Relevant bibliographies by topics / Transfert de mitochondries

Contents

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

Academic literature on the topic 'Transfert de mitochondries'

Author: Grafiati
Published: 4 June 2021
Last updated: 3 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Transfert de mitochondries.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Transfert de mitochondries"

1

GUEGUEN, N., L. LEFAUCHEUR, and P. HERPIN. "Relations entre fonctionnement mitochondrial et types contractiles des fibres musculaires." INRAE Productions Animales 19, no. 4 (September 13, 2006): 265–78. http://dx.doi.org/10.20870/productions-animales.2006.19.4.3494.

Full text
Abstract:
Le muscle, tissu d’importance économique majeure chez les animaux producteurs de viande, est un tissu composite comprenant en majeure partie des fibres musculaires qui constituent une population très hétérogène aux caractéristiques contractiles et métaboliques variées. Les relations entre type contractile des fibres et fonctionnement mitochondrial, un composant essentiel du métabolisme énergétique musculaire, restent mal connues. Leur compréhension est pourtant essentielle pour espérer mieux maîtriser l’impact du type de fibres sur les diverses composantes de la qualité de la viande. Une analyse fine de la composante mitochondriale du fonctionnement énergétique des fi-bres a donc été entreprise en relation avec leurs caractéristiques contractiles. Les résultats indiquent que, contrairement aux fibres rapides de types IIX et IIB, la régulation mitochondriale dans les fibres lentes de type I et, dans une moindre mesure, de type rapide IIA est hautement spécialisée avec une optimisation de l’efficacité des mitochondries (couplage entre oxydation et phosphorylation, capacité oxydative maximale), une restriction de leur perméabilité à l’ADP et un couplage fonctionnel entre les kinases mitochondriales et la production d’ATP, permettant un transfert efficace de l’énergie vers les myosines. De plus, la régulation mitochondriale et les transferts énergétiques sont modulés par l’activation calcium-dépendante des ATPases portées par les myosines.
APA, Harvard, Vancouver, ISO, and other styles
2

Lin, Tsu-Kung, Shang-Der Chen, Yao-Chung Chuang, Min-Yu Lan, Jiin-Haur Chuang, Pei-Wen Wang, Te-Yao Hsu, et al. "Mitochondrial Transfer of Wharton’s Jelly Mesenchymal Stem Cells Eliminates Mutation Burden and Rescues Mitochondrial Bioenergetics in Rotenone-Stressed MELAS Fibroblasts." Oxidative Medicine and Cellular Longevity 2019 (May 22, 2019): 1–17. http://dx.doi.org/10.1155/2019/9537504.

Full text
Abstract:
Wharton’s jelly mesenchymal stem cells (WJMSCs) transfer healthy mitochondria to cells harboring a mitochondrial DNA (mtDNA) defect. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is one of the major subgroups of mitochondrial diseases, caused by the mt.3243A>G point mutation in the mitochondrial tRNALeu(UUR) gene. The specific aim of the study is to investigate whether WJMSCs exert therapeutic effect for mitochondrial dysfunction in cells of MELAS patient through donating healthy mitochondria. We herein demonstrate that WJMSCs transfer healthy mitochondria into rotenone-stressed fibroblasts of a MELAS patient, thereby eliminating mutation burden and rescuing mitochondrial functions. In the coculture system in vitro study, WJMSCs transferred healthy mitochondria to rotenone-stressed MELAS fibroblasts. By inhibiting actin polymerization to block tunneling nanotubes (TNTs), the WJMSC-conducted mitochondrial transfer was abrogated. After mitochondrial transfer, the mt.3243A>G mutation burden of MELAS fibroblasts was reduced to an undetectable level, with long-term retention. Sequencing results confirmed that the transferred mitochondria were donated from WJMSCs. Furthermore, mitochondrial transfer of WJMSCs to MELAS fibroblasts improves mitochondrial functions and cellular performance, including protein translation of respiratory complexes, ROS overexpression, mitochondrial membrane potential, mitochondrial morphology and bioenergetics, cell proliferation, mitochondrion-dependent viability, and apoptotic resistance. This study demonstrates that WJMSCs exert bioenergetic therapeutic effects through mitochondrial transfer. This finding paves the way for the development of innovative treatments for MELAS and other mitochondrial diseases.
APA, Harvard, Vancouver, ISO, and other styles
3

Fu, Ailing. "Mitotherapy as a Novel Therapeutic Strategy for Mitochondrial Diseases." Current Molecular Pharmacology 13, no. 1 (January 15, 2020): 41–49. http://dx.doi.org/10.2174/1874467212666190920144115.

Full text
Abstract:
Background: The mitochondrion is a multi-functional organelle that is mainly responsible for energy supply in the mammalian cells. Over 100 human diseases are attributed to mitochondrial dysfunction. Mitochondrial therapy (mitotherapy) aims to transfer functional exogenous mitochondria into mitochondria-defective cells for recovery of the cell viability and consequently, prevention of the disease progress. Conclusion: Mitotherapy makes the of modulation of cell survival possible, and it would be a potential therapeutic strategy for mitochondrial diseases. Objective: The review summarizes the evidence on exogenous mitochondria that can directly enter mammalian cells for disease therapy following local and intravenous administration, and suggests that when healthy cells donate their mitochondria to damaged cells, the mitochondrial transfer between cells serve as a new mode of cell rescue. Then the transferred mitochondria play their roles in recipient cells, including energy production and maintenance of cell function.
APA, Harvard, Vancouver, ISO, and other styles
4

Adams, Keith L., Monica Rosenblueth, Yin-Long Qiu, and Jeffrey D. Palmer. "Multiple Losses and Transfers to the Nucleus of Two Mitochondrial Succinate Dehydrogenase Genes During Angiosperm Evolution." Genetics 158, no. 3 (July 1, 2001): 1289–300. http://dx.doi.org/10.1093/genetics/158.3.1289.

