Gotowe bibliografie tematyczne / Apoptosis

Gotowa bibliografia na temat „Apoptosis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 31 lipca 2024

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Artykuły w czasopismach na temat "Apoptosis"

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Cutrona, Giovanna, Nicolò Leanza, Massimo Ulivi, Giovanni Melioli, Vito L. Burgio, Giovanni Mazzarello, Giovanni Gabutti, Silvio Roncella i Manlio Ferrarini. "Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo". Blood 94, nr 9 (1.11.1999): 3067–76. http://dx.doi.org/10.1182/blood.v94.9.3067.

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Abstract This study shows that human postthymic T cells express CD10 when undergoing apoptosis, irrespective of the signal responsible for initiating the apoptotic process. Cells from continuous T-cell lines did not normally express CD10, but became CD10+ when induced into apoptosis by human immunodeficiency virus (HIV) infection and exposure to CD95 monoclonal antibody, etoposide, or staurosporin. Inhibitors of caspases blocked apoptosis and CD10 expression. Both CD4+ and CD8+ T cells purified from normal peripheral blood expressed CD10 on apoptotic induction. CD10 was newly synthesized by the apoptosing cells because its expression was inhibited by exposure to cycloheximide and CD10 mRNA became detectable by reverse transcription-polymerase chain reaction in T cells cultured under conditions favoring apoptosis. To show CD10 on T cells apoptosing in vivo, lymph node and peripheral blood T cells from HIV+ subjects were used. These suspensions were composed of a substantial, although variable, proportion of apoptosing T cells that consistently expressed CD10. In contrast, CD10+ as well as spontaneously apoptosing T cells were virtually absent in peripheral blood from normal individuals. Collectively, these observations indicate that CD10 may represent a reliable marker for identifying and isolating apoptosing T cells in vitro and ex vivo and possibly suggest novel functions for surface CD10 in the apoptotic process of lymphoid cells.
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Cutrona, Giovanna, Nicolò Leanza, Massimo Ulivi, Giovanni Melioli, Vito L. Burgio, Giovanni Mazzarello, Giovanni Gabutti, Silvio Roncella i Manlio Ferrarini. "Expression of CD10 by Human T Cells That Undergo Apoptosis Both In Vitro and In Vivo". Blood 94, nr 9 (1.11.1999): 3067–76. http://dx.doi.org/10.1182/blood.v94.9.3067.421a32_3067_3076.

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This study shows that human postthymic T cells express CD10 when undergoing apoptosis, irrespective of the signal responsible for initiating the apoptotic process. Cells from continuous T-cell lines did not normally express CD10, but became CD10+ when induced into apoptosis by human immunodeficiency virus (HIV) infection and exposure to CD95 monoclonal antibody, etoposide, or staurosporin. Inhibitors of caspases blocked apoptosis and CD10 expression. Both CD4+ and CD8+ T cells purified from normal peripheral blood expressed CD10 on apoptotic induction. CD10 was newly synthesized by the apoptosing cells because its expression was inhibited by exposure to cycloheximide and CD10 mRNA became detectable by reverse transcription-polymerase chain reaction in T cells cultured under conditions favoring apoptosis. To show CD10 on T cells apoptosing in vivo, lymph node and peripheral blood T cells from HIV+ subjects were used. These suspensions were composed of a substantial, although variable, proportion of apoptosing T cells that consistently expressed CD10. In contrast, CD10+ as well as spontaneously apoptosing T cells were virtually absent in peripheral blood from normal individuals. Collectively, these observations indicate that CD10 may represent a reliable marker for identifying and isolating apoptosing T cells in vitro and ex vivo and possibly suggest novel functions for surface CD10 in the apoptotic process of lymphoid cells.
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Park, Cheol, Cheng-Yun Jin, Tae Hyun Choi, Su Hyun Hong i Yung Hyun Choi. "Effect of Proapoptotic Bcl-2 on Naringenin-induced Apoptosis in Human Leukemia U937 Cells". Journal of Life Science 23, nr 9 (30.09.2013): 1118–25. http://dx.doi.org/10.5352/jls.2013.23.9.1118.

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Lizama, Carlos, Diego Rojas-Benítez, Marcelo Antonelli, Andreas Ludwig, Ximena Bustamante-Marín, Jurriaan Brouwer-Visser i Ricardo D. Moreno. "TACE/ADAM17 is involved in germ cell apoptosis during rat spermatogenesis". REPRODUCTION 140, nr 2 (sierpień 2010): 305–17. http://dx.doi.org/10.1530/rep-10-0104.

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The pathways leading to male germ cell apoptosisin vivoare poorly understood, but are highly relevant for the comprehension of sperm production regulation by the testis. In this work, we show the evidence of a mechanism where germ cell apoptosis is induced through the inactivation and shedding of the extracellular domain of KIT (c-kit) by the protease TACE/a disintegrin and metalloprotease 17 (ADAM17) during the first wave of spermatogenesis in the rat. We show that germ cells undergoing apoptosis lacked the extracellular domain of the KIT receptor. TACE/ADAM17, a membrane-bound metalloprotease, was highly expressed in germ cells undergoing apoptosis as well. On the contrary, cell surface presence of ADAM10, a closely related metalloprotease isoform, was not associated with apoptotic germ cells. Pharmacological inhibition of TACE/ADAM17, but not ADAM10, significantly prevented germ cell apoptosis in the male pubertal rat. Induction of TACE/ADAM17 by the phorbol-ester phorbol 12-myristate 13-acetate (PMA) induced germ cell apoptosis, which was prevented when an inhibitor of TACE/ADAM17 was present in the assay.Ex-vivorat testis culture showed that PMA induced the cleavage of the KIT extracellular domain. Isolation of apoptotic germ cells showed that even though protein levels of TACE/ADAM17 were higher in apoptotic germ cells than in nonapoptotic cells, the contrary was observed for ADAM10. These results suggest that TACE/ADAM17 is one of the elements triggering physiological germ cell apoptosis during the first wave of spermatogenesis.
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GETTI, G. T., R. A. CHEKE i D. P. HUMBER. "Induction of apoptosis in host cells: a survival mechanism forLeishmaniaparasites?" Parasitology 135, nr 12 (8.09.2008): 1391–99. http://dx.doi.org/10.1017/s0031182008004915.

