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Artykuły w czasopismach na temat "Apoptose mitochondriale"
Zweck, Elric, Julia Szendrödi, Malte Kelm i Michael Roden. "Das diabetische Herz und Herzinsuffizienz – Aktuelles zu Entstehung und Therapie". DMW - Deutsche Medizinische Wochenschrift 144, nr 03 (31.01.2019): 175–79. http://dx.doi.org/10.1055/a-0646-7871.
Pełny tekst źródłaAdhihetty, Peter J., Vladimir Ljubicic i 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, nr 3 (marzec 2007): E748—E755. http://dx.doi.org/10.1152/ajpendo.00311.2006.
Pełny tekst źródłaWissel, Kirsten, Elisabeth Berger, Gudrun Brandes, Gerrit Paasche, Thomas Lenarz i Martin Durisin. "Erratum: Wie beeinflussen Platin-Nanopartikel die Zellviabilität der Corti-Organ Zelllinie der Maus (HEI-OC1) und der Spiralganglienzellen postnataler Ratten in Kultur?" Laryngo-Rhino-Otologie 101, S 02 (maj 2022): e1-e2. http://dx.doi.org/10.1055/a-2004-8821.
Pełny tekst źródłaBreckenridge, David G., Marina Stojanovic, Richard C. Marcellus i Gordon C. Shore. "Caspase cleavage product of BAP31 induces mitochondrial fission through endoplasmic reticulum calcium signals, enhancing cytochrome c release to the cytosol". Journal of Cell Biology 160, nr 7 (31.03.2003): 1115–27. http://dx.doi.org/10.1083/jcb.200212059.
Pełny tekst źródłaBasu, Urmimala, Alicia M. Bostwick, Kalyan Das, Kristin E. Dittenhafer-Reed i Smita S. Patel. "Structure, mechanism, and regulation of mitochondrial DNA transcription initiation". Journal of Biological Chemistry 295, nr 52 (30.10.2020): 18406–25. http://dx.doi.org/10.1074/jbc.rev120.011202.
Pełny tekst źródłaKokkinopoulou, Ioanna, i Paraskevi Moutsatsou. "Mitochondrial Glucocorticoid Receptors and Their Actions". International Journal of Molecular Sciences 22, nr 11 (3.06.2021): 6054. http://dx.doi.org/10.3390/ijms22116054.
Pełny tekst źródłaKim, Sin Ri, Ji Won Park, You-Jin Choi, Seong Keun Sonn, Goo Taeg Oh, Byung-Hoon Lee i Tong-Shin Chang. "Mitochondrial H2O2 Is a Central Mediator of Diclofenac-Induced Hepatocellular Injury". Antioxidants 13, nr 1 (21.12.2023): 17. http://dx.doi.org/10.3390/antiox13010017.
Pełny tekst źródłaHeikaus, Sebastian, Linda van den Berg, Tobias Kempf, Csaba Mahotka, Helmut Erich Gabbert i Uwe Ramp. "HA14-1 is Able to Reconstitute the Impaired Mitochondrial Pathway of Apoptosis in Renal Cell Carcinoma Cell Lines". Analytical Cellular Pathology 30, nr 5 (1.01.2008): 419–33. http://dx.doi.org/10.1155/2008/693095.
Pełny tekst źródłaPeterson, Courtney M., Darcy L. Johannsen i Eric Ravussin. "Skeletal Muscle Mitochondria and Aging: A Review". Journal of Aging Research 2012 (2012): 1–20. http://dx.doi.org/10.1155/2012/194821.
Pełny tekst źródłaKroemer, Guido. "Heat Shock Protein 70 Neutralizes Apoptosis-Inducing Factor". Scientific World JOURNAL 1 (2001): 590–92. http://dx.doi.org/10.1100/tsw.2001.322.
Pełny tekst źródłaRozprawy doktorskie na temat "Apoptose mitochondriale"
Aure, Karine. "Physiopathologie moléculaire et cellulaire des maladies mitochondriales à présentation neurologique". Paris 6, 2007. http://www.theses.fr/2007PA066281.
Pełny tekst źródłaLandes, Thomas. "Dynamique mitochondriale et apoptose : rôle de l'interaction entre Opa1 et Bnip3". Toulouse 3, 2009. http://thesesups.ups-tlse.fr/671/.
Pełny tekst źródłaMitochondria are highly dynamic organelles that continually fuse and divide. Several studies suggest a link between mitochondrial dynamics and the intrinsic pathway of apoptosis, mediated by members of the Bcl-2 family, leading to the release of apoptogenic proteins, including cytochrome c, from the mitochondrial intermembrane space into the cytosol. We have previously identified Opa1 a dynamin of the inner membrane that regulates mitochondrial fusion. More recently, Opa1 has also been proposed to control, during apoptosis, cytochrome c redistribution through its capacity to locally form oligomers at mitochondrial cristae junctions. In this study, we identified Bnip3, a mitochondrial pro-apoptotic BH3-only protein of the Bcl-2 family, as a physical and functional partner of Opa1. Overall, our results give some insight into the relationship between mitochondrial dynamics and apoptosis and, in the future, may help to understand the aetiology of autosomal dominant optic atrophy, caused by Opa1 mutations
Desbourdes, Céline. "Nucléoside diphosphate kinase D : une protéine mitochondriale bifonctionnelle". Thesis, Université Grenoble Alpes (ComUE), 2017. http://www.theses.fr/2017GREAV004/document.
Pełny tekst źródłaThe nucleoside diphosphate kinases (NDPK) are essential for generation of nucleoside triphosphates (NTPs) using ATP and NDPs. The mitochondrial NDPK isoform (NDPK-D) located in the mitochondrial intermembrane space is found to have two modes of function. First, the phosphotransfer mode in which the protein has a kinase activity like other NDPK enzymes. In this mode, NDPK-D produces GTP for the optic atrophy 1 protein (OPA1), a GTPase involved in mitochondrial fusion, and ADP for the adenylate translocator (ANT) and the mitochondrial ATPase for ATP regeneration. The second mode of function is called lipid transfer and is related to the capacity of NDPK-D to bind anionic phospholipids, especially cardiolipin (CL). In this mode, the protein can cross-link the two mitochondrial membranes and transfer CL from the inner to the outer mitochondrial membrane, which can serve as a signal for mitophagy and apoptosis. This work aims to study these NDPK-D functions in more detail. With the use of HeLa cells stably expressing the wild-type, kinase inactive (H151N mutation) or lipid binding deficient (R90D mutation) NDPK-D and mouse lung epithelial cells, we show (i) the close proximity between NDPK-D and OPA1 that leads to GTP channeling from NDPK-D to OPA1, (ii) the essential role of NDPK-D for CL externalization to the mitochondrial surface during mitophagy, serving as a recognition signal for LC3-II-autophagosomes to eliminate damaged mitochondria, (iii) the possible inhibition of CL externalization due to the presence of NDPK-D/OPA1 complexes, and (iv) a pro-metastatic phenotype of HeLa cells expressing either of the NDPK-D mutants (H151N or R90D), characterized by high invasive and migratory potential, altered proteomic profile and changed mitochondrial network structure and function. Finally, a first bacterial expression and purification strategy for full-length OPA1 has been established for future in vitro studies of NDPK-D/OPA1 complexes
Olichon, Aurélien. "Morphologie mitochondriale : fonctions et dysfonctions de la dynamine humaine OPA1". Toulouse 3, 2004. http://www.theses.fr/2004TOU30295.
Pełny tekst źródłaMitochondria are essential organelles that provide energy to the cell and act as reservoirs of apoptogenic molecules. Mitochondrial morphology and dynamics are crucial for their function and their transmission, and drastically change during apoptosis. To explain the dynamic of the mitochondrial network morphology, a model conserved from yeast to human proposes that two antagonistic forces, fission versus fusion, are monitored by proteins localized on the mitochondrial outer membrane, such as Dnm1/DRP-1 or Fzo1/Mfn1-2. Conversely, dynamic of the inner membrane is largely unknown. Data on the large GTPase Msp1 in S. Pombe, OPA1 in human, and Mgm1 in S. Cerevisiae suggest that this dynamin related protein is involved in the inner-membrane structure and dynamic. We have isolated the OPA1 gene sequence encoding a human dynamin. Moreover, we have shown that OPA1 gene is mutated in patients suffering from an hereditary optic neuropathy leading to blindness (ADOA: Autosomal Dominant Optic Atrophy, OMIM 165500) My thesis project was to characterize OPA1 function in order to understand its dysfunction, impact on mitochondrial dynamics and function, and especially answer some questions about the pathological process of the ADOA. Orthology between OPA1 and Msp1 was confirmed by showing that OPA1 complements the lethal msp1 gene deletion in fission yeast. Using both biochemical and cytological approaches we have precisely localized OPA1 strongly associated with the inner membrane of the mitochondria, facing the innermembrane space. To investigate OPA1 dynamin function, we used total or selective downregulation or over-expression of wild type OPA1 variants or mutant, and showed that OPA1 could function in the inner-membrane dynamics and could have a role in structuring the cristae membrane. This later structural role suggests that OPA1 could be a key regulator of the mobilization of cytochrome c by remodeling the cristae membrane
Singh, François. "Skeletal muscle toxicity and statins : role of mitochondrial adaptations". Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ050/document.
Pełny tekst źródłaAlthough statins are the most prescribed class of lipid-lowering agents, adverse muscular toxicity has been reported, which can lead to the appearance of a myopathy. In the first part, we showed in Humans and animals that statins inhibit directly the mitochondrial respiratory chain, and induce the production of reactive oxygen species (ROS), that trigger apoptotic pathways in glycolytic skeletal muscles, whereas oxidative muscles are not impaired. We then showed in vitro that reductive stress can provoke mitochondrial oxidation, that could lead to an activation of mitochondrial biogenesis pathways. Moreover, the consequent increase in mitochondrial content enabled to protect cells against statin-induced apoptosis. Finally, we showed in vivo that the induction of mitochondrial biogenesis is necessary for statin tolerance in oxidative skeletal muscles. In conclusion, mitochondrial phenotype, both quantitatively and qualitatively, seems to be a key factor in the appearance of statin myopathy
Ferré, Cécile. "Mécanismes moléculaires et cellulaires à la base du pouvoir neuroprotecteur de la protéine "mitochondriale" X du bornavirus". Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30049/document.
Pełny tekst źródłaBornavirus, a non-cytolytic RNA virus establishes a long-lasting persistence in the central nervous system of infected animals. Viral persistence is facilitated by the expression of the non-structural X protein, which is addressed both to nucleus and mitochondria, where it interferes both with cellular antiviral responses and the initiation of apoptosis. Our team recently reported that the singled-out expression of the X protein could protect neurons against toxins of the mitochondrial respiratory chain, both in vitro and in a mouse model of Parkinson's disease (PD). During my Ph.D., we further demonstrated that the X protein triggered enhanced filamentation of the mitochondrial network, in physiological as well as in oxidative stress conditions. This effect is particularly interesting when considering the importance of mitochondrial dynamics in the pathophysiology of neurodegenerative diseases. Even if the therapeutic potential of this viral protein is now well established, the underlying molecular and cellular mechanisms are far from being elucidated. It is however clear that neuroprotection conferred by the X protein is strictly dependent on its mitochondrial localization. In this context, the goal of my Ph.D. project was to clarify the molecular mechanisms whereby the X protein is targeted to mitochondria and/or to the nucleus, in link with its protective capabilities. We focused on the amino terminal residues of X, by performing fusion proteins of various forms of these residues with GFP and by analyzing their cellular localization. We demonstrated that this region contains overlapping and interdependent signals for nuclear localization, nuclear export and mitochondrial targeting of the X protein. We also identified a point mutation or deletion leading to an almost exclusively mitochondrial localization of the X protein. As a consequence, these X mutants exhibited a better neuroprotective function. In order to get further insight into X-mediated neuroprotection, we also searched for the cellular partners of X in mitochondria. We revealed a direct and specific interaction of the X protein with the chaperone Hspa9, a protein that was recently shown to be involved in neurodegenerative diseases, notably in PD's patients. We observed that the down-regulation of Hspa9 triggered by mitochondrial toxins was attenuated by the coexpression of X, suggesting a functional link between these two proteins. We also demonstrated that Hspa9 overexpression could protect neurons from mitochondrial dysfunctions, similarly to the X protein. Altogether, these results have contributed to a better understanding of the mechanisms underlying the neuroprotective potential of the X protein, which may favor the development of novel therapeutic strategies
Carré, Manon. "Agents anti-tubuline et apoptose : du cytosquelette microtubulaire à la tubuline mitochondriale". Aix-Marseille 2, 2004. http://www.theses.fr/2004AIX22955.
Pełny tekst źródłaMartel, Cécile. "Rôle de la perméabilité membranaire mitochondriale, de la phosphorylation de VDAC et de la signalisation de l’apoptose dans la pathogenèse de la stéatose hépatique". Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T075.
Pełny tekst źródłaNon-alcoholic steatosis is a liver disease characterized by lipid accumulation in the cytoplasm of hepatocytes. For a long time, it has been considered as a benign condition. Now it is known that it can precede the development of a severe stage, non-alcoholic steatohepatitis (NASH). NASH is accompanied by severe dammages of the liver linked to the genesis of oxidative stress, inflammation and cell death. Mitochondrion is a central player of this disease; however, the knowledge of mitochondrial dysfunction and its consequences on apoptosis is still insufficient. Indeed, mitochondria are responsible for lipid degradation by -oxidation. Mitochondria act as a central integrator of apoptotic signals by triggering the mitochondrial membrane permeabilization (MMP) leading to the release of apoptogenic factors. This process is considered as the point of no return of the mitochondrial pathway of apoptosis. We aimed to better understand the molecular mechanisms linking mitochondrial liver apoptosis and steatosis. Combination of four experimental models of steatosis (human biopsies, isolated mitochondria from ob/ob obese mice, high fat diet-fed mice or hepatic cell lines) displayed, in steatotic livers, increased sensitivity to MMP induction and permeability of VDAC (Voltage dependent anion channel), a protein which forms a channel in the outer mitochondrial membrane. These findings are associated with the hypo-phosphorylation of VDAC on a threonine residue and the loss of its interaction with the anti-apoptotic Bcl-XL and GSK3 kinase, thus revealing a new lipid-induced signaling pathway. Our work is based on the use of functional assays on isolated mitochondria that we have developed and validated in several studies involving various strategies. To conclude, our study increases the knowledge on the lipid-induced mitochondrial weakness preceding hepatic apoptosis and opens perspectives in biomedical applications
Jelinek, Antje. "In-vitro-Toxizität grenzflächenaktiver Substanzen Wirkung auf Zellmembran, mitochondriale Funktion und Apoptose /". [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963587676.
Pełny tekst źródłaLefevre, Sophie. "Modèle levure de l'ataxie de Friedreich : stress oxydant, apoptose et dynamique mitochondriale". Paris 6, 2010. http://www.theses.fr/2010PA066204.
Pełny tekst źródłaKsiążki na temat "Apoptose mitochondriale"
Joza, Nicholas. Differential requirement for the mitochondrial apoptosis-inducing factor in apoptotic pathways. Ottawa: National Library of Canada, 2001.
Znajdź pełny tekst źródłaWadia, 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.
Znajdź pełny tekst źródłaSaavedra-Molina, Alfredo. Mitochondrial dysfunctions related to oxidative stress. Hauppauge, N.Y: Nova Science Publishers, 2010.
Znajdź pełny tekst źródłaLestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer, 2011.
Znajdź pełny tekst źródłaLestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer, 2011.
Znajdź pełny tekst źródłaLestienne, Patrick. Mitochondrial Diseases: Models and Methods. Springer London, Limited, 2012.
Znajdź pełny tekst źródłaLestienne, Patrick. Mitochondrial Diseases: Models and Methods. Redaktor Patrick Lestienne. SPRINGER-VERLAG, 1999.
Znajdź pełny tekst źródłaWadia, J. S. Changes in mitochondrial protein import during apoptosis. 2002.
Znajdź pełny tekst źródła(Editor), Guy C. Brown, David G. Nicholls (Editor) i Chris E. Cooper (Editor), red. Mitochondria and Cell Death. Princeton University Press, 1999.
Znajdź pełny tekst źródłaLee, Hong Kyu, Salvatore DiMauro, Masashi Tanaka i Yau-Huei Wei. Mitochondrial Pathogenesis: From Genes and Apoptosis to Aging and Disease. Springer London, Limited, 2014.
Znajdź pełny tekst źródłaCzęści książek na temat "Apoptose mitochondriale"
Mignotte, B., i G. Kroemer. "Roles of Mitochondria in Apoptosis". W Mitochondrial Diseases, 239–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59884-5_18.
Pełny tekst źródłaPeluso, G., O. Petillo, S. Margarucci, A. Calarco i M. Calvani. "Deregulation of Mitochondrial Apoptosis in Cancer". W Mitochondrial Disorders, 71–87. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0929-8_7.
Pełny tekst źródłaLee, Myung-Shik, Ja-Young Kim i Sun Young Park. "Resistance of ρ0 Cells against Apoptosis". W Mitochondrial Pathogenesis, 146–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2_15.
Pełny tekst źródłaServidei, S., S. Di Giovanni, A. Broccolini, A. D’amico, M. Mirabella i G. Silvestri. "Apoptosis and Oxidative Stress in Mitochondrial Disorders". W Mitochondrial Disorders, 37–45. Paris: Springer Paris, 2002. http://dx.doi.org/10.1007/978-2-8178-0929-8_4.
Pełny tekst źródłaAntonsson, Bruno. "The Mitochondrial Apoptosis Pathway". W Essentials of Apoptosis, 85–99. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-361-3_6.
Pełny tekst źródłaCleland, Megan M., i Richard J. Youle. "Mitochondrial Dynamics and Apoptosis". W Mitochondrial Dynamics and Neurodegeneration, 109–38. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1291-1_4.
Pełny tekst źródłaFernández-Checa, Jose C., i Carmen Garcia-Ruiz. "Apoptosis and Mitochondria". W Signaling Pathways in Liver Diseases, 439–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_29.
Pełny tekst źródłaPetit, Patrice Xavier, Naoufal Zamzami, Jean-Luc Vayssière, Bernard Mignotte, Guido Kroemer i Maria Castedo. "Implication of mitochondria in apoptosis". W Detection of Mitochondrial Diseases, 185–88. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6111-8_28.
Pełny tekst źródłaPetit, Patrice X., i Guido Kroemer. "Mitochondrial Regulation of Apoptosis". W 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.
Pełny tekst źródłaEl-Osta, Hazem, i Magdalena L. Circu. "Mitochondrial ROS and Apoptosis". W 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.
Pełny tekst źródłaStreszczenia konferencji na temat "Apoptose mitochondriale"
Kichkina, D. O., S. S. Patrushev, A. D. Moralev, E. E. Shults, M. A. Zenkova i 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". W 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.