Full text
Abstract:
Abstract Unlike in animals, the functional transfer of mitochondrial genes to the nucleus is an ongoing process in plants. All but one of the previously reported transfers in angiosperms involve ribosomal protein genes. Here we report frequent transfer of two respiratory genes, sdh3 and sdh4 (encoding subunits 3 and 4 of succinate dehydrogenase), and we also show that these genes are present and expressed in the mitochondria of diverse angiosperms. Southern hybridization surveys reveal that sdh3 and sdh4 have been lost from the mitochondrion about 40 and 19 times, respectively, among the 280 angiosperm genera examined. Transferred, functional copies of sdh3 and sdh4 were characterized from the nucleus in four and three angiosperm families, respectively. The mitochondrial targeting presequences of two sdh3 genes are derived from preexisting genes for anciently transferred mitochondrial proteins. On the basis of the unique presequences of the nuclear genes and the recent mitochondrial gene losses, we infer that each of the seven nuclear sdh3 and sdh4 genes was derived from a separate transfer to the nucleus. These results strengthen the hypothesis that angiosperms are experiencing a recent evolutionary surge of mitochondrial gene transfer to the nucleus and reveal that this surge includes certain respiratory genes in addition to ribosomal protein genes.
APA, Harvard, Vancouver, ISO, and other styles
5

Gao, Junjie, An Qin, Delin Liu, Rui Ruan, Qiyang Wang, Jun Yuan, Tak Sum Cheng, et al. "Endoplasmic reticulum mediates mitochondrial transfer within the osteocyte dendritic network." Science Advances 5, no. 11 (November 2019): eaaw7215. http://dx.doi.org/10.1126/sciadv.aaw7215.

Full text
Abstract:
Mitochondrial transfer plays a crucial role in the regulation of tissue homeostasis and resistance to cancer chemotherapy. Osteocytes have interconnecting dendritic networks and are a model to investigate its mechanism. We have demonstrated, in primary murine osteocytes with photoactivatable mitochondria (PhAM)floxed and in MLO-Y4 cells, mitochondrial transfer in the dendritic networks visualized by high-resolution confocal imaging. Normal osteocytes transferred mitochondria to adjacent metabolically stressed osteocytes and restored their metabolic function. The coordinated movement and transfer of mitochondria within the dendritic network rely on contact between the endoplasmic reticulum (ER) and mitochondria. Mitofusin 2 (Mfn2), a GTPase that tethers ER to mitochondria, predominantly mediates the transfer. A decline in Mfn2 expression with age occurs concomitantly with both impaired mitochondrial distribution and transfer in the osteocyte dendritic network. These data show a previously unknown function of ER-mitochondrial contact in mediating mitochondrial transfer and provide a mechanism to explain the homeostasis of osteocytes.
APA, Harvard, Vancouver, ISO, and other styles
6

Zampieri, Luca X., Catarina Silva-Almeida, Justin D. Rondeau, and Pierre Sonveaux. "Mitochondrial Transfer in Cancer: A Comprehensive Review." International Journal of Molecular Sciences 22, no. 6 (March 23, 2021): 3245. http://dx.doi.org/10.3390/ijms22063245.

Full text
Abstract:
Depending on their tissue of origin, genetic and epigenetic marks and microenvironmental influences, cancer cells cover a broad range of metabolic activities that fluctuate over time and space. At the core of most metabolic pathways, mitochondria are essential organelles that participate in energy and biomass production, act as metabolic sensors, control cancer cell death, and initiate signaling pathways related to cancer cell migration, invasion, metastasis and resistance to treatments. While some mitochondrial modifications provide aggressive advantages to cancer cells, others are detrimental. This comprehensive review summarizes the current knowledge about mitochondrial transfers that can occur between cancer and nonmalignant cells. Among different mechanisms comprising gap junctions and cell-cell fusion, tunneling nanotubes are increasingly recognized as a main intercellular platform for unidirectional and bidirectional mitochondrial exchanges. Understanding their structure and functionality is an important task expected to generate new anticancer approaches aimed at interfering with gains of functions (e.g., cancer cell proliferation, migration, invasion, metastasis and chemoresistance) or damaged mitochondria elimination associated with mitochondrial transfer.
APA, Harvard, Vancouver, ISO, and other styles
7

Peng, Wesley, Yvette C. Wong, and Dimitri Krainc. "Mitochondria-lysosome contacts regulate mitochondrial Ca2+dynamics via lysosomal TRPML1." Proceedings of the National Academy of Sciences 117, no. 32 (July 23, 2020): 19266–75. http://dx.doi.org/10.1073/pnas.2003236117.

Full text
Abstract:
Mitochondria and lysosomes are critical for cellular homeostasis, and dysfunction of both organelles has been implicated in numerous diseases. Recently, interorganelle contacts between mitochondria and lysosomes were identified and found to regulate mitochondrial dynamics. However, whether mitochondria–lysosome contacts serve additional functions by facilitating the direct transfer of metabolites or ions between the two organelles has not been elucidated. Here, using high spatial and temporal resolution live-cell microscopy, we identified a role for mitochondria–lysosome contacts in regulating mitochondrial calcium dynamics through the lysosomal calcium efflux channel, transient receptor potential mucolipin 1 (TRPML1). Lysosomal calcium release by TRPML1 promotes calcium transfer to mitochondria, which was mediated by tethering of mitochondria–lysosome contact sites. Moreover, mitochondrial calcium uptake at mitochondria–lysosome contact sites was modulated by the outer and inner mitochondrial membrane channels, voltage-dependent anion channel 1 and the mitochondrial calcium uniporter, respectively. Since loss of TRPML1 function results in the lysosomal storage disorder mucolipidosis type IV (MLIV), we examined MLIV patient fibroblasts and found both altered mitochondria–lysosome contact dynamics and defective contact-dependent mitochondrial calcium uptake. Thus, our work highlights mitochondria–lysosome contacts as key contributors to interorganelle calcium dynamics and their potential role in the pathophysiology of disorders characterized by dysfunctional mitochondria or lysosomes.
APA, Harvard, Vancouver, ISO, and other styles
8

SHIAO, Young-Ji, Bénédicte BALCERZAK, and Jean E. VANCE. "A mitochondrial membrane protein is required for translocation of phosphatidylserine from mitochondria-associated membranes to mitochondria." Biochemical Journal 331, no. 1 (April 1, 1998): 217–23. http://dx.doi.org/10.1042/bj3310217.

Full text
Abstract:
The mechanism of import of phosphatidylserine (PtdSer) into mitochondria was investigated using a reconstituted system of isolated organelles in vitroin which PtdSer was translocated from donor membranes to mitochondria and was decarboxylated therein. Neither phosphatidylcholine nor phosphatidylethanolamine (PtdEtn) was translocated under the same conditions. Transfer of PtdSer from its site of synthesis on the endoplasmic reticulum and mitochondria-associated membranes [J. E. Vance (1990) J. Biol. Chem. 265, 7248–7256] to its site of decarboxylation on mitochondrial inner membranes is predicted to be mediated by membrane contact. A mitochondrial membrane protein appears to be involved in the translocation event since proteolysis of proteins exposed on the mitochondrial surface potently inhibited PtdSer transfer, whereas proteolysis of surface proteins of mitochondria-associated membranes did not impair the transfer. The nature of the membranes that donate PtdSer to mitochondria in vitrois not crucial since PtdSer of mitochondria-associated membranes, endoplasmic reticulum and microsomes was decarboxylated to PtdEtn with approximately equal efficiency. The translocation of PtdSer to mitochondria was stimulated by magnesium and calcium ions and was inhibited by incubation of mitochondria with sulphydryl group-modifying reagents. Reconstitution of PtdSer translocation/decarboxylation using digitonin-solubilized mitochondria and PtdSer-donor membranes suggested that the putative PtdSer-translocation protein is primarily localized to contract sites between mitochondrial inner and outer membranes. These studies provide evidence for the involvement of a mitochondrial membrane protein in the import of newly-synthesized PtdSer into mitochondria.
APA, Harvard, Vancouver, ISO, and other styles
9