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SUMMARYLeishmaniaparasites invade host macrophages, causing infections that are either limited to skin or spread to internal organs. In this study, 3 species causing cutaneous leishmaniasis,L. major,L. aethiopicaandL. tropica, were tested for their ability to interfere with apoptosis in host macrophages in 2 different lines of human monocyte-derived macrophages (cell lines THP-1 and U937) and the results confirmed in peripheral blood mononuclear cells (PBMC). All 3 species induced early apoptosis 48 h after infection (expression of phosphatidyl serine on the outer membrane). There were significant increases in the percentage of apoptotic cells both for U937 and PBMC following infection with each of the 3 species. Early apoptotic events were confirmed by mitochondrial membrane permeabilization detection and caspase activation 48 and 72 h after infection. Moreover, the percentage of infected THP-1 and U937 macrophages increased significantly (up to 100%) following treatment with an apoptosis inducer. Since phosphatidyl serine externalization on apoptosing cells acts as a signal for engulfment by macrophages, induction of apoptosis in the parasitized cells could actively participate in spreading the infection. In summary, parasite-containing apoptotic bodies with intact membranes could be released and phagocytosed by uninfected macrophages.
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Langrová, Tereza, Zbyšek Sládek i Dušan Ryšánek. "The effect of the bacterial pathogens Staphylococcus aureus and Streptococcus uberis on morphological features of apoptosis of heifers mammary gland neutrophils". Acta Universitatis Agriculturae et Silviculturae Mendelianae Brunensis 53, nr 4 (2005): 61–74. http://dx.doi.org/10.11118/actaun200553040061.

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The aim of the student thesis was to review the effect of the significant bacterial pathogens,Staphylococcus aureusand Steptococcus uberis on programmed cell death – apoptosisin vitro, and to determine the dynamic of morphological changes during aging neutrophil granulocytes of heifers mammary glandin vitro. Using light and electron microscopy we have noted characteristic alterations of apoptotic neutrophils. These are running in three consequential phases. We found out, that the interaction of bacterial pathogens with neutrophils during the incubation have lead in expressive quantitative and qualitative changes in apoptotic cells proportion. Concretely, the influence of both pathogens on mammary gland neutrophils caused the defer of apoptosis expression. Here,S. aureuscaused lower number of apoptotic neutrophils in comprasion withS. uberis. The outcomes testified, thatS. aureusandS. uberisinteraction with heifers mammary gland neutrophilsin vitrocauses alterations relating to apoptosis of these cells. Looking at the results of the study, we can conclude, that the pathogensS. aureusandS. uberisare not only significant heifers mammary gland – affection causers, but they significantly influence the cells of defensive system in their functions too. They significantly decrease the appereance of morphological apoptosis manifestations on neotrophils of tissue pool of the heifers mammary gland. The numbers of apoptotic cells in neutrophil population confirm, that during the interaction with mentioned pathogens the defer of morphological apoptosis manifestations happens. Then, higher number of apoptotic neutrophils in stages of apoptotic corpuscles implies increasing dynamic of this process. Beside that, the dynamic of apoptotic process is influenced by the specifity of certain bacterious actor too.
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Aravani, Dimitra, Kirsty Foote, Nichola Figg, Alison Finigan, Anna Uryga, Murray Clarke i Martin Bennett. "Cytokine regulation of apoptosis-induced apoptosis and apoptosis-induced cell proliferation in vascular smooth muscle cells". Apoptosis 25, nr 9-10 (5.07.2020): 648–62. http://dx.doi.org/10.1007/s10495-020-01622-4.

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Abstract Vascular smooth muscle cells (VSMCs) are the main structural cell of blood vessels, and VSMC apoptosis occurs in vascular disease, after injury, and in vessel remodeling during development. Although VSMC apoptosis is viewed as silent, recent studies show that apoptotic cells can promote apoptosis-induced compensatory proliferation (AICP), apoptosis-induced apoptosis (AIA), and migration of both local somatic and infiltrating inflammatory cells. However, the effects of VSMC apoptosis on adjacent VSMCs, and their underlying signaling and mechanisms are unknown. We examined the consequences of VSMC apoptosis after activating extrinsic and intrinsic death pathways. VSMCs undergoing apoptosis through Fas/CD95 or the protein kinase inhibitor staurosporine transcriptionally activated interleukin 6 (IL-6) and granulocyte-macrophage colony stimulating factor (GM-CSF), leading to their secretion. Apoptosis induced activation of p38MAPK, JNK, and Akt, but neither p38 and JNK activation nor IL-6 or GM-CSF induction required caspase cleavage. IL-6 induction depended upon p38 activity, while Fas-induced GM-CSF expression required p38 and JNK. Conditioned media from apoptotic VSMCs induced VSMC apoptosis in vitro, and IL-6 and GM-CSF acted as pro-survival factors for AIA. VSMC apoptosis was studied in vivo using SM22α-DTR mice that express the diphtheria toxin receptor in VSMCs only. DT administration induced VSMC apoptosis and VSMC proliferation, and also signficantly induced IL-6 and GM-CSF. We conclude that VSMC apoptosis activates multiple caspase-independent intracellular signaling cascades, leading to release of soluble cytokines involved in regulation of both cell proliferation and apoptosis. VSMC AICP may ameliorate while AIA may amplify the effects of pro-apoptotic stimuli in vessel remodeling and disease.
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Hassan, Mohamed, Hidemichi Watari, Ali AbuAlmaaty, Yusuke Ohba i Noriaki Sakuragi. "Apoptosis and Molecular Targeting Therapy in Cancer". BioMed Research International 2014 (12.06.2014): 1–23. http://dx.doi.org/10.1155/2014/150845.

