Готові списки джерел за темами / Mitochondrial apoptosis

Добірка наукової літератури з теми "Mitochondrial apoptosis"

Автор: Grafiati
Опубліковано: 7 липня 2024

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Статті в журналах з теми "Mitochondrial apoptosis":

1

Adhihetty, Peter J., Vladimir Ljubicic, and David A. Hood. "Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 292, no. 3 (March 2007): E748—E755. http://dx.doi.org/10.1152/ajpendo.00311.2006.

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Chronic contractile activity of skeletal muscle induces an increase in mitochondria located in proximity to the sarcolemma [subsarcolemmal (SS)] and in mitochondria interspersed between the myofibrils [intermyofibrillar (IMF)]. These are energetically favorable metabolic adaptations, but because mitochondria are also involved in apoptosis, we investigated the effect of chronic contractile activity on mitochondrially mediated apoptotic signaling in muscle. We hypothesized that chronic contractile activity would provide protection against mitochondrially mediated apoptosis despite an elevation in the expression of proapoptotic proteins. To induce mitochondrial biogenesis, we chronically stimulated (10 Hz; 3 h/day) rat muscle for 7 days. Chronic contractile activity did not alter the Bax/Bcl-2 ratio, an index of apoptotic susceptibility, and did not affect manganese superoxide dismutase levels. However, contractile activity increased antiapoptotic 70-kDa heat shock protein and apoptosis repressor with a caspase recruitment domain by 1.3- and 1.4-fold ( P < 0.05), respectively. Contractile activity elevated SS mitochondrial reactive oxygen species (ROS) production 1.4- and 1.9-fold ( P < 0.05) during states IV and III respiration, respectively, whereas IMF mitochondrial state IV ROS production was suppressed by 28% ( P < 0.05) and was unaffected during state III respiration. Following stimulation, exogenous ROS treatment produced less cytochrome c release (25–40%) from SS and IMF mitochondria, and also reduced apoptosis-inducing factor release (≈30%) from IMF mitochondria, despite higher inherent cytochrome c and apoptosis-inducing factor expression. Chronic contractile activity did not alter mitochondrial permeability transition pore (mtPTP) components in either subfraction. However, SS mitochondria exhibited a significant increase in the time to Vmax of mtPTP opening. Thus, chronic contractile activity induces predominantly antiapoptotic adaptations in both mitochondrial subfractions. Our data suggest the possibility that chronic contractile activity can exert a protective effect on mitochondrially mediated apoptosis in muscle.
2

Parsons, Melissa J., and Douglas R. Green. "Mitochondria in cell death." Essays in Biochemistry 47 (June 14, 2010): 99–114. http://dx.doi.org/10.1042/bse0470099.

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Apoptosis can be thought of as a signalling cascade that results in the death of the cell. Properly executed apoptosis is critically important for both development and homoeostasis of most animals. Accordingly, defects in apoptosis can contribute to the development of autoimmune disorders, neurological diseases and cancer. Broadly speaking, there are two main pathways by which a cell can engage apoptosis: the extrinsic apoptotic pathway and the intrinsic apoptotic pathway. At the centre of the intrinsic apoptotic signalling pathway lies the mitochondrion, which, in addition to its role as the bioenergetic centre of the cell, is also the cell’s reservoir of pro-death factors which reside in the mitochondrial IMS (intermembrane space). During intrinsic apoptosis, pores are formed in the OMM (outer mitochondrial membrane) of the mitochondria in a process termed MOMP (mitochondrial outer membrane permeabilization). This allows for the release of IMS proteins; once released during MOMP, some IMS proteins, notably cytochrome c and Smac/DIABLO (Second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI), promote caspase activation and subsequent cleavage of structural and regulatory proteins in the cytoplasm and the nucleus, leading to the demise of the cell. MOMP is achieved through the co-ordinated actions of pro-apoptotic members and inhibited by anti-apoptotic members of the Bcl-2 family of proteins. Other aspects of mitochondrial physiology, such as mitochondrial bioenergetics and dynamics, are also involved in processes of cell death that proceed through the mitochondria. Proper regulation of these mitochondrial functions is vitally important for the life and death of the cell and for the organism as a whole.
3

Heikaus, Sebastian, Linda van den Berg, Tobias Kempf, Csaba Mahotka, Helmut Erich Gabbert, and Uwe Ramp. "HA14-1 is Able to Reconstitute the Impaired Mitochondrial Pathway of Apoptosis in Renal Cell Carcinoma Cell Lines." Analytical Cellular Pathology 30, no. 5 (January 1, 2008): 419–33. http://dx.doi.org/10.1155/2008/693095.

