Auswahl der wissenschaftlichen Literatur zum Thema „Mitochondria fusion“
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Zeitschriftenartikel zum Thema "Mitochondria fusion"
Murata, Daisuke, Kenta Arai, Miho Iijima und Hiromi Sesaki. „Mitochondrial division, fusion and degradation“. Journal of Biochemistry 167, Nr. 3 (04.12.2019): 233–41. http://dx.doi.org/10.1093/jb/mvz106.
Der volle Inhalt der QuelleSeo, Young Ah, Veronica Lopez und Shannon L. Kelleher. „A histidine-rich motif mediates mitochondrial localization of ZnT2 to modulate mitochondrial function“. American Journal of Physiology-Cell Physiology 300, Nr. 6 (Juni 2011): C1479—C1489. http://dx.doi.org/10.1152/ajpcell.00420.2010.
Der volle Inhalt der QuelleTwig, Gilad, Xingguo Liu, Marc Liesa, Jakob D. Wikstrom, Anthony J. A. Molina, Guy Las, Gal Yaniv, György Hajnóczky und Orian S. Shirihai. „Biophysical properties of mitochondrial fusion events in pancreatic β-cells and cardiac cells unravel potential control mechanisms of its selectivity“. American Journal of Physiology-Cell Physiology 299, Nr. 2 (August 2010): C477—C487. http://dx.doi.org/10.1152/ajpcell.00427.2009.
Der volle Inhalt der QuelleHaseeb, Abdul, Hong Chen, Yufei Huang, Ping Yang, Xuejing Sun, Adeela Iqbal, Nisar Ahmed et al. „Remodelling of mitochondria during spermiogenesis of Chinese soft-shelled turtle (Pelodiscus sinensis)“. Reproduction, Fertility and Development 30, Nr. 11 (2018): 1514. http://dx.doi.org/10.1071/rd18010.
Der volle Inhalt der QuelleHiguchi-Sanabria, Ryo, Joseph K. Charalel, Matheus P. Viana, Enrique J. Garcia, Cierra N. Sing, Andrea Koenigsberg, Theresa C. Swayne et al. „Mitochondrial anchorage and fusion contribute to mitochondrial inheritance and quality control in the budding yeast Saccharomyces cerevisiae“. Molecular Biology of the Cell 27, Nr. 5 (März 2016): 776–87. http://dx.doi.org/10.1091/mbc.e15-07-0455.
Der volle Inhalt der QuelleZheng, Yunsi, Anqi Luo und Xiaoquan Liu. „The Imbalance of Mitochondrial Fusion/Fission Drives High-Glucose-Induced Vascular Injury“. Biomolecules 11, Nr. 12 (27.11.2021): 1779. http://dx.doi.org/10.3390/biom11121779.
Der volle Inhalt der QuelleKnorre, Dmitry A., Konstantin Y. Popadin, Svyatoslav S. Sokolov und Fedor F. Severin. „Roles of Mitochondrial Dynamics under Stressful and Normal Conditions in Yeast Cells“. Oxidative Medicine and Cellular Longevity 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/139491.
Der volle Inhalt der QuelleKeng, T., E. Alani und L. Guarente. „The nine amino-terminal residues of delta-aminolevulinate synthase direct beta-galactosidase into the mitochondrial matrix“. Molecular and Cellular Biology 6, Nr. 2 (Februar 1986): 355–64. http://dx.doi.org/10.1128/mcb.6.2.355-364.1986.
Der volle Inhalt der QuelleKeng, T., E. Alani und L. Guarente. „The nine amino-terminal residues of delta-aminolevulinate synthase direct beta-galactosidase into the mitochondrial matrix.“ Molecular and Cellular Biology 6, Nr. 2 (Februar 1986): 355–64. http://dx.doi.org/10.1128/mcb.6.2.355.