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Apoptosis is the programmed cell death which maintains the healthy survival/death balance in metazoan cells. Defect in apoptosis can cause cancer or autoimmunity, while enhanced apoptosis may cause degenerative diseases. The apoptotic signals contribute into safeguarding the genomic integrity while defective apoptosis may promote carcinogenesis. The apoptotic signals are complicated and they are regulated at several levels. The signals of carcinogenesis modulate the central control points of the apoptotic pathways, including inhibitor of apoptosis (IAP) proteins and FLICE-inhibitory protein (c-FLIP). The tumor cells may use some of several molecular mechanisms to suppress apoptosis and acquire resistance to apoptotic agents, for example, by the expression of antiapoptotic proteins such as Bcl-2 or by the downregulation or mutation of proapoptotic proteins such as BAX. In this review, we provide the main regulatory molecules that govern the main basic mechanisms, extrinsic and intrinsic, of apoptosis in normal cells. We discuss how carcinogenesis could be developed via defective apoptotic pathways or their convergence. We listed some molecules which could be targeted to stimulate apoptosis in different cancers. Together, we briefly discuss the development of some promising cancer treatment strategies which target apoptotic inhibitors including Bcl-2 family proteins, IAPs, and c-FLIP for apoptosis induction.
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LaBelle, James L., Jill K. Fisher, Samuel G. Katz, Gregory H. Bird, Chelsea E. Lawrence, Amy M. Silverstein i Loren D. Walensky. "Pharmacologic Replacement of BIM BH3 Reactivates Apoptosis in Hematologic Cancer and Lymphoproliferative Disease." Blood 110, nr 11 (16.11.2007): 524. http://dx.doi.org/10.1182/blood.v110.11.524.524.

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Abstract Selective targeting of deregulated apoptotic protein networks is a promising pharmacologic strategy for subverting diseases of unrestrained cellular survival, such as cancer. BCL-2 family protein interactions constitute a critical control point for the regulation of apoptosis. Whereas multidomain anti-apoptotic proteins such as BCL-2 guard against cell death, multidomain pro-apoptotic proteins such as BAX constitute a gateway to cell death through mitochondrial damage. The BH3-only proteins function as death sentinels situated throughout the cell, poised to transmit signals of cellular injury to multidomain members. BH3-only proteins deliver their death messages via their conserved alpha-helical BH3 domains. Whereas the indirect activator class of BH3-only proteins (e.g. BAD) counteract anti-apoptotic proteins, the direct activator subgroup (e.g. BIM) is believed to trigger apoptosis both by neutralizing anti-apoptotics and by directly activating the mitochondrial executioners BAX and BAK. The essential roles of BH3-only proteins in maintaining cellular homeostasis is highlighted by the development of autoimmune disease and cancer in mouse models of BH3-only protein deficiency. By inserting hydrocarbon “staples” into native BH3 peptide sequences, we have produced a chemical toolbox of stabilized alpha-helices of BCL-2 domains (SAHBs) to dissect apoptotic signaling pathways in vivo and explore the pharmacodynamic effects of “BH3 replacement” in cancer cells and mouse models of deregulated apoptosis. Whereas SAHBs display high affinity binding to anti-apoptotic targets, BID and BIM SAHBs also directly engage BAX and are thus especially potent in inducing apoptosis of a panel of leukemia and lymphoma cell lines. To evaluate the impact of selective BH3 replacement in vivo, we tested the capacity of BIM SAHB to reactivate apoptosis in the lymphoproliferative disease of Bim-/- mice. Strikingly, Bim-/- mice treated with BIM SAHB displayed marked influx of tingible-body macrophages into the lymphoid infiltrates of affected organs, with scattered cells throughout the infiltrate robustly positive for activated caspase-3, suggestive of SAHB induced apoptosis induction. Our studies highlight the therapeutic potential of BH3 replacement to circumvent apoptotic blockade and restore the death pathway in hematologic cancer and lymphoproliferative disease.
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Resanović, Ivana, Emina Sudar-Milovanović, Nikola Bogdanović, Aleksandra Jovanović, Sonja Zafirović, Anastasija Panić i Esma Isenović. "Fundamentals of apoptosis". Medicinska istrazivanja 49, nr 3 (2015): 42–45. http://dx.doi.org/10.5937/medist1502042r.

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Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.
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Rozprawy doktorskie na temat "Apoptosis"

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Heiligtag, Sven. "Induction of apoptosis in neuroblastoma analysis of apoptotic pathways and putative apoptosis-mediating receptors /". [S.l.] : [s.n.], 2001. http://www.sub.uni-hamburg.de/disse/464/Disse.pdf.

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Devore, Casey Leigh. "DNR1 Regulates apoptosis: new insights into mosquito apoptosis". Thesis, Kansas State University, 2009. http://hdl.handle.net/2097/11972.

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Master of Science
Department of Biology
Rollie Clem
Apoptosis, or programmed cell death, is a crucial conserved process among organisms for deleting damaged unwanted cells, as well as for development and viral defense, and plays an important role in multiple diseases. Too much apoptosis may lead to Alzheimer’s disease, and too little may result in cancer. Therefore, the ability to understand this process is essential for improved medical knowledge today. Apoptosis has been explored in a number of species and pathways seem relatively conserved among most, with unique aspects contained in each, but little is known about apoptosis in mosquitoes. Improved knowledge and growing interest concerning apoptosis in mosquitoes is necessary considering the vast health effects seen across the globe as a result of diseases transferred by the mosquito vector. The Dengue virus mosquito vector Aedes aegypti was the focus here. A new player named defense repressor 1 was discovered in Drosophila melanogaster (DmDnr1), shown to play a role in apoptosis, and the homolog discovered in A. aegypti (AeDnr1). Silencing Dmdnr1 resulted in cells sensitized to apoptosis but was not enough to induce spontaneous apoptosis. In contrast, silencing Aednr1 in the A. aegypti cell line, Aag2, led to spontaneously induced apoptosis. This showed the importance of AeDnr1 as a member of the apoptotic pathway in this species. Epistasis experiments showed that apoptosis induced by silencing Aednr1 requires the initiator caspase Dronc and the effector caspase CASPS8, whereas apoptosis induced by silencing the inhibitor of apoptosis, Aeiap1, also requires Dronc but acts through the effector caspase CASPS7. Further epistasis experiments showed that apoptosis induced by silencing Aednr1 requires the IAP antagonist Mx, but not IMP. This showed for the first time a gene regulating upstream of an IAP antagonist. Biochemical studies showed that AeDnr1 regulates active CASPS8 but not CASPS7, and interacts with Mx and CASPS8 but not AeDronc, CASPS7 nor AeIAP1. Studies also showed Mx competes effectively with CASPS8 but not CASPS7 for AeIAP1 binding, and IMP competes effectively with CASPS7 but not CASPS8 for AeIAP1 binding. An improved apoptosis pathway for the mosquito A. aegypti emerged involving a potential feedback loop with explanations for the upstream IAP antagonist preference as well as the downstream effector caspase preference resulting from apoptosis induced by Aednr1 silencing. Through the discussed research, multiple unique findings resulted. Studying the mosquito model will allow us to find certain gene relations that are more difficult to uncover in the Drosophila model. Because Dnr1 is found in most systems, this improved pathway may shed light not only on a potential role of Dnr1 in apoptosis in insects but higher organisms as well.
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Seton, Kristina. "Eosinophil Apoptosis". Doctoral thesis, Uppsala University, Department of Medical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3427.