Chuang, Yao-Chung, Chia-Wei Liou, Shang-Der Chen, Pei-Wen Wang, Jiin-Haur Chuang, Mao-Meng Tiao, Te-Yao Hsu, Hung-Yu Lin, and Tsu-Kung Lin. "Mitochondrial Transfer from Wharton’s Jelly Mesenchymal Stem Cell to MERRF Cybrid Reduces Oxidative Stress and Improves Mitochondrial Bioenergetics." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–22. http://dx.doi.org/10.1155/2017/5691215.

Full text
Abstract:
Myoclonus epilepsy associated with ragged-red fibers (MERRF) is a maternally inherited mitochondrial disease affecting neuromuscular functions. Mt.8344A>G mutation in mitochondrial DNA (mtDNA) is the most common cause of MERRF syndrome and has been linked to an increase in reactive oxygen species (ROS) level and oxidative stress, as well as impaired mitochondrial bioenergetics. Here, we tested whether WJMSC has therapeutic potential for the treatment of MERRF syndrome through the transfer of mitochondria. The MERRF cybrid cells exhibited a high mt.8344A>G mutation ratio, enhanced ROS level and oxidative damage, impaired mitochondrial bioenergetics, defected mitochondria-dependent viability, exhibited an imbalance of mitochondrial dynamics, and are susceptible to apoptotic stress. Coculture experiments revealed that mitochondria were intercellularly conducted from the WJMSC to the MERRF cybrid. Furthermore, WJMSC transferred mitochondria exclusively to cells with defective mitochondria but not to cells with normal mitochondria. MERRF cybrid following WJMSC coculture (MF+WJ) demonstrated improvement of mt.8344A>G mutation ratio, ROS level, oxidative damage, mitochondrial bioenergetics, mitochondria-dependent viability, balance of mitochondrial dynamics, and resistance against apoptotic stress. WJMSC-derived mitochondrial transfer and its therapeutic effect were noted to be blocked by F-actin depolymerizing agent cytochalasin B. Collectively, the WJMSC ability to rescue cells with defective mitochondrial function through donating healthy mitochondria may lead to new insights into the development of more efficient strategies to treat diseases related to mitochondrial dysfunction.
APA, Harvard, Vancouver, ISO, and other styles
10

Singh, Abhishek K., Karin Golan, Mark J. Althoff, Ekaterina Petrovich-Kopitman, Ashley M. Wellendorf, Fatima Mohmoud, Mayla Bertagna, et al. "Bone Marrow Hematopoietic Connexin 43 Is Required for Mitotransfer and AMPK Dependent Mesenchymal Microenvironment Regeneration after Irradiation." Blood 132, Supplement 1 (November 29, 2018): 872. http://dx.doi.org/10.1182/blood-2018-99-118292.

Full text
Abstract:
Abstract Hematopoietic stem cell/progenitor (HSCP) transplantation (HSCT) is routinely used for the treatment of cancer and inborn hematopoietic defects. The bone marrow (BM) microenvironment (ME) is a major regulator of hematopoietic function and fate. Clinical data supports osteoblastic regeneration after HSCT despite the inability of BM mesenchymal stem cells (BM-MSC) to engraft. Therefore, understanding the hematopoietic-dependent mechanisms controlling ME mesenchymal regeneration is expected to provide molecular targets for intervention in the context of HSCT. Hematopoietic connexin-43 (H-Cx43) mediates HSCP survival and efficient blood formation by scavenging damaging excess reactive oxygen species (ROS) through transfer to BM mesenchymal stromal cells (BM-MSC) after chemotherapy, preventing lethal hematopoietic failure (Taniguchi-Ishikwawa E et al., PNAS 2012), while the expression of Cx43 on BM-MSC regulates CXCL12 secretion and HSCP homeostasis (Schajnovitz A et al., Nat. Immunol., 2011). Since Cx43 is expressed in mitochondria, we hypothesized that H-Cx43 mediated ROS transfer upon stress depends on hematopoietic mitochondria transfer and uptake by the BM-MSC. We created chimeric mice by transplanting Vav1-CreTg/-, Cox8 mitochondrial localization signal-Dendra2Tg/- wild-type (mDendra2/WT) or Cx43fl/fl(mDendra2/Cx43Δ/Δ) HSCP to lethally irradiated, congenic WT mice and assessed the recovery of stromal cell regeneration via transfer of mitochondria to BM-MSC. H-Cx43Δ/Δchimeric mice have delayed lympho-hematopoietic recovery after irradiation or chemotherapy which can be reversed by restoration of hematopoietic Cx43 expression. H-Cx43Δ/Δchimeric mice exhibit decreased (~60-80%) and delayed colony-forming-unit-fibroblast (CFU-F) and osteoblast (CFU-Ob) regeneration and hematopoietic recovery. The delayed hematopoietic response in H-Cx43Δ/Δchimeras associated with ~40% reduction in mitochondrial transfer from HSCP to Lin-/CD45-/PDGFRα+/Sca1- BM stromal cells (MSC/P). Reverse transplantation experiments indicate that stromal Cx43 is dispensable for mitochondrial transfer from BM stroma to HSCP. Impaired mitochondrial uptake in H-Cx43Δ/Δchimeras associated with ~30-40% decreased mitochondrial ROS (mROS), membrane potential (MMP) and proliferation (assessed by in vivo BrdU uptake) of recipient MSC/P, suggesting that the transferred mitochondria reprogram the recipient mesenchymal progenitor metabolism. Defects of mitotransfer from H-Cx43Δ/ΔHSCP to BM MSC/P and in recipient BM MSC/P mitochondrial activity were recapitulated in in vitro co-cultures. Interestingly, intracellular [ATP] is upregulated (~2 fold) in MSC/P from chimeric H-Cx43Δ/ΔBM that received donor-derived mitochondria, as compared to donor mitochondria containing MSC/P from WTchimeras. Hemichannel opening causes loss of ATP, we therefore speculated that ATP released from MSC/P upon irradiation and transplantation is uptaken by HSPC, activating mitochondrial transfer as part of BM regeneration. Forced glycolysis-dependent restoration of [ATP] in MSC/P but not in HSCP enhances transfer of mitochondria from HSCP to MSC/P, suggesting that BM stromal [ATP] is an irradiation-responsive positive regulator of mitochondria transfer. Hemichannel-derived exogenous ATP suppresses AMPK activation, which regulates cellular metabolic homeostasis by modulating mitochondrial ROS, mitochondria dynamics and the fate of mitochondria. We found that MSC/P recipient of H-Cx43Δ/Δ mitochondria have increased AMPK activity as assessed by increased phosphorylation of AMPK and its downstream effectors ULK1 and ACC (~2-fold) when compared with MSC/P recipient of H-WT mitochondria, whereas MSC/P containing no donor-derived mitochondria from either chimeric mice are insensitive to the effect of Cx43 deficiency. In vivo administration of the AMPK inhibitor BML-275 dramatically increased the mitochondria transfer from HSCP to MSC/P in WT and H-Cx43Δ/Δ chimeras, and completely restores the negative effect of H-Cx43 deficiency on BM mesenchymal and hematopoietic regeneration. Our data indicate that hematopoietic mitochondrial Cx43 is required to control both mitochondrial transfer and BM ME energetic balance and regeneration after myeloablative irradiation. Disclosures No relevant conflicts of interest to declare.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Transfert de mitochondries"