Der volle Inhalt der QuelleEisner, Verónica, Guy Lenaers und György Hajnóczky. „Mitochondrial fusion is frequent in skeletal muscle and supports excitation–contraction coupling“. Journal of Cell Biology 205, Nr. 2 (21.04.2014): 179–95. http://dx.doi.org/10.1083/jcb.201312066.
Der volle Inhalt der QuelleDissertationen zum Thema "Mitochondria fusion"
Heller, Anne Sabine [Verfasser], und Achim [Akademischer Betreuer] Göpferich. „Targeting mitochondria by mitochondrial fusion, mitochondria-specific peptides and nanotechnology / Anne Sabine Heller. Betreuer: Achim Göpferich“. Regensburg : Universitätsbibliothek Regensburg, 2013. http://d-nb.info/103321664X/34.
Der volle Inhalt der QuelleMacchi, Marc. „Contribution à l' étude de la morphogénèse des mitochondries chez la drosophile“. Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4051/document.
Der volle Inhalt der QuelleMitochondria are organelles which are a few micrometers long and are originated from the incorporation of an alpha-proteobacteria in the cytoplasm of eukaryotic cells through endosymbiosis. In eukaryotic cells, mitochondria play a central role in ATP production as well as in programmed cell death and in the biosynthesis of many molecules. Mitochondria are highly polymorphic in size and form. Their organization also varies considerably according to the cell type or physiological or pathological state of the cell. In the last two decades, the study of the mechanisms controlling morphogenesis, dynamic of mitochondrial fission and fusion and their physiological roles has become a major research field of mitochondria. In addition, the progress in video-microscopy enable to record mitochondrial dynamics in the cytoplasm of living cells. I participated in the research on the characterization of gene function called Pantagruelian Mitochondria I (PMI), a novel determinant of the mitochondrial morphology that we discovered in Drosophila. PMI, a protein of the inner membrane, is involved in its membrane organization and essential to form tubular mitochondria. I also contributed to the development of experimental tools and protocols to visualize and study the mitochondrial dynamics in living Drosophila embryos. Interestingly, a stereotyped process of mitochondrial remodeling during Drosophila embryogenesis has been found and it raised a question about its role in developmental processes through my work
Sauvanet, Cécile. „Caractérisation des acteurs et des mécanismes de la fusion mitochondriale“. Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21883/document.
Der volle Inhalt der QuelleMitochondria are dynamic organelles that continuously fuse and divide. This dynamic is required for mitochondrial biogenesis, function and degradation. The cross-talk between OXPHOS and dynamics and the mechanisms ensuring modulation of dynamics remain largely unraveled. We have investigated the relationship between fusion and OXPHOS in yeast cells carrying point mutations in the mitochondrial ATP6 gene that are associated to human diseases. We show that OXPHOS defects provoke severe defects of inner membrane, but not outer membrane fusion. Selective inhibition of inner membrane fusion can be recapitulated by ionophores that dissipate the inner membrane potential, but not by inhibitors of OXPHOS. We show a dominant inhibition of fusion that further provides a mechanism for the exclusion of defective mitochondria from the functional mitochondrial network, a pre-requisite for their selective targeting to mitophagy. These results suggest that defects of fusion could contribute to the pathology of diseases caused by mtDNA mutations. Moreover, these results imply that in cells, inhibition of dominant fusion could allow the exclusion of dysfunctional mitochondria mitochondrial network. Mitochondrial fusion involves many proteins of the superfamily of dynamin. If these proteins have been identified, the molecular mechanisms of fusion remain undetermined. In order to understand these mechanisms, we choose to characterize Mitofusin 1 and 2 proteins, essential for outer mitochondrial membrane fusion. These transmembrane proteins are consisting of two coiled-coil domains and one N-terminal GTPase domain. We have characterized GTPase activity of Mitofusin and reconstituted Mitofusins or fragments of Mitofusins into liposomes to study their capacity to fuse these liposomes. Full-length mitofusins can fuse liposomes containing cardiolipins. Surprisingly, these fusion events are independent of GTP but require Mg2+ in the buffer. Using electron microscopy, we show that mitofusin 1 and 2 induce local deformation of liposomes. This capacity of mitofusins to locally create highly curved (and thus fusogenic) membrane regions opens a new angle to understand the molecular mechanisms of mitochondrial fusion
Wang, Xinglong. „Impaired Balance of Mitochondria Fission and Fusion in Alzheimer Disease“. Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1228318762.