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Apoptosis or programmed cell death is crucial for the resolution of inflammation, and phagocytosis of apoptotic cells initiates the release of actively anti-inflammatory responses from the phagocytes. Eosinophils are one of the most potent inflammatory cells in the body and is involved in a number of diseases, most commonly associated with parasitic infections and allergic diseases. Apoptosis in eosinophils is therefore one of the most important systems to avoid inflammation. This aim of the present investigation was to examine the mechanisms behind, and the consequences of this process in eosinophils. Apoptotic eosinophils have a unique surface receptor expression that indicates abilities to communicate with T-, B- and antigen presenting cells. They have a novel expression of CD49f, indicating an importance for binding to laminin or unknown functions of the VLA-6 receptor, possibly in the concept of phagocytosis of the apoptotic cell.

In apoptotic eosinophils the granules are translocated to the periphery of the cell, probably through a disruption of the cytoskeleton. This translocation makes the granules easily accessible and the apoptotic eosinophil can release considerable amounts of granule proteins in response to specific stimuli. The spontaneous release however, is decreased as compared with living cells.

Furthermore, the survival of eosinophils in response to an allergen challenge is increased in healthy subjects, but not in allergic patients. Mechanistically, this needs further investigation, but one theory is that it is due to the presence of specific IgE in patients in combination with differences in the response from the epithelial cells.

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Quarrie, Lynda H. "Mammary apoptosis". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318886.

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Joza, Nicholas. "Differential requirement for the mitochondrial apoptosis-inducing factor in apoptotic pathways". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63071.pdf.

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Sani, Marc-Antoine. "Apoptosis Regulation via the Mitochondrial Pathway : Membrane Response upon Apoptotic Stimuli". Doctoral thesis, Umeå universitet, Kemiska institutionen, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1883.

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The aim of this thesis was the investigation of the mitochondrial response mechanisms upon apoptotic stimuli. The specific objectives were the biophysical characterization of membrane dynamics and the specific roles of lipids in the context of apoptotic regulation occurring at the mitochondrion and its complex membrane systems. The BH4 domain is an anti-apoptotic specific domain of the Bcl-2 protein. Solid phase peptide synthesis was used to produce large amount of the peptide for biophysical studies. A protocol has been established and optimized, guarantying the required purity for biophysical studies. In detail the purification by high performance liquid chromatography and the characterisation via mass spectroscopy are described. The secondary structure of BH4 changes significantly in the presence of lipid vesicles as observed by infrared spectroscopy and circular dichroism. The BH4 peptide aggregates at the membrane surface and inserts slightly into the hydrophobic part of the membrane. Using nuclear magnetic resonance (NMR) and calorimetry techniques, it could even be shown that the BH4 domain modifies the dynamic and organization of the liposomes which mimic a mitochondrial surface. The second study was on the first helix of the pro-apoptotic protein Bax. This sequence called Bax-α1 has the function to address the cytosolic Bax protein to the mitochondrial membrane upon activation. Once again a protocol has been established for the synthesis and purification of this peptide. The aim was to elucidate the key role of cardiolipin, a mitochondria-specific phospholipid, in the interaction of Bax-α1 with the mitochondrial membrane system. The NMR and circular dichroism studies showed that Bax-α1 interacts with the membrane models only if they contain the cardiolipin, producing a strong electrostatic lock effect which is located at the membrane surface. Finally, a new NMR approach was developed which allows the investigation of the lipid response of isolated active mitochondria upon the presence of apoptotic stimuli. The goal was there to directly monitor lipid specific the occurring changes during these physiological activities.
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Sani, Marc Antoine. "Apoptosis regulation via the mitochondrial pathway : membrane response upon apoptotic stimuli". Thesis, Bordeaux 1, 2008. http://www.theses.fr/2008BOR13651/document.