1

Le, Thi Phuong. "Transfert latéral de séquence." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5013.

Full text
Abstract:
Le transfert latéral de séquences (LST) joue un rôle critique dans l'évolution des bactéries. Les alphaprotéobactéries (ALPs), avec leurs différentes tailles, leurs divers modes de vie et leurs "mobilome", constituent un modèle idéal pour étudier l'histoire évolutive des bactéries. Le "rhizome" représente la diversité des origines des gènes chez ces alphaprotéobactéries : ceci est notamment observable chez les Rickettsiales, appartenant aux ALPs, qui possèdent des génomes en mosaïque. Toutefois, les ALPs contribuent également aux contenus génomiques de différents génomes bactériens comme eucaryotes. De plus, plusieurs gènes codant pour les ribosomes chez les ALPs ont participé à la formation des mitochondries. En premier lieu, nous avons ici mis en place une approche pour mettre en évidence l'histoire évolutive des LSTs. Cette approche est basée sur l'établissement de profils phylétiques, suivi de la recherche de séquences homologues, la reconstruction phylogénétique et enfin la définition des séquences transferts basée sur l'utilisation d'un motif spécifique. Nous avons ainsi montré que 42 gènes des Rickettsiales sont issus de transferts provenant de différentes espèces des trois domaines de la vie. Cette approche est applicable à l'étude de LSTs pour un grand nombre de génomes d'intérêt. Deuxièmement, nous avons séquencé et annoté le génome d'Odyssella thessalonicensis, puis étudié l'histoire évolutive de la mitochondrie, de Candidatus Pelagibacter ubique (CPu), d'O. thessalonicensis et des alphaprotéobactéries. Nos résultats montrent que CPu provient probablement d'un ancêtre intracellulaire facultatif en commun avec les espèces de Rickettsiales
Lateral sequence transfer (LST) plays a critical role in the bacterial evolu- tion. Alphaproteobacteria with different genomes in size, their diverse lifestyles and their "mobilome" are an ideal model for studying the evolutionary history of the bacteria. The different origins of genes of alphaproteobacteria species can be represented as a "rhizome". In constrast, the alphaproteobacteria contributed in the creation of different genomes such as bacteria, eukaryotes (the nematod, the insect). Moreover, many ribosomal genes of alphaproteobacteria have participated in the formation of the mitochondria. In the first part, we have done an approach to define LSTs. This approach is primarily based on the application of phylogenetic profiles, followed by the search for homologous sequences, then the phylogenetic reconstruction, and finally the definition of sequence transfer by a specific pattern. We found that 42 instances of transfers of Rickettsiales came from distantly related species of different domains of life (eukaryote, bacteria, archaea). We can apply this approach for studying LSTs of greater genomes of interest. In the second part, we sequenced and annotated the Odyssella thesalonicensis, then studied the evolutionary history of mitochondrion, Candidatus Pelagibacter ubique, O. thessalonicensis and alphaproteobacteria. Our results showed that Candidatus Pelagibacter ubique has probably originated from an ancestor facultative intracellular with Rickettsiales species
APA, Harvard, Vancouver, ISO, and other styles
2

Val, Romain. "Adressage d'ARN et manipulation génétique des mitochondries dans les cellules végétales et humaines." Université Louis Pasteur (Strasbourg) (1971-2008), 2008. http://www.theses.fr/2008STR13109.

Full text
Abstract:
La connaissance des mécanismes moléculaires qui contrôlent le système génétique des mitochondries reste très parcellaire. Ceci est largement dû à l'incapacité de manipuler leur génome avec les méthodologies conventionnelles. Nous développons une nouvelle approche basée sur l'import naturel des ARNt. Nous utilisons un mime d'ARNt comme navette pour importer dans les mitochondries des cellules végétales des séquences-passagères fixées en 5'. Après transcription dans le noyau, les ARN chimériques sont adressés aux mitochondries. L'import de séquences allant jusqu'à 154 nucléotides a été obtenu. Le processus suit la spécificité de l'import naturel des ARNt. Un trans-ribozyme à tête de marteau ciblé contre l'ARNm mitochondrial atp9 a été élaboré et importé dans les mitochondries grâce à ce système, entraînant ainsi le premier "knockdown" d'un ARN mitochondrial dans des cellules de plante. Le phénotype associé était un retard de croissance. L'analyse de la quantité d'une vingtaine d'ARNm a permis de démontrer une diminution de 70% de l'ARNm nucléaire de l'oxydase alternative 1 (aox-1) suite au knockdown de l'ARNm atp9, avec une forte chute de la protéine correspondante dans les mitochondries et une diminution de la consommation d'oxygène. Ces résultats mettent en évidence l'influence d'un événement mitochondrial sur l'expression d'un gène nucléaire, démontrant ainsi l'existence d'une régulation rétrograde. Dans une optique de thérapie génique, la transposition du système de navette a été tentée dans des cellules humaines. Tous les ARN chimériques élaborés étaient arrêtés dans l'espace intermembranaire des mitochondries. D'autres mimes d'ARNt devront donc être testés
The understanding of the molecular mechanisms which control the genetic system of mitochondria remains restricted. This is mainly due to the impossibility to manipulate their genome with conventional methods. We are developing an alternate approach based on the physiological mechanism of tRNA import. We use a tRNA mimic as a shuttle to import into mitochondria in plant cells passenger RNAs attached to its 5' end. Following nuclear transformation and transcription in the nucleus, the chimeric RNAs are targeted to mitochondria. So far, we obtained the import of passenger sequences up to 154 nucleotides in size into the mitochondria of transformed plant cells. The process follows the natural specificity of the tRNA import pathway. A trans-cleaving hammerhead ribozyme targeted to the mitochondrial atp9 mRNA was designed and imported into mitochondria as a passenger RNA attached to the tRNA mimic, yielding the first knockdown of a mitochondrial RNA in plant cells. The associated phenotype was a decrease in cell growth rate. The analysis of the level of about twenty mRNAs showed that the atp9 mRNA knockdown led to a 70% decrease of the nuclear-encoded alternative oxidase (aox-1) mRNA, with a strong drop in the amount of the corresponding protein in mitochondria and a decrease in the oxygen consumption. These results highlight the influence of a mitochondrial event on the expression of a nuclear gene, demonstrating the existence of a retrograde regulation. From a gene therapy point of view, we tried to transpose our shuttling system into human cells. All chimeric RNAs used were retained in the intermembrane space of the mitochondria. Thus, other tRNA mimics need to be tested
APA, Harvard, Vancouver, ISO, and other styles
3