Der volle Inhalt der QuelleDe, Vecchis Dario. „Gaining insights into mitochondrial membrane fusion through a structural and dynamic atomistic model of the mitofusin Fzo1p“. Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC001.
Der volle Inhalt der QuelleMitochondria are dynamic organelles whose morphology is determined by fusion and fission of their membranes. This essential process is known as mitochondrial dynamics. Defects in mitochondrial dynamics are associated with neurological disorders making the investigation of physiological relevance. However, the precise sequence of events that lead mitochondrial dynamics are still not well characterised. Fzo1p, a large GTPase of the Dynamin-Related Proteins superfamily, is a key component in mitochondrial outer membrane fusion in yeast. During this PhD project I built a model of the protein Fzo1p. The structure and dynamics of the model was investigated through molecular modelling and all-atom molecular dynamics simulation in a fully hydrated lipid bilayer environment. The Fzo1p structural model integrates information from several template structures, experimental knowledge, as well as ab initio models of the transmembrane segments. The model is validated experimentally through directed mutagenesis, for instance charge-swap mutations confirm predicted long-distance salt bridges. A series of mutants indicate that coiled-coil domains are required for protein function at variance with its N-terminal region. Overall, the experimental and in silico approaches pinpoint the hinge domains involved in the putative conformational change and identifies critical residues affecting protein stability. Finally, key Fzo1p-GDP interactions provide insights about the molecular mechanism of membrane fusion catalysis. The model provides insight on atomic level and proposes a structure that will be instructional to understanding mitochondrial membrane fusion
Macchi, Marc. „Contribution à l' étude de la morphogénèse des mitochondries chez la drosophile“. Electronic Thesis or Diss., Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4051.
Der volle Inhalt der QuelleMitochondria are organelles which are a few micrometers long and are originated from the incorporation of an alpha-proteobacteria in the cytoplasm of eukaryotic cells through endosymbiosis. In eukaryotic cells, mitochondria play a central role in ATP production as well as in programmed cell death and in the biosynthesis of many molecules. Mitochondria are highly polymorphic in size and form. Their organization also varies considerably according to the cell type or physiological or pathological state of the cell. In the last two decades, the study of the mechanisms controlling morphogenesis, dynamic of mitochondrial fission and fusion and their physiological roles has become a major research field of mitochondria. In addition, the progress in video-microscopy enable to record mitochondrial dynamics in the cytoplasm of living cells. I participated in the research on the characterization of gene function called Pantagruelian Mitochondria I (PMI), a novel determinant of the mitochondrial morphology that we discovered in Drosophila. PMI, a protein of the inner membrane, is involved in its membrane organization and essential to form tubular mitochondria. I also contributed to the development of experimental tools and protocols to visualize and study the mitochondrial dynamics in living Drosophila embryos. Interestingly, a stereotyped process of mitochondrial remodeling during Drosophila embryogenesis has been found and it raised a question about its role in developmental processes through my work
Norton, Matthew. „Genome-wide RNAi Screen Identifies Romo1 as a Novel Regulator of Mitochondrial Fusion and Cristae Integrity“. Thesis, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23701.
Der volle Inhalt der QuelleNguyen, Phuc Minh Chau. „Fusion Mitochondriale et Effets Vasculaires : rôle de OPA 1 dans l'hypertension artérielle et le vieillissement“. Thesis, Angers, 2015. http://www.theses.fr/2015ANGE0073.