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Le but de cette thèse est de montrer la réponse de la membrane mitochondriale au cours la régulation de l’apoptose en étudiant l’effet de domaines clés sur la dynamique membranaire et l’importance de la composition phospholipidiques des modèles utilisés. Le domaine BH4 est la partie spécifique anti-apoptotique de la famille Bcl-2. La première étape a été de synthétiser le peptide par voie chimique en utilisant la synthèse peptidique en phase solide. Un protocole décrivant les étapes de purification par chromatographie liquide et de caractérisation par spectroscopie de masse, garantissant une pureté indispensable pour des études biophysiques, a été établi. La modification de la structure secondaire du peptide interagissant avec des vésicules a été étudiée par spectroscopie infrarouge ainsi que par dichroïsme circulaire. Le peptide s’agrège à la surface et s’insère peu profondément dans la partie hydrophobe de la membrane. En utilisant la résonance magnétique nucléaire (RMN) et la calorimétrie, il a été montré que le peptide BH4 modifie l’organisation et la dynamique des liposomes mimant la surface mitochondriale. La deuxième étude a porté sur la première hélice de la protéine pro-apoptotique Bax (Bax-a1) qui a la propriété de diriger la protéine cytosolique vers la mitochondrie. Un protocole de synthèse et purification a été à nouveau établi. Le but de cette étude est de démontrer le rôle de l’interaction spécifique entre la cardiolipine, un phospholipide uniquement présent dans la mitochondrie et le peptide Bax-a1. Les études RMN ont montré que Bax-a1 n’interagissait uniquement que si la cardiolipine était présente, produisant un fort effet électrostatique piégeant le peptide à la surface de la membrane. Enfin, un nouveau protocole permettant d’étudier la réponse des lipides de mitochondries isolées toujours actives par RMN est présenté. Le but est de pouvoir directement observer les modifications subies par chaque phospholipide de la mitochondrie.
The aim of this thesis was the investigation of the mitochondrial response mechanisms upon apoptotic stimuli. The specific objectives were the biophysical characterization of membrane dynamics and the specific roles of lipids in the context of apoptotic regulation occurring at the mitochondrion and its complex membrane systems. The BH4 domain is an anti-apoptotic specific domain of the Bcl-2 protein. Solid phase peptide synthesis was used to produce large amount of the peptide for biophysical studies. A protocol has been established and optimized, guarantying the required purity for biophysical studies. In detail the purification by high performance liquid chromatography and the characterisation via mass spectroscopy are described. The secondary structure of BH4 changes significantly in the presence of lipid vesicles as observed by infrared spectroscopy and circular dichroism. The BH4 peptide aggregates at the membrane surface and inserts slightly into the hydrophobic part of the membrane. Using nuclear magnetic resonance (NMR) and calorimetry techniques, it could even be shown that the BH4 domain modifies the dynamic and organization of the liposomes which mimic a mitochondrial surface. The second study was on the first helix of the pro-apoptotic protein Bax. This sequence called Bax-a1 has the function to address the cytosolic Bax protein to the mitochondrial membrane upon activation. Once again a protocol has been established for the synthesis and purification of this peptide. The aim was to elucidate the key role of cardiolipin, a mitochondria-specific phospholipid, in the interaction of Bax-a1 with the mitochondrial membrane system. The NMR and circular dichroism studies showed that Bax-a1 interacts with the membrane models only if they contain the cardiolipin, producing a strong electrostatic lock effect which is located at the membrane surface. Finally, a new NMR approach was developed which allows the investigation of the lipid response of isolated active mitochondria upon the presence of apoptotic stimuli. The goal was there to directly monitor lipid specific the occurring changes during these physiological activities
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Schmeiser, Katja. "Expression of apoptosis specific proteins (ASPs) during apoptosis and autophagy". Thesis, University of Birmingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394165.

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ASPs (apoptosis specific proteins) are a protein family with a molecular weight betwccn 20K and 140K. Expression has been found mainly in apoptotic cells. However, some family members have also been detected in viable cells. It has been confirmed by confocal microscopy that these proteins are predominately located along the actin cytoskeleton vvith particular high concentrations corresponding to a-actinin. A gene encoding the 32K ASP component has been cloned from a human foetal liver expression library. This 32K ASP protein (termed Apg5L; ApgS [autophagy 5. S. cerevisiae]-like, human [h]Apg5; Apg5) is homologues to the product of the yeast Apg5 gene. In yeast. Apg5 is essential for a novel protein conjugation system during autophagy. It is believed that members of the ASP family (i.e. 32K ASP/Apg5L) are involved in a similar conjugation system in mammals. This assumption is based on the observation that polyclonal antibodies raised against ApgSL recognise a set of proteins with co-localise with members of the ASP family detected by immunofluorescence.
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Cabezas, Somalo Maria. "Polimorfismes genètics i tractament antitumoral: evolució dels pacients amb leucèmia limfoblàstica aguda i inducció de leucèmies secundàries". Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458541.

