammatory mediators such as damage-associated molecular patterns (DAMPs) by dying cells was not sufficient for CD8+ T cell cross-priming. Instead, robust cross-priming required RIPK1 signaling and NF-KB-induced transcription within dying cells. Decoupling NF-1(13 signaling from necroptosis or inflammatory apoptosis reduced priming efficiency and tumor immunity. Our results reveal that coordinated inflammatory and cell death signaling pathways within dying cells orchestrate adaptive immunity
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Janson, Veronica. "Cisplatin-resistance and cell death in malignant pleural mesothelioma cells." Doctoral thesis, Umeå universitet, Medicinsk biovetenskap, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1680.

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Malignant pleural mesothelioma (MPM) is an aggressive, treatment-resistant tumour. Cisplatin (cis-diamminedichloroplatinum (II)) is the best single-agent chemotherapy for MPM, but platinum-based combination therapies give the best overall response rates. However, cisplatin use is limited by resistance and severe side effects. This thesis has increased the knowledge concerning cisplatin-induced cell death in MPM by describing a novel potential therapeutic target, and three novel phenotypes of cisplatin-resistance in a human MPM cell line (P31) and its cisplatin-resistant sub-line (P31res1.2). The novel potential therapeutic target, and one of the novel phenotypes, was cisplatin-resistant pro-apoptotic BH3-only proteins. In the P31 cells, cisplatin transiently increased pro-apoptotic BH3-only proteins during 6 h of exposure. This response was almost completely abrogated in the P31res1.2 cells. De-regulated caspase activity and activation was the second novel phenotype identified. The P31res1.2 cells had earlier, possibly mitochondria-independent, caspase-3 activation, increased basal caspase-3 activity and increased basal cleavage of caspase-8 and -9. Despite these differences, 6-h equitoxic cisplatin exposures rendered 50-60% of the cells apoptotic in both cell lines. The third novel phenotype was abrogated Na+K+2Cl--cotransporter (NKCC1) activity. Although NKCC1 activity was dispensable for cisplatin-induced apoptosis, balanced potassium transport activity was essential for P31 cell survival. Finally, the survival signalling protein Protein Kinase B (PKB or Akt) isoforms α and γ were constitutively activated in a PI3K-independent manner in P31 cells. In the P31res1.2 cells, PKBα and γ activities were increased, and there was PI3K-dependent activation of PKBβ. However, this increase in PKB isoform activity was not strongly associated to the cisplatin-resistance of the P31res1.2 cells.
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Davies, Carwyn Children's Cancer Institute Australia for Medical Research UNSW. "The influence of p21WAF1 on cell death pathways in acute lymphoblastic leukaemia." Publisher:University of New South Wales. Children's Cancer Institute Australia for Medical Research, 2009. http://handle.unsw.edu.au/1959.4/44416.

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The p53 protein is a primary mediator of apoptosis and growth arrest after exposure to DNA-damaging agents. Previous work has categorised a wild type p53 gene in the majority of childhood acute lymphoblastic leukaemia (ALL) cases, in which instance the p53 protein functions as a modulator of chemotherapy-induced cell death. In contrast, certain p53-induced proteins, such as p21WAF1, can act in an anti-apoptotic manner, and bestow resistance to chemotherapy. Previous studies of the p53 pathway in ALL have utilised cell lines and primary material. In this study a model of ALL was utilised that had previously been developed from a heterogeneous panel of patient biopsies established as xenografts in immune-deficient mice, and are adaptable for short term in vitro culture. A wild-type p53 protein response to etoposide and nutlin-3 exposure was a feature of the whole ALL xenograft panel, irrespective of clinical characteristics and disease biology. While a range of p53 target genes were induced in B-cell precursor (BCP)-ALL and T-ALL xenografts after etoposide exposure, there was negligible induction of p21WAF1 in T- ALL samples. Further work with the histone deacetylase inhibitor vorinostat facilitated p53-independent induction of p21WAF1 in BCP-ALL samples, yet failed to induce p21WAF1 in T- ALL. An association was observed between reduced p21WAF1 expression in the T-ALL samples and decreased histone H3 acetylation in the p21WAF1 promoter together with increased cytosine methylation in the first exon/intron of the p21WAF1 gene. These results suggest that p21WAF1 in T-ALL cells is subject to epigenetic modifications that cause transcriptional silencing. Defective induction of p21WAF1 in T-ALL xenografts was associated with increased sensitivity to the death-inducing effects of drugs, phosphatidylserine (PS) externalisation and caspase-3/-7 activity after drug exposure, indicating that p21WAF1 may exert an anti-apoptotic activity. As proof of principle, p21WAF1 was silenced in Nalm-6 cells by micro-RNA transduction and these cells exhibited increased sensitivity and rapid PS externalisation after drug exposure. A combination of a p21WAF1 inhibitory agent and vorinostat gave some pharmacological evidence to suggest that p21WAF1 inhibition could enhance drug efficacy. Overall, these investigations provide insight into the epigenetic regulation of p21WAF1 and demonstrate an anti-apoptotic role for p21WAF1 in childhood ALL cells.
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Zhang, Tejia. "Discovery of bioactive lipids and lipid pathways in cell death and disease." Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11483.