Der volle Inhalt der QuelleDefects in mitochondrial dynamics have been associated with various disorders, including cardiovascular diseases. OPA1 is essential for mitochondrial inner membrane fusion. Mutation in Opa1 is associated with the autosomal dominant optic atrophy (ADOA). Since then, OPA1 has been reported to be associated with cell apoptosis, cell proliferation, mitochondrial ATP synthesis, calcium homeostasis and ROS production. These data suggest that OPA1 has a potential role in vascular cells and subsequently affects vascular function. On the other hand,OPA1 is also associated with age-related changes of mitochondria and simultaneously contribute to the development of many dysfunctions in different organs. In this study, we investigated impacts of OPA1 mutation on vascular function in physiological and pathological condition like hypertension and vascular aging. By using an Opa1+/- heterozygote mouse model, we show that the OPA1 protein plays a protective role in the vascular system. Indeed, Opa1+/- mice developed a hypertension more severe than WT mice which was associated with more important endothelial dysfunction and altered vascular remodeling. In addition, although initial vascular function was normal, at 12 months, Opa1+/- mice displayed vascular dysfunction which might predict onset of vascular diseases at a later time. These results suggest for the first time that mitochondrial dynamics might play an important role in vascular function and adaptation in pathological conditions and in vascular aging. More studies are needed to clarify the role of the protein OPA1 in hypertension. These data may help to identify novel therapeutic targets to prevent complications of hypertension and vascular age-related diseases
Frezza, Christian. „OPA1, a mitochondrial pro-fusion protein, regulates the cristae remodelling pathway during apoptosis“. Doctoral thesis, Università degli studi di Padova, 2007. http://hdl.handle.net/11577/3426739.
Der volle Inhalt der QuelleAlsayyah, Cynthia. „Régulation de la fusion mitochondriale par le Système Ubiquitine Protéasome et les contacts physiques mitochondrie - peroxysomes chez la levure Saccharomyces cerevisiae“. Electronic Thesis or Diss., Université Paris sciences et lettres, 2021. https://theses.hal.science/tel-03810525.
Der volle Inhalt der QuelleMitochondria are highly dynamic organelles that undergo constant fission and fusion of their outer and inner membranes. These processes are critical to maintain essential mitochondrial functions such as oxidative phosphorylation or calcium signaling. On a molecular basis, mitochondrial fusion and fission both depend on large GTPases of the Dynamin-Related Protein (DRP) family. The DRPs that mediate attachment and fusion of mitochondrial outer membranes are called the Mitofusins. The yeast mitofusin Fzo1 is located in the mitochondrial outer membrane. Its oligomerization promotes mitochondrial tethering followed by mitochondrial outer membrane fusion. Fzo1 has recently been proposed as a potential tether between peroxisomes and mitochondria when overexpressed. However, whether Fzo1 is present on peroxisomal membranes in WT cells or whether this extra-mitochondrial localization is a consequence of overexpression is unknown. In addition, we still don’t know how peroxisomal and mitochondrial Fzo1 mediate these contacts and their purpose in the cell. In my thesis, we were able to prove that Fzo1 naturally localizes to peroxisomes and oligomerizes with the mitochondrial Fzo1 thus creating Fzo1-Fzo1 contacts between peroxisomes and mitochondria which we will now call “Fzo1-mediated permit” contacts. We found that these contacts are modulated by Fzo1 levels which are tightly regulated by an SCF ubiquitin ligase called Mdm30 but also depending on fatty acid desaturation levels in the cell. From a functional standpoint, we found that the role of Fzo1-mediated permit contacts is to regulate mitochondrial fusion through the glyoxylate cycle, a process which allows cells to convert C2 unit compounds to C4 precursors for amino acid and carbohydrate biosynthesis. We discovered that Fzo1-mediated permit contacts allow the mitochondrial transfer of early byproducts of the glyoxylate cycle to stimulate mitochondrial fusion. In fine, the results obtained during my thesis enriched our knowledge on organelle contacts and allowed us to prove that Fzo1 is localized on both mitochondrial and peroxisomal membranes in wild type cells. Our studies also show that Fzo1-mediated permit contacts are modulated according to the cell’s needs as they play a crucial role in upkeeping mitochondrial fusion by providing a possible shortcut for byproducts of the glyoxylate cycle to reach mitochondria when direly needed
Bücher zum Thema "Mitochondria fusion"
Zick, Michael. Roles of the isoforms of the dynamin-like GTPases Mgm1/OPA1 in mitochondrial fusion. 2011.