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Renal cell carcinomas (RCCs) exhibit a marked resistance towards apoptosis. Although most apoptotic stimuli converge at the level of the mitochondria, little is known about the mitochondrial apoptosis pathway in renal cell carcinomas. The aim of the present study, therefore, was to investigate the functionality of the mitochondrial apoptosis pathway in renal cell carcinoma cell lines by exposure to TRAIL, etoposide, HA14-1 and betulinic acid activating the mitochondria by different mechanisms. Sensitivity to TRAIL-induced apoptosis correlated with cleavage of the initiator caspase-8, but the mitochondrial apoptosis pathway was not induced. Similarly, etoposide and betulinic acid could not induce mitochondrial damage. In contrast, HA14-1 was able to activate mitochondrial apoptosis, thereby demonstrating functionally inducible signalling pathways downstream of the mitochondria. The intactness of the pathways upstream of the mitochondria was shown by pretreatment of TRAIL-sensitive cell lines with HA14-1, which could reconstitute TRAIL-induced mitochondrial damage and resulted in a synergistic apoptosis induction.Our results demonstrate that the apoptotic pathways upstream and downstream of the mitochondria are intact and inducible in renal cell carcinoma cell lines. However, resistance towards mitochondrial apoptosis is located on the level of the mitochondria themselves.
4

Zamzami, N., S. A. Susin, P. Marchetti, T. Hirsch, I. Gómez-Monterrey, M. Castedo, and G. Kroemer. "Mitochondrial control of nuclear apoptosis." Journal of Experimental Medicine 183, no. 4 (April 1, 1996): 1533–44. http://dx.doi.org/10.1084/jem.183.4.1533.

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Anucleate cells can be induced to undergo programmed cell death (PCD), indicating the existence of a cytoplasmic PCD pathway that functions independently from the nucleus. Cytoplasmic structures including mitochondria have been shown to participate in the control of apoptotic nuclear disintegration. Before cells exhibit common signs of nuclear apoptosis (chromatin condensation and endonuclease-mediated DNA fragmentation), they undergo a reduction of the mitochondrial transmembrane potential (delta psi m) that may be due to the opening of mitochondrial permeability transition (PT) pores. Here, we present direct evidence indicating that mitochondrial PT constitutes a critical early event of the apoptotic process. In a cell-free system combining purified mitochondria and nuclei, mitochondria undergoing PT suffice to induce chromatin condensation and DNA fragmentation. Induction of PT by pharmacological agents augments the apoptosis-inducing potential of mitochondria. In contrast, prevention of PT by pharmacological agents impedes nuclear apoptosis, both in vitro and in vivo. Mitochondria from hepatocytes or lymphoid cells undergoing apoptosis, but not those from normal cells, induce disintegration of isolated Hela nuclei. A specific ligand of the mitochondrial adenine nucleotide translocator (ANT), bongkreik acid, inhibits PT and reduces apoptosis induction by mitochondria in a cell-free system. Moreover, it inhibits the induction of apoptosis in intact cells. Several pieces of evidence suggest that the proto-oncogene product Bcl-2 inhibits apoptosis by preventing mitochondrial PT. First, to inhibit nuclear apoptosis, Bcl-2 must be localized in mitochondrial but not nuclear membranes. Second, transfection-enforced hyperexpression of Bcl-2 directly abolishes the induction of mitochondrial PT in response to a protonophore, a pro-oxidant, as well as to the ANT ligand atractyloside, correlating with its apoptosis-inhibitory effect. In conclusion, mitochondrial PT appears to be a critical step of the apoptotic cascade.
5

Majewski, Nathan, Veronique Nogueira, R. Brooks Robey, and Nissim Hay. "Akt Inhibits Apoptosis Downstream of BID Cleavage via a Glucose-Dependent Mechanism Involving Mitochondrial Hexokinases." Molecular and Cellular Biology 24, no. 2 (January 15, 2004): 730–40. http://dx.doi.org/10.1128/mcb.24.2.730-740.2004.

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ABSTRACT The serine/threonine kinase Akt/protein kinase B inhibits apoptosis induced by a variety of stimuli, including overexpression or activation of proapoptotic Bcl-2 family members. The precise mechanisms by which Akt prevents apoptosis are not completely understood, but Akt may function to maintain mitochondrial integrity, thereby preventing cytochrome c release following an apoptotic insult. This effect may be mediated, in part, via promotion of physical and functional interactions between mitochondria and hexokinases. Here we show that growth factor deprivation induced proteolytic cleavage of the proapoptotic Bcl-2 family member BID to yield its active truncated form, tBID. Activated Akt inhibited mitochondrial cytochrome c release and apoptosis following BID cleavage. Akt also antagonized tBID-mediated BAX activation and mitochondrial BAK oligomerization, two downstream events thought to be critical for tBID-induced apoptosis. Glucose deprivation, which impaired the ability of Akt to maintain mitochondrion-hexokinase association, prevented Akt from inhibiting BID-mediated apoptosis. Interestingly, tBID independently elicited dissociation of hexokinases from mitochondria, an effect that was antagonized by activated Akt. Ectopic expression of the amino-terminal half of hexokinase II, which is catalytically active and contains the mitochondrion-binding domain, consistently antagonized tBID-induced apoptosis. These results suggest that Akt inhibits BID-mediated apoptosis downstream of BID cleavage via promotion of mitochondrial hexokinase association and antagonism of tBID-mediated BAX and BAK activation at the mitochondria.
6

Seo, Young Ah, Veronica Lopez, and Shannon L. Kelleher. "A histidine-rich motif mediates mitochondrial localization of ZnT2 to modulate mitochondrial function." American Journal of Physiology-Cell Physiology 300, no. 6 (June 2011): C1479—C1489. http://dx.doi.org/10.1152/ajpcell.00420.2010.

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Female reproductive tissues such as mammary glands, ovaries, uterus, and placenta are phenotypically dynamic, requiring tight integration of bioenergetic and apoptotic mechanisms. Mitochondrial zinc (Zn) pools have emerged as a central player in regulating bioenergetics and apoptosis. Zn must first be imported into mitochondria to modulate mitochondrion-specific functions; however, mitochondrial Zn import mechanisms have not been identified. Here we documented that the Zn transporter ZnT2 is associated with the inner mitochondrial membrane and acts as an auxiliary Zn importer into mitochondria in mammary cells. We found that attenuation of ZnT2 expression significantly reduced mitochondrial Zn uptake and total mitochondrial Zn pools. Moreover, expression of a ZnT2-hemagglutinin (HA) fusion protein was localized to mitochondria and significantly increased Zn uptake and mitochondrial Zn pools, directly implicating ZnT2 in Zn import into mitochondria. Confocal microscopy of truncated and point mutants of ZnT2-green fluorescent protein (GFP) fusion proteins revealed a histidine-rich motif (51HH XH54) in the NH2 terminus that is important for mitochondrial targeting of ZnT2. More importantly, the expansion of mitochondrial Zn pools by ZnT2 overexpression significantly reduced ATP biogenesis and mitochondrial oxidation concurrent with increased apoptosis, suggesting a functional role for ZnT2-mediated Zn import into mitochondria. These results identify the first Zn transporter directly associated with mitochondria and suggest that unique secretory tissues such as the mammary gland require novel mechanisms to modulate mitochondrion-specific functions.
7

Tang, Ho Lam, Anh-Huy Phan Le, and Hong Lok Lung. "The increase in mitochondrial association with actin precedes Bax translocation in apoptosis." Biochemical Journal 396, no. 1 (April 26, 2006): 1–5. http://dx.doi.org/10.1042/bj20060241.

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Accumulating evidence indicates the potential role of actin cytoskeleton in facilitating the mitochondrial recruitment of various pro-apoptotic proteins from the cytosol to initiate apoptosis. In the present paper, we report the observation of the increase in mitochondrial association of actin in early apoptosis. Using cell fractionation and Western blot analysis, we found that mitochondrial accumulation of β-actin occurred before the mitochondrial insertion of Bax and release of cytochrome c in apoptosis. The mitochondrial accumulation of β-actin was observed with various apoptotic stimuli in various cell lines, suggesting that this is a general apoptotic phenomenon in mammalian systems. Using fluorescence microscopy, we have shown that an apoptotic induction triggered the reorganization of the F-actin (filamentous actin) network with an increase in the association with mitochondria, which was observed before mitochondrial fission and nuclear condensation. Perhaps actin could contribute to the initiation of apoptosis by enabling cytosolic pro-apoptotic proteins to be carried to mitochondria by the cytoskeleton-driven trafficking system.
8

Mayer, Bernd, and Rainer Oberbauer. "Mitochondrial Regulation of Apoptosis." Physiology 18, no. 3 (June 2003): 89–94. http://dx.doi.org/10.1152/nips.01433.2002.

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Mitochondria play a central part in cellular survival and apoptotic death. These processes are highly regulated by pro- and antiapoptotic Bcl-2 superfamily members. A key feature within apoptosis cascades is disruption of mitochondrial transmembrane potential and apoptogenic protein release, caused by opening of the permeability transition pore (PT). New data, however, indicate that mitochondrial apoptosis may occur without PT involvement.
9

Sugioka, Rie, Shigeomi Shimizu, and Yoshihide Tsujimoto. "Fzo1, a Protein Involved in Mitochondrial Fusion, Inhibits Apoptosis." Journal of Biological Chemistry 279, no. 50 (September 30, 2004): 52726–34. http://dx.doi.org/10.1074/jbc.m408910200.

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Mitochondrial morphology and physiology are regulated by the processes of fusion and fission. Some forms of apoptosis are reported to be associated with mitochondrial fragmentation. We showed that overexpression of Fzo1A/B (rat) proteins involved in mitochondrial fusion, or silencing of Dnm1 (rat)/Drp1 (human) (a mitochondrial fission protein), increased elongated mitochondria in healthy cells. After apoptotic stimulation, these interventions inhibited mitochondrial fragmentation and cell death, suggesting that a process involved in mitochondrial fusion/fission might play a role in the regulation of apoptosis. Consistently, silencing of Fzo1A/B or Mfn1/2 (a human homolog of Fzo1A/B) led to an increase of shorter mitochondria and enhanced apoptotic death. Overexpression of Fzo1 inhibited cytochromecrelease and activation of Bax/Bak, as assessed from conformational changes and oligomerization. Silencing of Mfn or Drp1 caused an increase or decrease of mitochondrial sensitivity to apoptotic stimulation, respectively. These results indicate that some of the proteins involved in mitochondrial fusion/fission modulate apoptotic cell death at the mitochondrial level.
10

Su, Ching-Chieh, Jia-Ying Yang, Hsin-Ban Leu, Yumay Chen, and Ping H. Wang. "Mitochondrial Akt-regulated mitochondrial apoptosis signaling in cardiac muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (February 2012): H716—H723. http://dx.doi.org/10.1152/ajpheart.00455.2011.

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We recently reported translocation and activation of Akt in cardiac mitochondria. This study was to determine whether activation of Akt in mitochondria could inhibit apoptosis of cardiac muscle cells. Insulin stimulation induced translocation of phosphorylated Akt to the mitochondria in primary cardiomyocytes. A mitochondria-targeted constitutively active Akt was overexpressed via adenoviral vector and inhibited efflux of cytochrome c and apoptosis-inducing factor from mitochondria to cytosol and partially prevented loss of mitochondria cross-membrane electrochemical gradient. Activation of caspase 3 was suppressed in the cardiomyocytes transduced with mitochondria-targeted active Akt, whereas a mitochondria-targeted dominant negative Akt enhanced activation of caspase 3. Terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling assay showed that mitochondrial activation of Akt significantly reduced the number of apoptotic cells. When the endogenous Akt was abolished by LY294002, the antiapoptotic actions of mitochondrial Akt remained effective. These experiments suggested that mitochondrial Akt suppressed apoptosis signaling independent of cytosolic Akt in cardiac muscle cells.
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Статті в журналах Дисертації Книги

Дисертації з теми "Mitochondrial apoptosis":

1

Sun, Mei Guo. "Mitochondrial structure during apoptosis." Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3273480.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed August 31, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 129-140).
2

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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3

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.
4

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
5

Zhao, Ming. "The lysosomal-mitochondrial axis theory of apoptosis /." Linköping : Univ, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med747s.pdf.

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6

Bender, Cheryl E. "The mitochondrial pathway of apoptosis in invertebrates." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC IP addresses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3288845.

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Thesis (Ph. D.)--University of California, San Diego, 2007.
Title from first page of PDF file (viewed June 2, 2008). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 190-218).
7

Wang, Jianming. "Life without mitochondrial DNA : studies of transgenic mice /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4491-1/.

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8

Cipolat, Sara. "From mitochondrial morphology to apoptosis: genetic analysis of OPA1 function and regulation." Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425557.