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Apoptosis is an intricately regulated cellular process required for the health and homeostasis of living systems. The mitochondrial apoptotic pathway depends on the BCL-2 family of pro- and anti-apoptotic members whose interactions regulate cell fate. BAX and BAK are key pro-apoptotic proteins required for mitochondrial permeabilization during apoptosis. While the mitochondrial death program relies heavily on its protein components, evidences support equally crucial roles for lipids and lipid metabolism in promoting or hindering apoptosis at the mitochondria. To gain insight into the interplay between lipids and BCL-2 proteins we used a liquid chromatography (LC)-mass spectrometry (MS)-based comparative lipidomics approach to uncover lipid changes in the absence of BAX and/or BAK. Our analysis revealed novel functions for BAX and BAK in inflammation and ceramide metabolism. A targeted LC-MS workflow was also developed for characterization of a novel lipid class involved in type 2 diabetes. Targeted LC-MS revealed altered oxysterol metabolism following perturbation of the Sonic hedgehog pathway. Taken together, our findings demonstrate interesting connections among lipids, cell death and disease.
Chemistry and Chemical Biology
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Books on the topic "Cell death pathways"

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Bromfield, Gillian. Cell death pathways in irradiated prostate cells. Ottawa: National Library of Canada, 2002.

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Aft, Rebecca, ed. Targeting New Pathways and Cell Death in Breast Cancer. InTech, 2012. http://dx.doi.org/10.5772/1744.

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(Editor), Jochen Schacht, Arthur N. Popper (Editor), and Richard R. Fay (Editor), eds. Auditory Trauma, Protection, and Repair (Springer Handbook of Auditory Research). Springer, 2008.

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Phosphoinositide 3-kinase Signalling Pathway: The Key to Cell Proliferation And Death. Imperial College Press, 2006.

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Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
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Anning, Lin, ed. The JNK signaling pathway. Georgetown, Tex: Landes Bioscience, 2006.

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Plutynski, Anya. Causation, Causal Selection, and Causal Parity. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199967452.003.0004.

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It is typical to refer to cancer as a “genetic” or “genomic” disease. This claim is ambiguous; one of the central goals of this chapter is to disambiguate this claim. I first distinguish different types of causal claims: claims about causal relevance, causal role, and causal specificity. As a backdrop to this discussion, I introduce what I call the “mechanistic research program” in cancer, according to which progression to cancer involves breakdowns in regulatory controls on gene expression in ways that affect cell birth and death. While this research program has been successful, it has downplayed the role of context in cancer progression, and the fact that disorderly cellular growth is affected by many pathways. I conclude by considering several philosophers’ accounts of “causal selection” and argue that ultimately the causal selection problem is not one but several different problems, requiring different, context-specific solutions.
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Pleniceanu, Oren, and Benjamin Dekel. Kidney stem cells. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0344.

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End-stage renal failure is a major cause of death with currently only dialysis and transplantation available as therapeutic options, each with its own limitations and drawbacks. To allow regenerative medicine-based kidney replacement therapies and due to the fact that neither haematopoietic stem cells nor mesenchymal stem cells, the most accessible human stem cells, can be used to derive genuine nephron progenitors, much attention has been given to finding adult renal stem cells. Several candidates for this have been described, but their true identity as stem or progenitor cells and their potential use in therapy has not yet been shown. However, the analysis of embryonic renal stem cells, specifically stem/progenitor cells that are induced into the nephrogenic pathway to form nephrons until the 34th week of gestation, has been much more conclusive.
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Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.