Baleva, Mariia. "Etudes des mécanismes d'adressage d'ARN de transfert dans les mitochondries de levure et humaines." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ096/document.

Full text
Abstract:
Des mutations dans le génome mitochondrial donnent lieu à l’apparition de maladies neuro-dégénératives ou de myopathies. Pour développer des approches de thérapie génique pour prévenir de ces syndromes, nous devons mieux comprendre les mécanismes moléculaires d’import mitochondrial des ARN. Pour cela nous tentons de récapituler in vitro l’import des ARN à partir d’extraits cellulaires fractionnés par différentes méthodes telles que la chromatographie d’exclusion ou d’affinité à l’aide d’étiquettes d’ARN ou de protéines. Nos résultats affinent nos connaissances de ces mécanismes et permettent d’avancer l’idée que l’énolase, une enzyme de la glycolyse, n’agit pas seule lors de la première étape de l’import de l’ARNtLys avec anticodon CUU (tRK1). En effet nous avons montré que l’énolase ultra-purifiée ne se fixait plus à tRK1 in vitro, alors que des préparations de mitochondries de levure récapitulaient l’import lorsque diverses fractions ajoutées à l’énolase étaient testées. Les fractionnements d’extraits opérés permettent de cerner certaines protéines qui pourraient fonctionner de concert avec l’énolase pour véhiculer tRK1 vers la mitochondrie
Mutations in the mitochondrial genome give rise to neurodegenerative diseases or myopathies. To develop gene therapy for preventing the appearance of these syndromes, we need to better understand the molecular mechanisms of mitochondrial RNA. For this purpose we try to recapitulate in vitro the import of RNA from cell extracts fractionated by different methods such as exclusion or affinity chromatography using tagged RNAs or proteins. Our results refine our knowledge of these mechanisms and allow to advance the idea that enolase, an enzyme of glycolysis, does not act alone during the first stage of import of tRNALys with anticodon CUU (tRK1). Indeed, we have shown that ultra-purified enolase no longer binds to tRK1 in vitro, while preparations of yeast mitochondria recapitulate the import when various fractions mixed with enolase were tested. The performed extracts fractionation make it possible to point to certain proteins which could work in concert with the enolase to convey tRK1 to mitochondria
APA, Harvard, Vancouver, ISO, and other styles
4

Salinas, Thalia Drouard Laurence. "Mécanisme d'importation des ARN de transfert cytosoliques dans la mitochondrie de plante." Strasbourg : Université Louis Pasteur, 2007. http://eprints-scd-ulp.u-strasbg.fr:8080/711/01/Salinas2006.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Salinas, Thalia. "Mécanisme d'importation des ARN de transfert cytosoliques dans la mitochondrie de plante." Université Louis Pasteur (Strasbourg) (1971-2008), 2006. https://publication-theses.unistra.fr/public/theses_doctorat/2006/SALINAS_Thalia_2006.pdf.

Full text
Abstract:
Au cours de l’évolution, les génomes mitochondriaux de plante ont subi de multiples réarrangements, aboutissant à la perte d’information génétique. Une des conséquences est que le nombre d’ARN de transfert (ARNt) codés par le génome mitochondrial n’est pas suffisant pour permettre la traduction mitochondriale et des ARNt codés dans le génome nucléaire sont importés du cytosol vers la mitochondrie. Trois points de ce processus ont été abordés dans ce travail de thèse. Une approche transgénique a mis en évidence le rôle de l’anticodon et de la boucle D dans l’importation des ARNtGly. Ensuite, des études in vitro et biochimiques ont permis l’identification de la protéine « Voltage Dependent Anion Channel » (VDAC) et des protéines du complexe TOM comme étant des facteurs protéiques membranaires impliqués dans le transport des ARNt cytosoliques dans la mitochondrie. Finalement, une étude biochimique a été initiée pour mieux comprendre l’interaction entre les ARNt et la protéine VDAC
During evolution, plant mitochondrial genomes underwent multiple rearrangements leading to the loss of genetic information. One of the consequences is that the number of mitochondrial encoded tRNA genes is not sufficient to ensure plant mitochondrial translation. In order to compensate this deficiency, cytosolic tRNAs have to be imported into mitochondria. Although this phenomenon is an essential process for mitochondrial biogenesis in most eukaryotic cells, it remains poorly understood. Three aspects of this process in plants have been studied during my PhD thesis. A transgenic approach showed that the anticodon and D-domain are essential for tRNAGly import. Moreover, in vitro and biochemical studies allowed the identification of outer mitochondrial proteins, namely the "Voltage Dependent Anion Channel" (VDAC) and TOM proteins, involved in tRNA import into plant mitochondria. Finally, biochemical studies were initiated in order to understand the tRNA-VDAC interaction
APA, Harvard, Vancouver, ISO, and other styles
6

Sieber, François. "Development of a tool to address nucleic acids into mitochondria." Strasbourg, 2011. http://www.theses.fr/2011STRA6123.