Pełny tekst źródłaLiu, G., S. Soberanes, N. Bruce, SA Weitzman, GR Budinger, PT Schumacker i DW Kamp. "A Mitochondria-Targeted DNA Repair Enzyme, hOgg1, Prevents Oxidant-Induced Alveolar Epithelial Cell Apoptosis by Chaperoning and Preserving Mitochondrial Aconitase." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4178.
Pełny tekst źródłaLuo, Yu, Zhuoyan Zhang i David Kessel. "Role of mitochondrial photodamage in PDT-induced apoptosis". W BiOS '98 International Biomedical Optics Symposium, redaktor Thomas J. Dougherty. SPIE, 1998. http://dx.doi.org/10.1117/12.308138.
Pełny tekst źródłaPourzia, Alexandra, Michael Olson, Stefanie Bailey, Aditi Aryal, Jeremy Ryan, Marcela Maus i Anthony Letai MD. "269 Mitochondrial apoptosis mediates CAR T cell cytotoxicity". W SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0269.
Pełny tekst źródłaHamacher-Brady, Anne, Verena Lang i Nathan R. Brady. "Abstract 3324: FATE1 promotes mitochondrial hyperfusion and supports maintenance of mitochondrial networks following apoptosis stimulation". W 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.
Pełny tekst źródłaZebo, Tang, Liu Yanbo, Li Chun, Wen Na i Gai Xiaodong. "pLXSN-Tum-5 inducing HUVEC apoptosis through mitochondrial pathway". W 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027904.
Pełny tekst źródłaLee, Yuan-Hao, Exing Wang, Neeru Kumar i Randolph D. Glickman. "Ursolic acid mediates photosensitization by initiating mitochondrial-dependent apoptosis". W SPIE BiOS, redaktorzy E. Duco Jansen i Robert J. Thomas. SPIE, 2013. http://dx.doi.org/10.1117/12.2000225.
Pełny tekst źródłaZhuang, Cai-ping, Qian Liang, Xiao-ping Wang i Tong-sheng Chen. "Hydrogen peroxide induces apoptosis via a mitochondrial pathway in chondrocytes". W SPIE BiOS, redaktorzy Daniel L. Farkas, Dan V. Nicolau i Robert C. Leif. SPIE, 2012. http://dx.doi.org/10.1117/12.905786.
Pełny tekst źródłaSui, Cliff, i Nada Boustany. "Potential application of the FDTD technique to study mitochondrial apoptosis". W Biomedical Optics (BiOS) 2007, redaktorzy Adam Wax i Vadim Backman. SPIE, 2007. http://dx.doi.org/10.1117/12.702151.
Pełny tekst źródłaKamp, David, Paul Cheresh, Humberto Trejo, Katie Knister, Jing Liu i Anna Lam. "Asbestos-Induced Alveolar Epithelial Cell Apoptosis: Mitochondria-ER Crosstalk". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4277.
Pełny tekst źródłaRaporty organizacyjne na temat "Apoptose mitochondriale"
Myers, Charles. Mitochondrial Apoptosis: A New Foundation for Combining Agents in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, marzec 2001. http://dx.doi.org/10.21236/ada402436.
Pełny tekst źródłaTweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality,Apoptosis, Inflammation and Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2013. http://dx.doi.org/10.21236/ada612817.
Pełny tekst źródłaTweardy, David J. Prevention of Trauma/Hemorrhagic Shock-Induced Mortality, Apoptosis, Inflammation and Mitochondrial Dysfunction. Fort Belvoir, VA: Defense Technical Information Center, grudzień 2012. http://dx.doi.org/10.21236/ada612818.
Pełny tekst źródłaMyers, Charles E. Mitochondrial Apoptosis: A New Foundation for Combing Agents in Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, marzec 2000. http://dx.doi.org/10.21236/ada392324.
Pełny tekst źródłaTweardy, 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, grudzień 2011. http://dx.doi.org/10.21236/ada612819.
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