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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.
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Noordenbos, Troy, and Dominique Baeten. Immune mechanisms: innate immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0007.

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Innate immune mechanisms are strongly implied in the pathophysiology of spondyloarthritis (SpA). This chapter discusses available data on the role of the innate immune system in relation to HLA-B27, genetic associations, and the cellular and molecular characteristics of disease target tissue. Regarding the linkage with MCH-class I molecule HLA-B27, the chapter discusses the arthritogenic peptide hypothesis and three popular antigen-independent theories. The genetic architecture of the disease argues against a role for the adaptive immune system and identifies cytokine pathways, such as IL-1, TNF, and IL-23/IL-17. In experimental as well as in human SpA, the importance of these cytokine pathways are confirmed by effective reduction of signs and symptoms upon blockade of specific molecules. In-depth cellular and molecular analysis of the target tissue identifies a contribution of cells with strong innate features, rather than cells of the adaptive immune system.
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Book chapters on the topic "Cell death pathways"

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McDonald, E. Robert, and Wafik S. El-Deiry. "Mammalian Cell Death Pathways." In Death Receptors in Cancer Therapy, 1–41. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-851-x:001.

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Horowitz, Stuart. "Pathways to Oxidative Cell Death." In Acute Respiratory Distress Syndrome, 215–24. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4419-8634-4_26.

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Marín-García, José. "Cell-Death Pathways and Mitochondria." In Mitochondria and Their Role in Cardiovascular Disease, 225–41. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4599-9_11.

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Lin, Yong. "RIP1-Mediated Signaling Pathways in Cell Survival and Death Control." In Necrotic Cell Death, 23–43. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8220-8_2.

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Wardle, E. Nigel. "Programmed Cell Death: Apoptosis." In Guide to Signal Pathways in Immune Cells, 111–28. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_8.

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Morley, Simon J. "The Regulation of eIF4F During Cell Growth and Cell Death." In Signaling Pathways for Translation, 1–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-09889-9_1.

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Meuer, Katrin, Mathias Bähr, and Jochen H. Weishaupt. "CDK5 and Mitochondrial Cell Death Pathways." In Cyclin Dependent Kinase 5 (Cdk5), 91–106. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-78887-6_7.

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Kessel, David, and Nancy L. Oleinick. "Photodynamic Therapy and Cell Death Pathways." In Methods in Molecular Biology, 35–46. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-697-9_3.

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Singh, Gurmit, Omar Alqawi, and Myrna Espiritu. "Metronomic PDT and Cell Death Pathways." In Methods in Molecular Biology, 65–78. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-697-9_5.

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Andersen, Joshua L., and Jeffrey C. Rathmell. "Cell Death Pathways in Toxicological Response." In Mammalian Toxicology, 75–83. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118683484.ch4.

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Conference papers on the topic "Cell death pathways"

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Kessel, David, and John J. Reiners, Jr. "Cell death pathways associated with PDT." In Biomedical Optics 2006, edited by David Kessel. SPIE, 2006. http://dx.doi.org/10.1117/12.639925.

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Wright, Neil T. "Parameter Correlation in Models of Hyperthermic Cell Death." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53933.

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A number of mathematical models have been developed to predict the survival of cells after heating. Some of these models have been based on first principle arguments, while others have been empirically motivated. Some models have been inspired by analogs of damage to cells by ionizing radiation. Evidence exists for multiple targets leading to cell death, although precise definition of the pathways for the various temperature ranges and environmental conditions remains in question. For reviews of the cellular targets of heating, see [1], [2], or [3].
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Belashov, A. V., A. A. Zhikhoreva, D. A. Rogova, T. N. Belyaeva, E. S. Kornilova, A. V. Salova, I. V. Semenova, and O. S. Vasyutinskii. "Holographic monitoring of cell death pathways induced by reactive oxygen species." In 2018 International Conference Laser Optics (ICLO). IEEE, 2018. http://dx.doi.org/10.1109/lo.2018.8435688.

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Arumugam, Arunkumar, and Rajkumar Lakshmanaswamy. "Abstract 5361: Progesterone alters cell survival and cell death pathways in estrogen-induced mammary carcinogenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5361.

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Barbee, Kenneth A., Gulyeter Serbest, and Joel Horwitz. "Membrane Integrity as a Therapeutic Target in Neural Cell Injury." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-61566.

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The importance of cell membrane integrity for normal cell function and indeed survival is well established, yet the role of membrane disruption in cellular pathology is seldom considered except as a prelude to, or indication of, cell death. However, evidence from diverse fields strongly implicates membrane disruption as a key precipitating event in the pathological responses to various stimuli. Dynamic mechanical loading of neural cells produces an acute disruption of the plasma membrane as indicated by a rapid and transient release of LDH from the cytoplasm of injured cells. In this report, we show that this cellular level injury is not immediately fatal, but rather gives rise to a cascade of signaling events that lead to cell death in the long term. In our model, over 50% of the cells were dead at 24 hours post injury, the majority of which were apoptotic as assessed by the TUNEL assay using flow cytometry. Though many of the signaling pathways involved in this response to injury have been studied, the link between the initial membrane damage and the subsequent signaling is poorly understood. We report for the first time that treating injured neurons with an agent that promotes resealing of membrane pores can rescue the cells from both necrotic cell death and apoptosis at 24 hours post injury. Treatment with the nonionic surfactant, poloxamer 188 (P188), at 15 minutes post injury restored cell viability at 24 hours to control values. The role of the pro-apoptosis MAP kinase, p38, in cell death following injury was investigated using Western blot analysis. Activation of p38 was increased over 2-fold at 15 minutes post injury. P188 treatment at 10 minutes inhibited p38 activation. However, treatment with a specific inhibitor of p38 activation produced only a partial reduction in apoptosis and had no effect on necrotic cell death. These data suggest multiple signaling pathways are involved in the long term response of neurons to mechanical injury. Furthermore, the putative mechanism of action of P188 to promote membrane resealing suggests that the acute membrane damage due to trauma is a critical precipitating event lying upstream of the many signaling cascades that contribute to the subsequent pathology.
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Turubanova, Victoria, Iuliia Efimova, Tatiana Mishchenko, Irina Balalaeva, Maria Vedunova, and Dmitri Krysko. "IMMUNOGENIC PATHWAYS OF CONTROLLED CELL DEATH IN THE TREATMENT OF NEURO-ONCOLOGICAL DISEASES." In XV International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2019. http://dx.doi.org/10.29003/m584.sudak.ns2019-15/415.

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Shah, Pooja A., Tuhina Mazumdar, Reid T. Powell, Li Shen, Jing Wang, Clifford C. Stephen, Mitchell J. Frederick, and Faye M. Johnson. "Abstract 369: Identification of pathways that enhance cell death in NOTCH1-mutant HNSCC." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-369.

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Abdi, A. "Computational modeling of molecular pathways regulating cell survival and death by the SigFlux algorithm." In 2017 IEEE Signal Processing in Medicine and Biology Symposium (SPMB). IEEE, 2017. http://dx.doi.org/10.1109/spmb.2017.8257047.

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Turubanova, Victoria, Iuliia Efimova, Irina Balalaeva, Tatiana Mishchenko, Maria Savuk, Maria Vedunova, and Dmitri Krysko. "IMMUNOGENIC PATHWAYS OF CONTROLLED CELL DEATH IN THE TREATMENT OF NEURO-ONCOLOGICAL DISEASES USING PORPHYRAZINES." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1291.sudak.ns2020-16/464-465.

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Oliver, David J., Anusha Chaparala, Emeka Okafor, Carlos J. Camacho, Alexander S. Doemling, Felix T. Wieland, Igor B. Roninson, and Michael Shtutman. "Abstract 5104: Identification of cancer-specific COPI inhibitors and their associated apoptotic cell death pathways." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5104.

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Reports on the topic "Cell death pathways"

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Vincenz, Claudius. Identification of Components of the Cell Death Pathway. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada372429.

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Reed, John C. Yeast Genetics for Delineating Bax/Bc1 Pathway of Cell Death Regulation. Fort Belvoir, VA: Defense Technical Information Center, July 1997. http://dx.doi.org/10.21236/ada329121.

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Xu, Qunli. Training in Support of Research Project Entitled Genetic Regulation of the Bcl-2/Bax Cell Death Pathway".". Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada368475.

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