Full text
Abstract:
Les mitochondries, organelles présentes chez la majorité des cellules eucaryotes, proviennent de l’endosymbiose d’une α-protéobactérie à l’intérieur d’une cellule proto-eucaryotique ancestrale. Elles sont impliquées dans de nombreux processus fondamentaux comme la production d’ATP par phosphorylation oxydative, la synthèse d’acides aminés ou l’apoptose. Leur dysfonctionnement engendre des répercussions dramatiques sur le fonctionnement des cellules eucaryotes. Ils peuvent être associés par exemple à la stérilité mâle cytoplasmique chez les plantes ou à de nombreuses maladies chez l’homme telles que des maladies neurodégénératives et musculaires. Au cours de l’évolution la majorité des gènes bactériens ancestraux ont été perdus ou transférés dans le génome nucléaire et l’ADN mitochondrial ne code plus que pour un nombre limité de gènes. Ainsi, la majorité des protéines mitochondriales sont codées par des gènes nucléaires. De plus, les mitochondries d’un grand nombre d’espèces ne contiennent pas un nombre suffisant de gènes d’ARNt et importent des ARNt cytosoliques pour effectuer la traduction des ARNm de l’organelle. Le nombre et la nature des ARNt importés dans les mitochondries varient selon les espèces. Contrairement aux mécanismes d’importation des protéines qui sont maintenant bien connus (Neupert and Herrmann, 2007), les mécanismes gouvernant le transport des ARNt dans la mitochondrie restent très mal compris (Salinas et al. , 2008; Sieber et al. , 2011a). Par ailleurs, plusieurs défis majeurs restent à relever afin de comprendre l’ensemble des processus fondamentaux liés à la biogenèse mitochondriale. Ils se heurtent à plusieurs verrous scientifiques et techniques. L’un des verrous les plus importants est le suivant : à ce jour, aucune approche ne permet de transformer de manière stable l’ADN mitochondrial végétal ou humain. Pour tenter de répondre à cette problématique, la stratégie employée repose sur 2 principes majeurs : l’interaction possible entre un acide nucléique et une protéine, et l’existence de séquences d’adressage permettant l’importation dans les mitochondries de protéines codées par des gènes nucléaires. Ainsi, une protéine fusionnée à une séquence d’adressage mitochondriale capable d’interagir avec un acide nucléique allogène devrait entraîner ce dernier dans les mitochondries. [. . . ]
Mitochondria are organelles found in nearly all eukaryotes. They are considered to be the energetic center of the cell because they generate ATP by oxidative phosphorylation, but they are also involved in many more biological processes such as lipid and amino acid metabolism, iron-sulphur (FeS) cluster biogenesis, calcium homeostasis and apoptosis. Mitochondria originate from the endosymbiosis of an alpha-proteobacterium ancestor into a proto-eukaryotic cell. Classical mitochondria have retained a highly reduced vestige of the genome of the ancestral bacteria such that most mitochondrial proteins but also numerous tRNAs have to be imported from the cytosol to the mitochondria (Sieber et al. , 2011a). Mitochondrial genomes are subject to numerous mutations that can result in mitochondrial dysfunctions, which are often dramatic for cell viability. Such mitochondrial disorders can be at the center of human neurodegenerative and neuromuscular diseases, diabetes, aging and also cancers (Florentz et al. , 2003). In plants, mitochondrial disorders can originate from the presence of chimeric sequences in mitochondrial genomes, which lead to cytoplasmic male sterility (CMS). CMS plants are incapable of producing functional pollen and constitute a valuable tool in agronomy to produce hybrid plants that are more vigorous in culture (Budar and Pelletier, 2001). Mitochondrial transformation is thus of great interest, both for the study of mitochondrial disorders, and as a biotechnological tool for example in agronomy. Mitochondrial gene expression also remains poorly characterized and awaits reverse genetics tools for a better understanding. Except for the yeast S. Cerevisiae and the unicellular algae C. Reinhardtii where stable mitochondrial transformation has been achieved by biolistic approaches (Fox et al. , 1988; Remacle et al. , 2006), no means exist to stably transform mitochondrial DNA of higher eukaryotes. In my Ph. D. , I focused on developing a tool for efficient introduction of exogenous RNA into mitochondria of various model organisms. The strategy was to use a nucleic acid binding protein fused to a mitochondrial targeting sequence to create a protein shuttle capable of targeting RNA substrates to the mitochondrial matrix. As a shuttle candidate, I chose the mouse dihydrofolate reductase (DHFR) that binds nucleic acids non-specifically in vitro. A mitochondrial targeting sequence fused to the protein allows it to be imported into isolated mitochondria. DHFR fused to a mitochondrial targeting sequence (pDHFR) is conventionally used to dissect the mechanism of protein import into mitochondria of yeast (Pfanner et al. , 1987), and was used as a starting point for this study
APA, Harvard, Vancouver, ISO, and other styles
7

Kamenskiy, Petr Tarassov Ivan Krasheninnikov Igor. "Studying the role of the precursor of mitochondrial lysyl-tRNA synthetase in the targeting of a cytosolic tRNA-Lys in the mitochondria of S. cerevisiae." Strasbourg : Université Louis Pasteur, 2007. http://eprints-scd-ulp.u-strasbg.fr:8080/778/01/KAMENSKIY2007.pdf.

Full text
Abstract:
Thèse de doctorat : Aspects moléculaires et cellulaires de la biologie : Strasbourg 1 : 2007. Thèse de doctorat : Aspects moléculaires et cellulaires de la biologie : Université M. V. Lomonossov, Moscou : 2007.
Thèse soutenue en co-tutelle. Titre provenant de l'écran-titre. Bibliogr. p. 58-69.
APA, Harvard, Vancouver, ISO, and other styles
8

Delage, Ludovic. "Etude du mécanisme d'importation des ARN de transfert dans les mitochondries de plantes." Université Louis Pasteur (Strasbourg) (1971-2008), 2001. http://www.theses.fr/2001STR13142.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

El, Farouk-Ameqrane Samira. "Etude des protéines VDAC dans le cadre de l’importation des ARNt dans les mitochondries de plantes." Strasbourg, 2009. http://www.theses.fr/2009STRA6111.