Den vollen Inhalt der Quelle findenHill, Geoffrey E. Mitonuclear Ecology. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198818250.001.0001.
Der volle Inhalt der QuelleHinder, Lucy M., Kelli A. Sullivan, Stacey A. Sakowski und Eva L. Feldman. Mechanisms Contributing to the Development and Progression of Diabetic Polyneuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0114.
Der volle Inhalt der QuelleBuchteile zum Thema "Mitochondria fusion"
Ichikawa, H., L. Tanno-Suenaga und J. Imamura. „Transfer of Mitochondria Through Protoplast Fusion“. In Plant Protoplasts and Genetic Engineering II, 360–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74454-9_21.
Der volle Inhalt der QuelleKennedy, Barry E., Mark Charman und Barbara Karten. „Measurement of Mitochondrial Cholesterol Import Using a Mitochondria-Targeted CYP11A1 Fusion Construct“. In Methods in Molecular Biology, 163–84. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6875-6_12.
Der volle Inhalt der QuelleKarbowski, Mariusz. „Mitochondria on Guard: Role of Mitochondrial Fusion and Fission in the Regulation of Apoptosis“. In Advances in Experimental Medicine and Biology, 131–42. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6706-0_8.
Der volle Inhalt der QuelleGriparic, Lorena, Brian Head und Alexander M. van der Bliek. „Mitochondrial fission and fusion machineries“. In Mitochondrial Function and Biogenesis, 227–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/b95718.
Der volle Inhalt der QuelleMeeusen, Shelly L., und Jodi Nunnari. „Mitochondrial Fusion In Vitro“. In Methods in Molecular Biology, 461–66. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-365-3_32.
Der volle Inhalt der QuelleChan, Eliana Y. L., Jarungjit Rujiviphat und G. Angus McQuibban. „The Genetics of Mitochondrial Fusion and Fission“. In Mitochondrial Dynamics and Neurodegeneration, 1–46. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1291-1_1.
Der volle Inhalt der QuelleGiannakis, Konstantinos, und Theodore Andronikos. „Mitochondrial Fusion Through Membrane Automata“. In Advances in Experimental Medicine and Biology, 163–72. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09012-2_10.
Der volle Inhalt der QuelleLenaers, Guy, Dominique Bonneau, Cécile Delettre, Patrizia Amati-Bonneau, Emmanuelle Sarzi, Dan Miléa, Christophe Verny, Vincent Procaccio, Christian Hamel und Pascal Reynier. „Neurological Diseases Associated with Mutations in the Mitochondrial Fusion Machinery“. In Mitochondrial Dynamics and Neurodegeneration, 169–96. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1291-1_6.
Der volle Inhalt der QuelleChu, Charleen T., und Sarah B. Berman. „Mitochondrial Fission-Fusion and Parkinson’s Disease: A Dynamic Question of Compensatory Networks“. In Mitochondrial Dynamics and Neurodegeneration, 197–213. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1291-1_7.
Der volle Inhalt der QuelleSamanas, Nyssa Becker, und Suzanne Hoppins. „Cell-Free Analysis of Mitochondrial Fusion by“. In Methods in Molecular Biology, 129–40. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0676-6_10.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Mitochondria fusion"
Waggoner, AA, A. Wright, T. Moore, SA Gebb, J. King, G. Wilson und MN Gillespie. „A Fusion Protein Construct Targeting a DNA Repair Enzyme to Mitochondria Protects Against Oxidant-Induced Edema Formation in Perfused Rat Lungs.“ In 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.a5559.
Der volle Inhalt der QuelleChouteau, Joshua, Olena Gorodnya, Mykhaylo Ruchko, Boniface Obiako, Glenn Wilson und Mark N. Gillespie. „Novel Fusion Protein Constructs Targeting DNA Repair Enzymes To Mitochondria Protect Against Pseudomonas Aeruginosa-Induced Acute Lung Injury In Intact Rats“. In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3763.
Der volle Inhalt der QuelleSuzuki, Sozo, Kazuo Mori, Koji Sugai, Yasuyuki Akutsu, Masaaki Ishikawa, Hideaki Sakai und Katsuhide Hiwatashi. „ELECTRONMICROSCOPIC STUDIES ON PLATELETS AND MEGAKARYOCYTES IN GIANT PLATELET SYNDROME“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644560.
Der volle Inhalt der QuelleSchwarz, Johannes, und Oliver Eickelberg. „Mitochondrial Fusion Processes Modulate Lung Fibroblast Activation“. In 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.a1926.
Der volle Inhalt der QuelleKim, So Ri, Yong Chul Lee, Hae Jin Park, Dong Im Kim und Soon Ha Kim. „Mitochondrial fusion in the pathogenesis of severe asthma with fungal sensitization“. In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa1082.
Der volle Inhalt der QuelleChang, Zee-Fen. „Abstract 1402: NME3 links mitochondrial fusion to DNA repair in nuclear genome“. 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.am2017-1402.
Der volle Inhalt der QuelleGraves, J. Anthony, Kristi D. Rothermund, Yudong Wang, Jennifer Elster, Jerry Vockley, Bennett Van Houten und Edward V. Prochownik. „Abstract 1259: c-Myc influences mitochondrial structure and function by regulating fusion and fission“. In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1259.
Der volle Inhalt der QuelleArumugam, P. I., M. Wessendarp, Y. Ma, M. Imbrogno, M. Collins, B. C. Carey, J. Stock, C. Chalk, B. C. Trapnell und M. D. Filippi. „GM-CSF Is Required for Regulation of Mitochondrial Fusion, Fission, and Mitophagy in Macrophages“. In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2600.
Der volle Inhalt der QuelleNguyen, Nicholas D., Meifang Yu, Tara N. Fujimoto, Abagail Delahoussaye, Yanqing Huang, Manuel A. Estrada und Cullen M. Taniguchi. „Abstract 555: Mitochondrial fusion exertsKRAS-dependent therapeutic synergy with gemcitabine/nab-paclitaxel in preclinical models of pancreatic cancer“. In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-555.
Der volle Inhalt der QuelleLyu, Mi-Ae, Lawrence H. Cheung, John W. Marks und Michael G. Rosenblum. „Abstract 2579: Bax345/BLyS: A novel, completely human fusion construct targeting malignant B cells and delivering a unique mitochondrial toxin“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2579.
Der volle Inhalt der QuelleBerichte der Organisationen zum Thema "Mitochondria fusion"
Izhar, Shamay, Maureen Hanson und Nurit Firon. Expression of the Mitochondrial Locus Associated with Cytoplasmic Male Sterility in Petunia. United States Department of Agriculture, Februar 1996. http://dx.doi.org/10.32747/1996.7604933.bard.
Der volle Inhalt der QuelleGranot, David, Richard Amasino und Avner Silber. Mutual effects of hexose phosphorylation enzymes and phosphorous on plant development. United States Department of Agriculture, Januar 2006. http://dx.doi.org/10.32747/2006.7587223.bard.
Der volle Inhalt der QuelleSadot, Einat, Christopher Staiger und Mohamad Abu-Abied. Studies of Novel Cytoskeletal Regulatory Proteins that are Involved in Abiotic Stress Signaling. United States Department of Agriculture, September 2011. http://dx.doi.org/10.32747/2011.7592652.bard.
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