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Els pacients amb la leucèmia limfoblàstica aguda (LLA) infantil responen diferentment a la quimioteràpia. Els polimorfismes genètics, juntament amb les alteracions genètiques en les cèl·lules leucèmiques, podrien ser responsables de la variabilitat en aquesta resposta. En la present tesi es va estudiar l’associació de copy number variants i/o single nucleotide polymorphisms (SNPs) en gens que codifiquen enzims metabolitzadors de fàrmacs i proteïnes apoptòtiques (CYP2D6, GSTT1, GSTM1, SULT1A1, UGT2B17 i TP53) amb l’evolució dels pacients amb LLA infantil. Es va observar que els pacients amb el genotip GSTM1 non-null mostraven una supervivència inferior i que els pacients portadors d’almenys un al·lel amb la variant Pro del polimorfisme Arg72Pro de TP53 també mostraven una tendència a una supervivència inferior. A més, la combinació d’ambdós genotips va resultar en una major reducció de la supervivència, comparat amb GSTM1 per si sol. Per avaluar la base biològica d’aquests resultats, es va dissenyar un model in vitro amb cèl·lules leucèmiques Jurkat transfectades amb l’al·lel Arg o Pro de TP53 i amb un siRNA de GSTM1. Els resultats van mostrar que les cèl·lules Jurkat p53Arg GSTM1 null tenien una sensibilitat més gran a un fàrmac antitumoral glucocorticoide, la dexametasona, confirmant els resultats observats en els pacients. S’ha descrit que GSTM1 inhibeix la mort cel·lular induïda per glucocorticoides, i p53Arg indueix l’apoptosi més eficientment que p53Pro, la qual és més eficient en activar l’aturada del cicle cel·lular i la reparació del DNA. Per tant, tenir almenys una còpia del gen GSTM1 i p53Pro, suficient en heterozigosi, podria conduir a una apoptosi menys eficaç en les cèl·lules leucèmiques després del tractament antitumoral i per tant, podria relacionar-se amb una menor supervivència dels pacients amb LLA. Per altra banda, una de les complicacions més greus després de la teràpia antitumoral és el desenvolupament d’un càncer secundari, generalment una neoplàsia mieloide (t-NM). Fins un 20% dels pacients tractats per un càncer primari poden desenvolupar una t-NM. És probable que les variacions genètiques constitucionals estiguin implicades en el risc individual de desenvolupar un càncer secundari. En la present tesi es va analitzar l’impacte de dos polimorfismes en gens de la via de p53 en el desenvolupament de t-NM i es va observar que la variant p53Pro de l’SNP Arg72Pro de TP53 i l’al·lel G de l’SNP309 de MDM2 estaven sobrerepresentats en pacients amb t-NM comparat amb els controls. Per analitzar el possible efecte biològic del polimorfisme de TP53, es va desenvolupar un model amb línies cel·lulars Jurkat isogèniques, que expressaven p53Arg o p53Pro. Després del tractament amb un agent alquilant o un inhibidor de la topoisomerasa II es van avaluar els següents paràmetres: dany en el DNA, nombre de cèl·lules apoptòtiques i formació d’alteracions cromosòmiques característiques de t-NM després d’un cultiu cel·lular a llarg termini. Les cèl·lules Jurkat p53Arg van presentar més foci de γ-H2AX per cèl·lula, un nivell més elevat de dany en el DNA i un potencial apoptòtic més elevat, respecte a les p53Pro. A més a més, es va detectar la translocació t(15;17) i la deleció en 5q33 en les cèl·lules p53Pro, però no en les p53 Arg. Per això, s’ha proposat que les diferències en el risc de desenvolupar t-NM en pacients tractats amb les mateixes dosis de quimioteràpia i/o radioteràpia serien degudes a la capacitat de cada individu de dur a terme més o menys eficientment l’apoptosi o la reparació de les lesions al DNA, segons el polimorfisme que tingui a TP53.
Children with acute lymphoblastic leukemia (ALL) respond differently to chemotherapy. Genetic polymorphisms together with genetic abnormalities in leukemic cells are probably behind variability in response to chemotherapy in childhood ALL. In the present thesis, we investigated whether copy number variants and/or single nucleotide polymorphism (SNPs) in genes coding for proteins involved in drug metabolism or apoptosis (CYP2D6, GSTT1, GSTM1, SULT1A1, UGT2B17 and TP53) have an impact on the therapeutic outcome of childhood ALL. We observed that patients with GSTM1 non-null genotype showed poor survival and patients carrying at least one allele of the Pro variant of the TP53 Arg72Pro SNP also showed a tendency to poor survival. When combining GSTM1 and TP53 genotypes, our data indicated that they can predict survival with higher significance than GSTM1 alone. To validate these results, an in vitro model was created with leukemic Jurkat cell line by transfection of the two TP53 variants at codon 72, either Pro or Arg and a GSTM1 siRNA into Jurkat cells. Results revealed that Jurkat p53Arg GSTM1 null cells exhibited higher sensitivity to dexamethasone, confirming the results observed in patients. It has been reported that GSTM1 inhibits glucocorticoids-induced cell death and that p53Arg induces apoptosis more efficiently than p53Pro, which is a more efficient activator of cell cycle arrest and DNA damage repair. Therefore, at least one copy of the gene GSTM1 and p53Pro, enough in heterozygosis, would lead to less efficient apoptosis in leukemic cells after the antileukemic treatment and could therefore be related to lower survival. On the other hand, one of the most severe complications after successful cancer therapy is the development of a secondary cancer, mostly a myeloid neoplasm (t-MN). Up to 20% of patients treated for a primary cancer develop t-MN. Constitutional genetic variation is likely to impact on an individual’s risk of developing t-MN. In the present thesis, we analyzed the impact of two polymorphisms in the p53 pathway on the development of t-MN. Results revealed that the TP53 Arg72Pro polymorphism and the MDM2 SNP309 were associated with t-MN risk. The p53Pro and the G allele of MDM2 were overrepresented in t-MN patients. To assess the biological effect of the TP53 polymorphism, we established Jurkat isogenic cell lines expressing p53Arg or p53Pro and assessed the number of γ-H2AX foci, chromosome alterations, sister chromatid exchanges, and apoptotic cells, as well as development of chromosomal alterations typical of t-MN, after treatment with an alkylating agent, or a topoisomerase II poison. Jurkat p53Arg cells presented more γ-H2AX foci per cell, higher level of DNA damage and higher apoptotic potential than p53Pro cells. Moreover, Jurkat p53Pro cells presented the t(15;17) translocation and 5q33 deletion whereas Jurkat p53Arg cells did not present the alterations. Therefore, it could be possible that differences in t-MN risk in patients treated with the same doses of chemotherapy and/or radiation are due to the ability of individuals to undergo apoptosis or to repair DNA lesions more or less efficiently related to the TP53 polymorphism.
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Deng, Diana Xi. "Metallothionein and apoptosis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq21105.pdf.

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Książki na temat "Apoptosis"

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Erhardt, Peter, i Ambrus Toth, red. Apoptosis. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-017-5.

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Al-Rubeai, M., red. Apoptosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102303.

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Reed, John C., i Douglas R. Green, red. Apoptosis. Cambridge: Cambridge University Press, 2011. http://dx.doi.org/10.1017/cbo9780511976094.

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Kuchino, Y., i W. E. G. Müller, red. Apoptosis. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4.

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Mihich, Enrico, i Robert T. Schimke, red. Apoptosis. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9217-1.

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D, Jacobson Michael, i McCarthy Nicola J, red. Apoptosis. Oxford, OX: Oxford University Press, 2002.

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Pérez, Lidia Gómez. Apoptosis. [Madrid]: Legados Ediciones, 2015.

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R, Preedy Victor, red. Apoptosis. Enfield NH: Science Publishers, 2010.

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R, Preedy Victor, red. Apoptosis. Enfield, N.H: Science Publishers, 2010.

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1948-, Al-Rubeai Mohamed, red. Apoptosis. Berlin: Springer, 1998.

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Części książek na temat "Apoptosis"

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McKenna, Sharon L., Adrian J. McGowan i Thomas G. Cotter. "Molecular mechanisms of programmed cell death". W Apoptosis, 1–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102304.

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Darzynkiewicz, Zbigniew, i Frank Traganos. "Measurement of apoptosis". W Apoptosis, 33–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102305.

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Bruckheimer, E. M., S. H. Cho, M. Sarkiss, J. Herrmann i T. J. McDonnell. "The Bcl-2 gene family and apoptosis". W Apoptosis, 75–105. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102306.

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Harvey, Natasha L., i Sharad Kumar. "The role of caspases in apoptosis". W Apoptosis, 107–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102307.

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Autuori, Francesco, Maria Grazia Farrace, Serafina Oliverio, Lucia Piredda i Mauro Piacentini. "“Tissue” transglutaminase and apoptosis". W Apoptosis, 129–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102308.

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O'Connor, Rosemary. "Survival factors and apoptosis". W Apoptosis, 137–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102309.

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Singh, R. P., i M. Al-Rubeai. "Apoptosis and bioprocess technology". W Apoptosis, 167–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/bfb0102310.

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Tanuma, S., i D. Shiokawa. "An Endonuclease Responsible for Apoptosis". W Apoptosis, 1–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_1.