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Mitochondria are essential organelles for life and death of the cell: they produce most of the cellular ATP (Danial et al., 2003), regulate cytosolic Ca2+ signalling (Rizzuto et al., 2000), and integrate and amplify different apoptotic stimuli (Green and Kroemer, 2004). Such a functional versatility is matched by a complex and dynamic morphology, both at the ultrastructural and at the cellular level (Griparic and van der Bliek). At the ultrastructural level, the mitochondrial cristae constitute a separate compartment connected to the thin intermembrane space by narrow tubular junctions (Frey and Mannella, 2000). In the cytosol, mitochondria are organized in a network of individual organelles that dynamically fuse and divide. Mitochondrial morphology results from the equilibrium between fusion and fission processes, controlled by a family of "mitochondria-shaping" proteins, many of which are dynamin-related proteins initially identified by genetic screens in buddying yeast (Dimmer et al., 2002; Shaw and Nunnari, 2002). Dynamins are ubiquitous mechano-enzymes that hydrolyze GTP to regulate fusion, fission, tubulation and elongation of cellular membranes (McNiven et al., 2000). In mammalians, mitochondrial fission is controlled by a cytosolic dynamin related protein DRP-1 (Smirnova et al., 2001) that translocates to sites of mitochondrial fragmentation where it binds to FIS1, its adapter in the outer membrane (Yoon et al., 2003) (James et al., 2003). Fusion is controlled by mitofusin-1 (MFN1) and-2 (MFN2), two large GTPases of the outer mitochondrial membrane, orthologues of S. cerevisiae Fzo1p (Rapaport et al., 1998). OPA1, the mammalian homologue of S. cerevisiae Mgm1p, is the only dynamin-related protein of the inner mitochondrial membrane (Olichon et al., 2002). Loss-of-function or dominant-negative mutations in Opa1 are associated with autosomal dominant optic atrophy (DOA), the leading cause of inherited optic neuropathy, characterized by retinal ganglion cells degeneration followed by ascending atrophy of the optic nerve (Alexander et al., 2000; Delettre et al., 2000). The aim of my PhD has been to generate, use and analyze genetic models in order to unravel the biological function of OPA1 as well as its regulation. In order to dissect the biological function of OPA1, we undertook a combination of genetics and imaging to address its role in regulating mitochondrial fusion/fission equilibrium. Imaging of wild type mouse embryonic fibroblasts (MEFs) cotransfected with a mitochondrially targeted cyan fluorescent protein (mtCFP) showed mitochondria as individual organelles, rod or round-shaped, with an average length of 3±0.34 µm along their major axis. Morphometric analysis confirmed that only 23% of the analyzed cells displayed elongated mitochondria, i.e. cells with axial length >5 µm and roundness index <0.5 in more than 50% of mitochondria. Cotransfection of OPA1 with mtCFP induced visible changes in the shape of the mitochondrial reticulum. The rod-shaped mitochondria appeared now to be interconnected in a branched network. Morphometric analysis confirmed this mitochondria-shaping effect of OPA1, with more than 50% of the cells analyzed showing elongated mitochondria. Furthermore, we analyzed the effect of pathogenic mutations of OPA1 on its ability to elongate mitochondria. A missense mutation in the GTPase domain (K301A) that reduces the GTPase activity of more than 80%, as well as a truncative one in the coiled coil domain (R905stop), which eliminates the C-terminal coiled-coil domain required in protein-protein interactions, abolished the ability of OPA1 to elongate mitochondria, indicating that it requires a functional GTPase and coiled-coil domain. To address the effect of reduced OPA1 levels on mitochondrial morphology we turned to stable, plasmid-generated RNA interference (RNAi). In cell clones where OPA1 was ablated, mitochondria appeared globular and fragmented as opposed to the rod, elongated organelles of the control clones. Tubulation induced by OPA1 is not the results of simple juxtaposition of mitochondria, but it represents the steady state appearance of increased mitochondrial fusion events, as substantiated by assays of mitochondrial fusion in polykarions induced by PEG treatment. Expression of OPA1 significantly speeded up mixing of matricial content, whereas its downregulation reduced mitochondrial fusion. In yeast, the pro-fusion activity of Mgm1p, the orthologue of OPA1, depends on the outer membrane mitochondria-shaping protein Fzo1p. We therefore wished to ascertain whether this paradigm was maintained in higher eukaryotes. We turned to a genetic approach, testing the ability of overexpressed OPA1 to promote mitochondrial tubulation in MEFs deficient for either Mfn1 or Mfn2. Expression of OPA1 induced mitochondrial tabulation and fusion in wt and in Mfn2-/- but not in Mfn1-/- cells. This defect was complemented by re-introduction of MFN1 but not MFN2, unequivocally identifying outer membrane MFN1 as an essential functional partner of OPA1. Moreover, MFN1 was unable to promote mitochondrial elongation if OPA1 had been ablated. Thus, OPA1 and MFN1 appear to functionally depend one on each other. To address whether Mfn1-/- MEFs displayed any defect in the preparatory events of mitochondrial juxtaposition and docking, we performed 4D-imaging of mitochondria, i.e. time series of z-stacks of mitochondrial images. The total number of contacts between mitochondria was not affected by OPA1 overexpression or by MFN deficiency. OPA1 facilitated fusion following contacts between wt and Mfn2-/- but not Mfn1-/- mitochondria. Taken together, our results suggested that OPA1 requires MFN1 to fuse the membranes of two juxtaposed mitochondria and not to produce inter-mitochondrial contacts. Our genetic analysis provided the first evidence of a functional diversity between MFN1 and MFN2, suggesting a functional axis between OPA1 and MFN1 (Cipolat et al., 2004). The discovery that OPA1 is a pro-fusion protein raised the question of whether this protein participated in the regulation of apoptosis, during which fusion is impaired. We therefore decided to genetically dissect the role of OPA1 in fusion and apoptosis. We could demonstrate that OPA1 has an antiapoptotic activity, controlling the cristae remodelling pathway of apoptosis, independently of mitochondrial fusion. OPA1 did not interfere with the activation of the core mitochondrial apoptotic pathway of BAX and BAK activation. Yet OPA1 inhibited the release of cytochrome c by preventing the remodelling of the cristae and the intramitochondrial redistribution of cytochrome c. Inactivating mutations in the GTPase domain of OPA1 impaired its anti-apoptotic activity, enhancing susceptibility to apoptosis induced by stimuli that recruit the mitochondrial pathway. While our results contributed to clarify the biological function of OPA1, they left open a number of questions. In particular, if the pro-fusion activity of OPA1 was dispensable for the inhibition of apoptosis, how was this function controlled? In yeast Mgm1p is processed by the inner mitochondrial membrane rhomboid protease Rbd1/Pcp1 into a short active form, responsible for the effects of Mgm1p on mitochondrial morphology (Herlan et al., 2003; McQuibban et al., 2003). The mammalian orthologue of Rbd1p, PARL, could similarly play a role in the regulation of one of the two biological functions we ascribed to OPA1, i.e. its effect in mitochondrial fusion and its anti-apoptotic activity. In order to address this issue, we decided to analyze the phenotype of a mouse model of Parl deletion. Parl-/- mice were born with normal Mendelian frequency and developed normally up to 4 weeks. From then on, mice displayed severe growth retardation and progressive atrophy in multiple tissues, leading to cachexia and death. The atrophy of Parl-/- tymi, spleens and muscular tissues was caused by an increased apoptosis of double-positive (CD4+CD8+) thymic lymphocytes, splenic B lymphocytes (B220+) and myoblasts, respectively. We investigated to what extent mitochondrial dysfunction and morphology dysregulation contributed to this multisystemic atrophy. PARL was not required for normal mitochondrial function: Parl-/- mitochondria did not display primary respiratory defects or latent mitochondrial dysfunction in hepatocytes, MEFs, primary myocytes and myotubes. Mitochondrial dysfunction therefore did not explain Parl-/- muscular atrophy and multisystem failure. Moreover Parl was not required for maintenance of mitochondrial shape and fusion, even in tissues severely affected by Parl ablation like muscle, and Parl was dispensable for regulation of mitochondrial dynamics by OPA1. We therefore investigated whether PARL regulates mitochondrial apoptotic machinery by analyzing apoptosis in MEFs treated with different intrinsic mitochondria utilizing stimuli. Parl-/- MEFs were more sensitive to all the stimuli tested as compared to their wt counterparts. Reintroduction of a catalytically active PARL showed that the defect was specific. PARL exerted its antiapoptotic effect at the mitochondrial level, since cytochrome c release and mitochondrial dysfunction following treatment with an apoptotic stimulus occurred faster in Parl-/- fibroblasts than in their relative wt counterparts. PARL did not regulate activation of the core BAX, BAK dependent apoptotic pathway, but it was required to keep in check the cristae remodelling pathway and to prevent mobilization of the cristae stores of cytochrome c during apoptosis. Since these results pointed to a role for PARL in the cristae remodelling pathway, regulated by OPA1, we ought to understand whether OPA1 required PARL to regulate apoptosis. OPA1 protected wt but not Parl-/- MEFs from apoptosis; furthermore, expression of OPA1 in Parl-/- MEFs did not reduce cytochrome c release, or mitochondrial depolarization following intrinsic stimuli. When Opa1 was silenced by siRNA in Parl-/- cells, they were no longer rescued by re-expression of PARL, demonstrating that PARL is genetically positioned upstream of OPA1. This genetic interaction was confirmed at multiple levels, since PARL and OPA1 interacted in a yeast two-hybrid and co-immunoprecipitation assays. PARL participated in the production of a soluble, IMS located, "anti-apoptotic" form of OPA1. The catalytic activity of PARL was required for the efficient production of soluble OPA1 and the re-introduction of a form of OPA1 in the IMS rescued the pro-apoptotic phenotype of Parl-/- cells. Thus, this IMS form resulted pivotal in controlling the pathway of cristae remodelling and cytocrome c redistribution. IMS and integral IM OPA1 indeed were both found to participate in the assembly of OPA1-containing oligomers that are early targets during cristae remodelling and greatly reduced in Parl /- mitochondria. The reduced level of OPA1 oligomers could account for the faster remodelling and cytochrome c mobilization observed in the absence of PARL. OPA1 affects complex cellular functions other than apoptosis, as substantiated in overexpression studies showing a role for this protein in movement of leukocytes (Campello et al., 2006) and formation of dendritic spines (Li et al., 2004). Furthermore, Opa1 knockout mice demonstrated that OPA1 is required for embryonic development. Homozygous mutant mice die in uterus at 13.5 dpc, with first notable developmental delay at E8.5 (Alavi et al., 2007). We therefore reasoned that levels of OPA1 are likely to affect development and function of multiple organs, by regulating mitochondrial fusion or apoptosis. In the last part of this Thesis, we therefore decided to study whether ablation of OPA1 influences differentiation of embryonic stem (ES) cells in vitro using a hanging-drop differentiation system. To this end, we analyzed an ES cell line where Opa1 had been gene trapped (Opa1gt), resulting in an Opa1+/- genotype. We compared the differentiation potential into cardiomyocytes and neurons of this Opa1gt ES cell line to its relative wt ES cell line. Opa1gt ES cells displayed a decreased capacity to differentiate into beating cardiomyocytes, while they retained a normal neuronal differentiation potential. These preliminary results indicate that OPA1 is a good candidate to regulate differentiation of ES cells in vitro. We now aim at understanding the molecular mechanism by which levels of OPA1 influence differentiation into cardiomyocytes. In conclusion, the data presented in this Thesis demonstrate genetically distinct roles of the mitochondrial dynamin related protein OPA1 in the regulation of organellar shape and apoptosis. The individuation that the functional axis between OPA1 and MFN1 (that regulates mitochondrial fusion) and the regulatory IMM network comprised of the couple substrate-protease Parl-Opa1 could perhaps even control embryonic differentiation opens novel, unexpected avenues to investigate the role of mitochondria in life and death of the cell.
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Katz, Elad. "Mitochondrial regulation of apoptosis during B cell selection." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327569.

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10

Okaro, Madubuchi Chiedu. "Mitochondrial directed apoptosis sensitising studies in cholangiocarcinoma cells." Thesis, University College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.412629.

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Книги з теми "Mitochondrial apoptosis":

1

Joza, Nicholas. Differential requirement for the mitochondrial apoptosis-inducing factor in apoptotic pathways. Ottawa: National Library of Canada, 2001.

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2

Wadia, Jehangir S. R(-)-deprenyl treatment blocks apoptosis in PC12 cells by affecting mitochondrial membrane potential, mitochondrial calcium and superoxide radical generation. Ottawa: National Library of Canada, 1996.

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3

Saavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Hauppauge, N.Y: Nova Science Publishers, 2010.

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Wadia, J. S. Changes in mitochondrial protein import during apoptosis. 2002.

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5

Lee, Hong Kyu, Salvatore DiMauro, Masashi Tanaka, and Yau-Huei Wei. Mitochondrial Pathogenesis: From Genes and Apoptosis to Aging and Disease. Springer London, Limited, 2014.

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6

Mitochondrial Pathogenesis: From Genes and Apoptosis to Aging and Disease (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2004.

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7

Seth, Rohit. Zinc deficiency induces apoptosis via mitochondrial p53- and caspase-dependent pathways in human neuronal precursor cells. Elseveir, 2014.

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8

Joza, Nicholas. Genetic elucidation of the roles of apoptosis-inducing factor (AIF) in mitochondrial respiration and programmed cell death. 2005.

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9

Korea) Asian Society for Mitochondrial Research and Medicine. Scientific Meeting (1st : 2003 : Seoul and Hong Kyu Lee. Mitochondrial Pathogenesis: From Genes and Apoptosis to Aging and Disease (Annals of the New York Academy of Sciences, V. 1011). New York Academy of Sciences, 2004.

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10

Lestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer, 2011.

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Частини книг з теми "Mitochondrial apoptosis":

1

Mignotte, B., and G. Kroemer. "Roles of Mitochondria in Apoptosis." In Mitochondrial Diseases, 239–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_18.

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2

Antonsson, Bruno. "The Mitochondrial Apoptosis Pathway." In Essentials of Apoptosis, 85–99. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-361-3_6.

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3

Peluso, G., O. Petillo, S. Margarucci, A. Calarco, and M. Calvani. "Deregulation of Mitochondrial Apoptosis in Cancer." In Mitochondrial Disorders, 71–87. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0929-8_7.

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Lee, Myung-Shik, Ja-Young Kim, and Sun Young Park. "Resistance of ρ0 Cells against Apoptosis." In Mitochondrial Pathogenesis, 146–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2_15.

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Cleland, Megan M., and Richard J. Youle. "Mitochondrial Dynamics and Apoptosis." In Mitochondrial Dynamics and Neurodegeneration, 109–38. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1291-1_4.

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6

Servidei, S., S. Di Giovanni, A. Broccolini, A. D’amico, M. Mirabella, and G. Silvestri. "Apoptosis and Oxidative Stress in Mitochondrial Disorders." In Mitochondrial Disorders, 37–45. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0929-8_4.

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Petit, Patrice X., and Guido Kroemer. "Mitochondrial Regulation of Apoptosis." In Mitochondrial DNA Mutations in Aging, Disease and Cancer, 147–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-12509-0_8.

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El-Osta, Hazem, and Magdalena L. Circu. "Mitochondrial ROS and Apoptosis." In Mitochondrial Mechanisms of Degeneration and Repair in Parkinson's Disease, 1–23. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-42139-1_1.

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Petit, Patrice Xavier, Naoufal Zamzami, Jean-Luc Vayssière, Bernard Mignotte, Guido Kroemer, and Maria Castedo. "Implication of mitochondria in apoptosis." In Detection of Mitochondrial Diseases, 185–88. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8_28.

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Campello, Silvia, and Luca Scorrano. "The Mitochondrial Pathway: Focus on Shape Changes." In Essentials of Apoptosis, 151–75. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-381-7_6.

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Тези доповідей конференцій з теми "Mitochondrial apoptosis":

1

Luo, Yu, Zhuoyan Zhang, and David Kessel. "Role of mitochondrial photodamage in PDT-induced apoptosis." In BiOS '98 International Biomedical Optics Symposium, edited by Thomas J. Dougherty. SPIE, 1998. http://dx.doi.org/10.1117/12.308138.

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Pourzia, Alexandra, Michael Olson, Stefanie Bailey, Aditi Aryal, Jeremy Ryan, Marcela Maus, and Anthony Letai MD. "269 Mitochondrial apoptosis mediates CAR T cell cytotoxicity." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0269.

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3

Zebo, Tang, Liu Yanbo, Li Chun, Wen Na, and Gai Xiaodong. "pLXSN-Tum-5 inducing HUVEC apoptosis through mitochondrial pathway." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027904.

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4

Lee, Yuan-Hao, Exing Wang, Neeru Kumar, and Randolph D. Glickman. "Ursolic acid mediates photosensitization by initiating mitochondrial-dependent apoptosis." In SPIE BiOS, edited by E. Duco Jansen and Robert J. Thomas. SPIE, 2013. http://dx.doi.org/10.1117/12.2000225.

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5

Hamacher-Brady, Anne, Verena Lang, and Nathan R. Brady. "Abstract 3324: FATE1 promotes mitochondrial hyperfusion and supports maintenance of mitochondrial networks following apoptosis stimulation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3324.

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6

Zhuang, Cai-ping, Qian Liang, Xiao-ping Wang, and Tong-sheng Chen. "Hydrogen peroxide induces apoptosis via a mitochondrial pathway in chondrocytes." In SPIE BiOS, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2012. http://dx.doi.org/10.1117/12.905786.

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Sui, Cliff, and Nada Boustany. "Potential application of the FDTD technique to study mitochondrial apoptosis." In Biomedical Optics (BiOS) 2007, edited by Adam Wax and Vadim Backman. SPIE, 2007. http://dx.doi.org/10.1117/12.702151.

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8

Kichkina, D. O., S. S. Patrushev, A. D. Moralev, E. E. Shults, M. A. Zenkova, and A. V. Markov. "NEW SEMISYNTHETIC SESQUITERPENE LACTONES AS INDUCERS OF OXIDATIVE STRESS IN TUMOR CELLS AND BLOCKERS OF THE AGGRESSIVE PHENOTYPE OF GLIOBLASTOMA MULTIFORME CELLS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-331.

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Анотація:
Screening for the antitumor potency of novel derivatives of isoalanotlactone revealed: (1) compound pat_651p, demonstrating high selectivity of action in respect to tumor cells and triggering oxidative stress and mitochondrial-dependent apoptosis in them; (2) compound pat_651_6p capable of passing through the blood-brain barrier and effectively inhibiting the motility, invasion, and adhesive traits of glioblastoma multiforme cells.
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Dasari, Venkata Ramesh, Swapna Asuthkar, Arun Kumar Nalla, and Jasti S. Rao. "Abstract 1731: Decreased cyclin B1 expression contributes to mitochondrial apoptosis in medulloblastoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1731.

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10

Hambright, Heather G., Addanki P. Kumar, and Rita Ghosh. "Abstract 5466: Mitochondrial superoxide inhibits autophagy and induces apoptosis through SQSTM1-mediated mechanism." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5466.

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Звіти організацій з теми "Mitochondrial apoptosis":

1

Myers, Charles. Mitochondrial Apoptosis: A New Foundation for Combining Agents in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada402436.

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2

Tweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality,Apoptosis, Inflammation and Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada612817.

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3

Tweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality, Apoptosis, Inflammation and Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, December 2012. http://dx.doi.org/10.21236/ada612818.

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4

Myers, Charles E. Mitochondrial Apoptosis: A New Foundation for Combing Agents in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, March 2000. http://dx.doi.org/10.21236/ada392324.

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5

Tweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality, Apoptosis, Inflammation and Mitochondrial Dysfunction Using IL-6 as a Resuscitation Adjuvant. Fort Belvoir, VA: Defense Technical Information Center, December 2011. http://dx.doi.org/10.21236/ada612819.

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6

Marassi, Francesca M. Structural Basis for Bc12-Regulated Mitochondrion-Dependent Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada437659.

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Marassi, Francesca M. Structural Basis for Bcl-2-Regulated Mitochondrion-Dependent Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada429719.

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8

Sick, Thomas J. Pro-Apoptotic Changes in Brain Mitochondria After Toxic Exposure. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada397717.

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9

Sick, Thomas J. Pro-Apoptotic Changes in Brain Mitochondria After Toxin Exposure. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada434079.

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Chandra, Dhyan. A Novel Mitochondria-Dependent Apoptotic Pathway (MAP) in Prostate Cancer (PCa) Cells. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada415386.

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