Full text
Abstract:
Ces travaux de thèse se sont intéressés aux protéines VDAC et au transport des ARNt dans les mitochondries végétales. En effet, ces protéines interviennent dans le transport des ARNt et de l’ADN dans les mitochondries végétales. Ma thèse s’est donc focalisée dans un premier temps sur l’étude de l’interaction entre VDAC et les ARNt puisqu’aucun site potentiel de liaison avec l’ARN connu n’a pu être prédit. Cette étude a permis de montrer que l’interaction implique plusieurs acides aminés distribués le long de la séquence protéique et en particulier l’hélice a, la Gly2 ainsi que les Lys47 et Lys48. Cette interaction nécessite une protéine de taille entière et vraisemblablement sa structure en tonneau β. Ainsi dans un second temps, il semblait nécessaire de déterminer sa structure spatiale. Nous avons donc produit et purifié les protéines VDAC en grande quantité puis nous avons mis au point leurs conditions de cristallisation. Comme VDAC peut interagir avec différents acides nucléiques et avec des ARNt qu’ils soient importés ou non, nous avons recherché à quel niveau se faisait la sélectivité lors du transport des ARNt dans les mitochondries végétales. Les résultats nous ont montré que la sélectivité est un processus complexe mettant en jeu différentes barrières lors du transport des ARNt. Enfin pour décortiquer plus finement le processus d’importation des ARNt dans les mitochondries, nous avons recherché les partenaires des protéines VDAC potentiellement impliqués dans le transport des ARNt dans les mitochondries végétales. Cette étude a permis de mettre en évidence 8 protéines qui pourraient aussi interagir avec les ARNt
During this work, I was interested in plant VDAC proteins and in the mechanism of tRNA import into plant mitochondria. These proteins are known to be involved in several mechanisms such as transport of metabolites or apoptosis. Recently it was shown that these proteins are implicated in tRNA and DNA import into plant mitochondria. Thus we studied how VDAC can interact with nucleic acids as no binding site can be predicted. The results show that the interaction imply several aminoacids of the protein in particular the Gly2, Lys47, Lys48 and the a helix. As VDAC proteins form a β barrel, we tried to determine their spatial structure to better understand how it can interacts with tRNA. So we express and purify these proteins in big quantity and we get cristallisation conditions. Then as VDAC can interact with different kind of nucleic acids and with imported or not imported tRNA, we tried to understand where is performed the selectivity in the transport of tRNA into mitochondria. This study show that the process of selectivity is complex and imply several barrieres. Finally, we looked for VDAC partners involved in tRNA transport. We identified 8 proteins that can potentially interact with tRNA too
APA, Harvard, Vancouver, ISO, and other styles
10

Besagni, Céline. "Mutations des ARNt mitochondriaux de la levure Saccharomyces cerevisiae et implications pathologiques." Paris 11, 2007. http://www.theses.fr/2007PA112153.

Full text
Abstract:
Il existe de nombreuses pathologies mitochondriales, certaines dues à des mutations dans le noyau, d’autres dans le génome mitochondrial. Parmi ces dernières, une grande partie est due a des mutations des ARNt. Les malades présentent alors des dystrophies musculaires plus ou moins sévères pouvant atteindre différents organes. De plus, la quantité de molécules mutées ainsi que le contexte nucléaire influent sur la gravité des symptomes. C es divers paramètres associés aux limites techniques rendent l’étude de ces mutations difficile chez l’homme ainsi que la recherche d’un traitement. Notre choix c’est alors portés sur la levure S. Cerevisiae (homoplasmique, simple a manipuler, permettant la transformation de ses mitochondriaux par biolistique, et possédant une conservation structurale entre ses ARNt mitochondriaux et ceux de l’homme) comme organisme modèle pour la recherche de gène capable de corriger l’effet de ces mutations. Pour cela, il était préalablement nécessaire de valider le modèle levure en créant des mutations équivalentes (position, substitutions) aux mutations humaines dans les gènes qui codent les ARNt de levure. Ainsi nous avons pu observer une corrélation entre la sévérité des pathologies humaines et le phénotype mutant de levure associé à la même mutation. De plus, comme il est constaté chez l’homme, ce phénotype est dépendant du contexte nucléaire. Par la suite, la recherche de gène correcteurs nous a permis d’identifier le facteur d’élongation de la traduction EF-Tu comme suppresseur de toutes les mutations ARNt obtenues jusqu’à présent ce qui laisse penser à un effet chaperon de la protéine en plus de son rôle durant la traduction ce qui est prometteur d’un point de vue thérapeutique
115 mutations have been identified in the human tRNA genes responsible of human degenerative diseases. The severity of the pathologies is mainly due to the mutations, the affected tissues, the level of heteroplasmy and the nuclear context. In order to find a solution to correct the effect of these mutations, it’s necessary to better understand their molecular mechanisms. Studying such mutaitons in human cultured cells has limits (notably for experimental reasons) and it would be easier at first to use a simple organism as a model. Hence the idea to work with the yeast S. Cerevisiae that is homoplasmic allows a lot of molecular and genetics methods, particularly the possibility to transform the mitochondria by biolistic and creating equivalent mutations to the human ones in the yeast Trna. Once the yeast model validated, for an equivalent mutation in human and yeast, we observed a good correlation between the severity of the human pathology and the mutant phenotype in yeast. Like in human, the yeast phenotype depends of the nuclear context. We found that overexpression of the translation factor EF-Tu is able to correct all the tRNA mutations (even tRNA mutations which lead to a defect on tRNA maturation). Because of this general effect, the possibility to use EF-Tu in human cells is promising and parameters of this effect have been established
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Transfert de mitochondries"

1

International Symposium on Structure, Function, and Biogenesis of Energy Transfer Systems (1989 Bari, Italy). Structure, function, and biogenesis of energy transfer systems: Proceedings of the International Symposium on Structure, Function, and Biogenesis of Energy Transfer Systems, Bari, Italy, 9-11 July 1989. Edited by Quagliariello E. Amsterdam: Elsevier Science, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lestienne, Patrick, ed. Mitochondrial Diseases: Models and Methods. SPRINGER-VERLAG, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Mitochondrial Diseases: Models and Methods. Springer, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Adams, Keith Lee. Evolution of the Peperomia coxi gene intron: A mitochondrial group I intron acquired by horizontal transfer. 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

de Melo-Martín, Inmaculada. Enhancing the Assessment of Reprogenetic Technologies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190460204.003.0008.

Full text
Abstract:
Mitochondrial replacement, a new technological development that allows the creation of an embryo with genetic material from three different people, two of whom are women, has been enthusiastically embraced by reprogenetic proponents. Unlike other reprogenetic technologies currently in use, mitochondrial transfer results in germline modifications. This chapter offers a more adequate assessment of reprogenetic technologies, one that attends to context, is gendered, and recognizes the value-laden nature of these technologies. It points out that even if one were to accept that these techniques have a reasonable safety profile—something for which current evidence is actually lacking—attention to the ends that these techniques will presumably help achieve, and to the values that they reinforce and oppose, calls for skepticism about their moral permissibility.
APA, Harvard, Vancouver, ISO, and other styles
7

de Melo-Martín, Inmaculada. Reprogenetic Technologies. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190460204.003.0002.