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Rojko, J. L., J. R. Hartke, C. M. Cheney, A. J. Phipps i J. C. Neil. "Cytopathic Feline Leukemia Viruses Cause Apoptosis in Hemolymphatic Cells". W Apoptosis, 13–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_2.

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Müller, W. E. G., G. Pergande, H. Ushijima, C. Schleger, M. Kelve i S. Perovic. "Neurotoxicity in Rat Cortical Cells Caused by N-Methyl-D-Aspartate (NMDA) and gp120 of HIV-1: Induction and Pharmacological Intervention". W Apoptosis, 44–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-79850-4_3.

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Streszczenia konferencji na temat "Apoptosis"

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van der Meer, Freek J., Dirk J. Faber, Riëtte de Bruin, Maurice C. Aalders, Jop Perrée i Ton G. van Leeuwen. "Changes in optical properties of cells and tissue after induction of apoptosis". W European Conference on Biomedical Optics. Washington, D.C.: Optica Publishing Group, 2001. http://dx.doi.org/10.1364/ecbo.2001.4431_122.

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Apoptosis is the effector of regulated cell death and plays a role in many physiologic and pathologic processes. It is characterized by a highly regulated condensation and fragmentation of the cell nucleus, and breakup of the entire cell into vesicles, (apoptotic bodies) containing cell organelles and fragments of the nucleus. Previous experiments indicate that changes in optical properties after induction of apoptosis might be detected using optical imaging systems, such as optical coherence tomography (OCT), due to an increase in scattering of apoptotic cells. The previous in vitro experiments are extended to ex vivo and in vivo experiments. A nearly two-fold increase in attenuation coefficient is observed in a tissue culture of porcine carotid artery, in which apoptosis is induced by balloon dilation, and a significant 20 % increase in an in vivo setup. The preliminary results of this study indicate that the apoptotic process may also be detected ex vivo and in vivo using optical imaging systems, such as optical coherence tomography (OCT), due to an increase in scattering by the typical disintegration of cellular material.
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Zhao, Ruogang, Lina Lin i Craig A. Simmons. "The Effects of Cell Contraction and Loss of Adhesion on the Apoptosis of Valve Interstitial Cells". W ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19249.

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Dystrophic calcification in sclerotic aortic valves is associated with apoptosis of myofibroblasts that differentiate from valve interstitial cells (VICs). The factors that regulate apoptosis in sclerotic valves are not known, but may include mechanical stimuli, as is the case in other fibrotic tissues. In support of this hypothesis, we have observed that VICs on stiff collagen matrices that simulate fibrotic tissue differentiate to myofibroblasts and form calcified aggregates that contain apoptotic cells [1]. However, the mechanisms by which cell aggregation leads to VIC apoptosis are unknown. In other cell types, cell contraction caused by release of matrix tension can induce cell apoptosis, but the mechanical transduction pathway regulating this process is unknown [2]. Similarly, cell rounding caused by disrupting the cytoskeletal network has been found to induce apoptosis [3], indicating the cytoskeletal network may play an important role in the cell shape-change related apoptosis pathways. Loss of adhesion between the cell and its matrix is also a well-documented cause for apoptosis of adherent cell types [4].
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Kuttikrishnan, Shilpa, Kirti S. Prabhu, Tamam Elimat, Ashraf Khalil, Nicholas H. Oberlies, Feras Q. Alali i Shahab Uddin. "Anticancer Activity of Neosetophomone B, An Aquatic Fungal Secondary Metabolite, Against Hematological Malignancie S". W Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0106.

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Cancer is one of the most life threatening diseases, causing nearly 13% death in the worldwide. Leukemia, cancer of the hematopoetic cells is the main cause of cancer death in adults and children. Therapeutic agents used in treatment of cancer are known to have narrow therapeutic window and tendency to develop resistance against some cancer cell lines thus, proposing a need to discover some novel agents to treat cancer. In the present study we investigated the anticancer activity of Neosetophomone B(NSP-B), an aquatic fungal metabolite isolated from Neosetophoma sp against leukemic cells (K562 and U937). MTT results demonstrated a dose dependent inhibition of cell proliferation in K562 and U937 cell lines. Annexin staining using flow cytometry indicated that NSP-B treatment cause a dose dependent apoptosis in leukemic cells.Western blot analysis showed that NSP-B mediated apoptosis involves sequential activation of caspase 9, 3 and poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore NSP-B treatment of leukemic cells resulted in upregulation of pro-apoptotic proteins (Bax) with downregulation of anti-apoptotic proteins ( Bcl-2 ).Thus, present study focuses on exploring the mechanism of anticancer activity of NSP-B on leukemic cells, raising the possibility of its use as a novel therapeutic agent for hematological malignancies. Results: We sought to determine whether NSP-B suppresses the growth of leukemic cell lines. We tested a panel of leukemic cell lines with different doses of NSP-B. Cell viability decreased in a concentration-dependent manner in K562 and U937 cell lines. NSP-B induced apoptosis in K562 and U937 cell lines via downregulation of anti-apoptotic proteins and enhancement of pro-apoptotic proteins. NSP-B induced the activation of caspase cascade signaling pathway. Altogether our results suggest that the NSP-B plays an important role in apoptosis in leukemic cell lines .Conclusions: Our data provides insight on anticancer activities of NSP-B in leukemic cell lines (K562 and U937). NSP-B inhibit cell viability via inducing apoptosis. The NSP-B mediated apoptosis occurs via downregulation of anti-apoptotic proteins and enhancement of pro-apototic proteins, thereby activating the caspase-cascade signaling. Further studies are required to elicit role of NSP-B in regulating molecular pathway involved in the progression of cancer. Taken together, above results suggest that NSP-B may have a future therapeutic role in leukemia and possibly other hematological malignancies.
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Dereli-Korkut, Zeynep, i Sihong Wang. "Microfluidic Cell Arrays to Mimic 3D Tissue Microenvironment". W ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80411.

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We developed a functional high throughput 3D microfluidic living cell array (MLC) for anti-cancer drug screening and mechanism discovery. Contemporary drug screening methods suffer from low sample throughput and lack of abilities of mimicking the 3D microenvironment of mammalian tissues. The poor performance of anti-cancer drugs limits the efficacy at controlling the complex disease system like cancer. Systematic studies of apoptotic signaling pathways can be prominent approaches for searching active and effective treatments with less drug resistance. Hence, innovative bio-devices are needed to represent tumor microenvironment to understand the molecular signatures of apoptosis for testing new anticancer therapies targeting apoptosis. Our novel 3D MLC design is the prototype of a high-throughput drug screening platform targeting apoptotic signaling pathways.
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Baust, John M., Robert G. Van Buskirk i John G. Baust. "Cryopreservation of an Engineered Skin Equivalent: The Apoptosis Paradigm". W ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0586.

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Abstract The emergence of the tissue engineering sciences has led to an immediate need for cryopreservation protocols compatible with cell survival, cell-matrix binding and “scaffold” integrity. While numerous problems exist related to directional restrictions in cryoprotectant transport in tissue models, recent findings have demonstrated that the induction of specific molecular events, especially gene regulated cell death (apoptosis) is of significance. Accordingly, we report on a new strategy for the successful cryopreservation of a human skin equivalent. The integration of an intracellular-type cryopreservation solution containing dimethyl sulfoxide with and without apoptotic inhibitors provides a successful model for tissue preservation. With optimized formulations, post-thaw improvement of viability upwards of three-fold has been demonstrated when compared with traditional preservation methodologies. We conclude that 1) the use of an intracellular-type cryopreservation medium, Hypothermosol®, can improve post-thaw tissue construct integrity and cell viability, and 2) the inclusion of apoptotic inhibitors significantly improves cryopreservation outcome.
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Трушина, Элеонора Николаевна. "APOPTOSIS OF BRAIN NEURONS IN ISCHEMIA". W Психология. Спорт. Здравоохранение: сборник избранных статей по материалам Международной научной конференции (Санкт-Петербург, Апрель 2021). Crossref, 2021. http://dx.doi.org/10.37539/psm296.2021.47.78.003.

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В статье приводится краткий обзор литературы о механизмах развития апоптоза нейронов головного мозга при ишемии. Ингибирование путей апоптоза оказывает нейропротективный эффект и предотвращает расширение зоны поражения. The article provides a brief review of the literature on the mechanisms of the development of apoptosis of cerebral neurons during ischemia. Inhibition of the pathways of apoptosis has a neuroprotective effect and prevents the expansion of the affected area.
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Liu, Lei, Yingjie Zhang i Xianwang Wang. "Involvement of caspase-dependent and -independent apoptotic pathways in cisplatin-induced apoptosis". W SPIE BiOS: Biomedical Optics, redaktor Wei R. Chen. SPIE, 2009. http://dx.doi.org/10.1117/12.808431.

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Cheng, Chao-Min, i Philip R. LeDuc. "Effects of Local Mechanical Stimulation on Cellular Behavior". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176082.

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Cell response to mechanical stimulation is a controlled and complex set of events that has been investigated by numerous groups. Understanding the behavior of cells from a localized perspective is even more challenging due to the integrated responses that play significant roles. After investigating the effect of local mechanical stimulation with respect to cell apoptosis, we find that the resulting ratio of apoptotic cells with respect to the deformation of the cells through using soft pyramid shaped microstructure versus rectangular microstructures is increased by 200% percent. These results may also have implications in understanding cell behaviors such as cell-cell communication under the mechanical stimulation and mechanotransduction.
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"APOPTOSIS AND ASSESSMENT OF CYTOGENETIC DISORDERS APOPTOSIS AND ASSESSMENT OF CYTOGENETIC DISORDERS IN THE POPULATION OF THE ARCTIC ZONE OF THE RUSSIAN FEDERATION". W СОВРЕМЕННЫЕ ПРОБЛЕМЫ ЭКОЛОГИИ И ЗДОРОВЬЯ НАСЕЛЕНИЯ. ЭКОЛОГИЯ И ЗДОРОВЬЕ НАСЕЛЕНИЯ. Иркутский научный центр хирургии и травматологии, 2023. http://dx.doi.org/10.12731/978-5-98277-383-8-art1.

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The intensity of apoptosis and the level of cytogenetic damage in the indigenous population and migrants of the Arctic were studied depending on age, smoking status, lifestyle and northern seniority. It was found that the frequency of occurrence of nuclear protrusions was higher in the group of examined indigenous people against the background of a lower level of apoptosis (2,03 ± 0,08 and 1,8 ± 0,09, p < 0,05) compared with migrants. Significant excess of apoptosis indicators in the indigenous settlement population relative to residents leading a nomadic lifestyle is shown. The assessment of the intensity of apoptosis and cytogenetic indices depending on the length of residence of the population in the Arctic zone of the Russian Federation showed that the number of proliferating cells and the index of accumulation of cytogenetic disorders in a group of migrants with 10-20 years of experience is significantly lower compared to a group of migrants living in extreme Arctic conditions for up to 5 years.
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Kessel, David, Yu Luo i Hyeong-Reh C. Kim. "Determinants of PDT-induced apoptosis". W BiOS 2000 The International Symposium on Biomedical Optics, redaktor Thomas J. Dougherty. SPIE, 2000. http://dx.doi.org/10.1117/12.379884.

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Raporty organizacyjne na temat "Apoptosis"

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Donato, Nicholas J. Calcium-Mediated Apoptosis and Apoptotic Sensitization in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2003. http://dx.doi.org/10.21236/ada418675.

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Holley, Christopher L. Reaper-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2002. http://dx.doi.org/10.21236/ada411241.

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Perry, Jennifer. Reaper-Induced Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2005. http://dx.doi.org/10.21236/ada462723.

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Kornbluth, Sally A., i Erica K. Evans. Regulation of Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 1999. http://dx.doi.org/10.21236/ada381256.

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Liu, Junwei. Apoptosis-Dependent and Apoptosis-Independent Functions Bim in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, marzec 2004. http://dx.doi.org/10.21236/ada439201.

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Marcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2001. http://dx.doi.org/10.21236/ada398042.

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Marcelli, Marco. Apoptosis in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2002. http://dx.doi.org/10.21236/ada407231.

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Vogel, Kristine S. Neurofibromin and Neuronal Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2004. http://dx.doi.org/10.21236/ada429612.

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Vogel, Kristine S. Neurofibromin and Neuronal Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2003. http://dx.doi.org/10.21236/ada420881.

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Zhang, Hong. A Novel Apoptosis Regulator. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2000. http://dx.doi.org/10.21236/ada390571.

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