Full text
Abstract:
This chapter offers a brief description of the main reprogenetic technologies in use today as well as some of the most significant ones being developed. Because of their relevance in the field, particular attention is given to in vitro fertilization (IVF) and preimplantation genetic diagnosis (PGD). The chapter discusses the differences between somatic and germline modifications, the most common uses of reprogenetic technologies today, and some possible and likely future uses. It also includes a description of recent technological advances such as mitochondrial transfer and gene editing techniques.
APA, Harvard, Vancouver, ISO, and other styles
8

Dickenson, Donna. The Common Good. Edited by Roger Brownsword, Eloise Scotford, and Karen Yeung. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199680832.013.75.

Full text
Abstract:
In conventional thinking, the promise of scientific progress gives automatic and unquestioned legitimacy to any new development in biotechnology. It is the nearest thing we have in a morally relativistic society to the concept of the common good. This chapter begins by examining a recent case study, so-called ‘mitochondrial transfer’ or three-person IVF, in which policymakers appeared to accept that this new technology should be effectively deregulated because that would serve UK national scientific progress and the national interest, despite serious unanswered concerns about its effectiveness and safety. The historical and philosophical underpinnings of the concept of the common good should make us more sceptical of the manner in which the concept can be perverted by particular interests. But there are also hopeful signs that the common good and the biomedical commons are being taken seriously in new models for governance of genomics and biotechnology more generally.
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Transfert de mitochondries"

1

Guerin, Martine, Nadine Camougrand, Alain Cheyrou, and Michèle-France Henry. "Another type of Alternative Electron Transfer Pathway in the Yeast Candida parapsilosis." In Plant Mitochondria, 243–46. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-3517-5_42.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Jefcoate, Colin, and Irina Artemenko. "From electron transfer to cholesterol transfer; molecular regulation of steroid synthesis in the mitochondrion." In Mitochondrial Function and Biogenesis, 293–330. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/b97159.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Ferguson-Miller, S., K. Rajarathnam, J. Hochman, and M. Schindler. "Is Electron Transfer Mediated by Random Diffusion Alone?" In Integration of Mitochondrial Function, 23–31. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2551-0_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lenaz, G., R. Fato, C. Castelluccio, M. Degli Esposti, C. M. Samworth, M. Battino, and G. Parenti Castelli. "Role of Ubiquinone Diffusion in Mitochondrial Electron Transfer." In Integration of Mitochondrial Function, 33–52. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2551-0_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sanchez, Viviana, and Alicia Brusco. "Mitochondrial Transfer by Intercellular Nanotubes." In Biochemistry of Oxidative Stress, 95–108. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45865-6_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Wojtczak, Lech, Jerzy Duszyński, Małgorzata Puka, and Anna Żółkiewska. "Nonlinearity of the Flux/Force Relationship in Respiring Mitochondria as a Possible Consequence of Heterogeneity of Mitochondrial Preparations." In Ion Interactions in Energy Transfer Biomembranes, 111–18. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-8410-6_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Rottenberg, Hagai. "Surface Potential in Energized Mitochondria." In Ion Interactions in Energy Transfer Biomembranes, 29–37. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-8410-6_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Maréchal-Drouard, Laurence, André Dietrich, and Jean-Michel Grienenberger. "Mitochondrial Transfer RNAs and RNA Editing." In The molecular biology of plant mitochondria, 93–130. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0163-9_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Siedow, James N. "Bioenergetics: The Mitochondrial Electron Transfer Chain." In The molecular biology of plant mitochondria, 281–312. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0163-9_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Frei, Balz, and Christoph Richter. "Mono(ADP-Ribosyl)ation in Rat Liver Mitochondria." In ADP-Ribose Transfer Reactions, 433–36. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-8507-7_82.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Transfert de mitochondries"

1

Rahman, I., K. Maremanda, and I. K. Sundar. "Mitochondrial Dysfunction, Mitostress and Mitochondria Transfer In Cigarette Smoke-induced Lung Epithelial Senescence." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7228.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

"Pollen parent transfer mitochondria to offspring." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/plantgen2019-027.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Frankenberg Garcia, J., C. Michaeloudes, B. Xu, K. F. Chung, S. E. Harding, T. A. Rodriguez, and P. K. Bhavsar. "Mechanisms of Mitochondrial Transfer in Health and Disease." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a7217.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ortiz, Luis A., Daniel Winnica, Fabrizio Fazzi, Michelangelo Di Giuseppe, Ernest Sala, Claudette St. Croix, Simmon Watkins, and Donnald Phinney. "The Mesenchymal Stem Cell (MSC) Secretome Involves Mitochondrial Transfer." 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.a3768.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Frankenberg Garcia, J., B. Xu, K. F. Chung, C. Hui, T. Rodriguez, C. Micheloudes, and P. Bhavsar. "Transfer of mitochondria between COPD airway smooth muscle cells." In ERS Lung Science Conference 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/23120541.lsc-2020.69.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Shakoor, Adnan, Mingyang Xie, Fei Pan, Wendi Gao, Jiayu Sun, and Dong Sun. "A Robotic Surgery Approach to Mitochondrial Transfer Amongst Single Cells." In 2019 IEEE/RSJ International Conference on Intelligent Robots and Systems (IROS). IEEE, 2019. http://dx.doi.org/10.1109/iros40897.2019.8968588.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Schneckenburger, Herbert, Michael H. Gschwend, Reinhard Sailer, Wolfgang S. L. Strauss, Lars Schoch, Alexander Schuh, Karl Stock, Rudolf W. Steiner, and Peter Zipfl. "Selective detection of mitochondrial malfunction in situ by energy transfer spectroscopy." In BiOS Europe '98, edited by Irving J. Bigio, Herbert Schneckenburger, Jan Slavik, Katarina Svanberg, and Pierre M. Viallet. SPIE, 1999. http://dx.doi.org/10.1117/12.336827.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gschwend, Michael H., Wolfgang S. L. Strauss, H. Brinkmeier, R. Ruedel, Rudolf W. Steiner, and Herbert Schneckenburger. "Microscopic energy transfer spectroscopy to determine mitochondrial malfunction in human myotubes." In BiOS Europe '96, edited by Irving J. Bigio, Warren S. Grundfest, Herbert Schneckenburger, Katarina Svanberg, and Pierre M. Viallet. SPIE, 1996. http://dx.doi.org/10.1117/12.260816.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Konstantinov, Yu M. "HORIZONTAL GENE TRANSFER INTO PLANT MITOCHONDRIA IN VIVO AND IN EXPERIMENTS." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-1439-1440.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

dela Cruz, A., J. Frankenberg Garcia, C. Michaeloudes, and P. Bhavsar. "S105 Paracrine-mediated transfer of mitochondria between airway smooth muscle cells." In British Thoracic Society Winter Meeting 2019, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 4 to 6 December 2019, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2019. http://dx.doi.org/10.1136/thorax-2019-btsabstracts2019.111.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Transfert de mitochondries' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography