Gotowa bibliografia na temat „Lysosomes”
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Artykuły w czasopismach na temat "Lysosomes":
Nakae, Isei, Tomoko Fujino, Tetsuo Kobayashi, Ayaka Sasaki, Yorifumi Kikko, Masamitsu Fukuyama, Keiko Gengyo-Ando, Shohei Mitani, Kenji Kontani i Toshiaki Katada. "The Arf-like GTPase Arl8 Mediates Delivery of Endocytosed Macromolecules to Lysosomes inCaenorhabditis elegans". Molecular Biology of the Cell 21, nr 14 (15.07.2010): 2434–42. http://dx.doi.org/10.1091/mbc.e09-12-1010.
Trivedi, Purvi C., Jordan J. Bartlett i Thomas Pulinilkunnil. "Lysosomal Biology and Function: Modern View of Cellular Debris Bin". Cells 9, nr 5 (4.05.2020): 1131. http://dx.doi.org/10.3390/cells9051131.
Amick, Joseph, Arun Kumar Tharkeshwar, Catherine Amaya, i Shawn M. Ferguson. "WDR41 supports lysosomal response to changes in amino acid availability". Molecular Biology of the Cell 29, nr 18 (wrzesień 2018): 2213–27. http://dx.doi.org/10.1091/mbc.e17-12-0703.
Bonet-Ponce, Luis, Alexandra Beilina, Chad D. Williamson, Eric Lindberg, Jillian H. Kluss, Sara Saez-Atienzar, Natalie Landeck i in. "LRRK2 mediates tubulation and vesicle sorting from lysosomes". Science Advances 6, nr 46 (listopad 2020): eabb2454. http://dx.doi.org/10.1126/sciadv.abb2454.
Bakker, A. C., P. Webster, W. A. Jacob i N. W. Andrews. "Homotypic fusion between aggregated lysosomes triggered by elevated [Ca2+]i in fibroblasts". Journal of Cell Science 110, nr 18 (15.09.1997): 2227–38. http://dx.doi.org/10.1242/jcs.110.18.2227.
Xu, Miao, Ke Liu, Manju Swaroop, Wei Sun, Seameen J. Dehdashti, John C. McKew i Wei Zheng. "A Phenotypic Compound Screening Assay for Lysosomal Storage Diseases". Journal of Biomolecular Screening 19, nr 1 (27.08.2013): 168–75. http://dx.doi.org/10.1177/1087057113501197.
Cuervo, A. M., E. Knecht, S. R. Terlecky i J. F. Dice. "Activation of a selective pathway of lysosomal proteolysis in rat liver by prolonged starvation". American Journal of Physiology-Cell Physiology 269, nr 5 (1.11.1995): C1200—C1208. http://dx.doi.org/10.1152/ajpcell.1995.269.5.c1200.
Liu, Ji, Wennan Lu, Sonia Guha, Gabriel C. Baltazar, Erin E. Coffey, Alan M. Laties, Ronald C. Rubenstein, William W. Reenstra i Claire H. Mitchell. "Cystic fibrosis transmembrane conductance regulator contributes to reacidification of alkalinized lysosomes in RPE cells". American Journal of Physiology-Cell Physiology 303, nr 2 (15.07.2012): C160—C169. http://dx.doi.org/10.1152/ajpcell.00278.2011.
Alquier, C., P. Guenin, Y. Munari-Silem, C. Audebet i B. Rousset. "Isolation of pig thyroid lysosomes. Biochemical and morphological characterization". Biochemical Journal 232, nr 2 (1.12.1985): 529–37. http://dx.doi.org/10.1042/bj2320529.
Zeng, Wenping, Canjun Li, Ruikun Wu, Xingguo Yang, Qingyan Wang, Bingqian Lin, Yanan Wei i in. "Optogenetic manipulation of lysosomal physiology and autophagy-dependent clearance of amyloid beta". PLOS Biology 22, nr 4 (23.04.2024): e3002591. http://dx.doi.org/10.1371/journal.pbio.3002591.
Rozprawy doktorskie na temat "Lysosomes":
Ebrahim, Roshan. "Biogenesis of lysosomes in macrophages : intracellular pathway of lysosomal membrane protein to lysosomes". Doctoral thesis, University of Cape Town, 2008. http://hdl.handle.net/11427/3126.
Salgues, Frédéric. "Ciblage des lysosomes pour la thérapie enzymatique substitutive ou pour la thérapie photodynamique". Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20148.
The cation independent mannose-6-phosphate receptor (CI-M6PR) allows the endocytosis and the transfer of molecules bearing the M6P marker to lysosomes. To improve both the affinity for the CI-M6PR and stability of the M6P residue, we carried out the synthesis of isosteric M6P analogues functionalized at the anomeric position to allow efficient coupling to molecules of therapeutic interest. First, the coupling on human recombinant enzymes was performed. The remodelling of the oligosaccharide part of the lysosomal enzyme GAA, whose deficiency is responsible for Pompe disease, helped to highlight the neoglycoGAA is recognized efficiently by CI-M6PR and its enzymatic activity is completely preserved. Second, the coupling of these analogues of M6P to porphyrins for photodynamic therapy of cancer was considered. The model developed in the mannose series has validated our strategy of ligation of saccharides to photosensitizers. The employed methods avoid the conventional steps of deprotection of saccharides after coupling. The biological study with the prepared glycosylporphyrins demonstrated the photoinduced cytotoxicity
Deng, Yuping. "Studies of intraorganelle dynamics : the lysosome, the pre-lysosomal compartment, and the golgi apparatus /". Diss., This resource online, 1991. http://scholar.lib.vt.edu/theses/available/etd-07282008-134815/.
Boutry, Maxime. "Dysfonctions des lysosomes et neurodégénérescence : l'exemple de la paraplégie spastique de type SPG11". Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066295/document.
Lysosomal dysfunctions are involved in a large number of neurodegenerative diseases highlightingthe crucial function of lysosomes in neuron survival and function. The mechanism of lysosomereformation from autolysosomes allow cells to maintain the ool of functional lysosomes.Disruptions of this rocess are involved in athologies affecting the central nervous system. Inparticular, spatacsin that lays a role in lysosome recycling is implicated in hereditary spasticparaplegia type SPG11, a severe disease characterized by motors and cognitive alterations. Thispathology is caused by loss of function mutations in SPG11, encoding spatacsin. The study ofSPG11 cellular models gives the opportunity to decipher the hysiopathological mechanismsunderlying lysosomal reformation disruptions.During my thesis, I showed that loss of spatacsin function induces lipid accumulation in lysosomesand articularly in autolysosomes both in fibroblasts and neurons from Spg11-/- mice. Gangliosidesand cholesterol are among lipids that accumulate in autolysosomes impairing lysosomal membranerecycling by disrupting the recruitment of keys roteins. Neurons with ganglioside accumulationsare more sensitive to glutamate induced neuronal death, suggesting that these accumulations areinvolved in neurodegeneration. These results could be of great importance since accumulations ofgangliosides in lysosomes arise in many diseases.I also showed that loss of spatacsin disrupts extracellular calcium import by the store-operatedcalcium entry (SOCE) leading to an increase in cytosolic calcium levels. Lysosomal calcium contentis also increased in Spg11-/- cells and calcium release from lysosome by TRPML1 is reduced.Inhibiting SOCE and stimulating lysosomal calcium release by TRPML1 reduced lipidsaccumulations in lysosomes and artially restored lysosome reformation.Our data suggest that absence of spatacsin is responsible for a disruption of calcium homeostasisthat contributes to lipid accumulation in autolysosomes, disturbing reformation of lysosomes fromautolysosomes. Inhibiting gangliosides synthesis could be used as a therapeutic strategy. However,understanding how loss of function of spatacsin alters these cellular athways will allow thedevelopment of targeted therapeutic approaches
Moule, Christie Joy. "The synthesis and kinetic studies of substrate analogues for N-acetylgalactosamine-4-sulfatase". Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phm926.pdf.
Piccolo, Enzo. "Rôle de la protéine HMGB1 dérivée des macrophages au cours d'une réaction inflammatoire". Thesis, Toulouse 3, 2021. http://www.theses.fr/2021TOU30035.
The Inflammatory reaction is the first necessary step to combat all pathogens and tissue injuries and restore damaged tissue homeostasis. The immune system is particularly involved during each step, in particular the macrophages which display various inflammatory and metabolic changes. Macrophages can modify and adapt their cellular metabolism to meet their energy needs and efficiently perform the inflammatory reaction according to signals from the surrounding environment. These deep metabolic adaptations influence mitochondria physiology and oxidative phosphorylations (OXPHOS), the secretions of pro and anti-inflammatory molecules, as well as the ability to phagocytize various inflammatory compounds (pathogens, cell debris, and autophagy). These deep metabolic adaptations are under the control of several transcription factors such as NFkB, TFEB or HIF1alpha. The compaction and accessibility of chromatin are crucial for the regulation of the activity of these transcription factors. In the nucleus, DNA compaction is regulated by histones but also by High Mobility Group (HMG) proteins. Among this family of HMG proteins, the High Mobility Group B1 (HMGB1) protein, mainly located in the nucleus, is capable of regulating indirectly the transcription of genes in many tissues. In addition to its nuclear role, HMGB1 can be actively relocated into the cytoplasm and then secreted by innate immune cells during acute or chronic inflammation. Once in the bloodstream, HMGB1 acts as alarmine which initiates and maintains inflammation. Furthermore, during acute or chronic inflammation, concentrations of circulating HMGB1 are increased compared to the basal condition in mice. All these results suggest a role of HMGB1 in the immunometabolism of macrophages as well as in acute or chronic inflammatory processes. In this context, this thesis work has two objectives: I /: To study the role of HMGB1 derived from macrophages and its consequences on the occurrence of tissue fibrosis. II /: To study the intracellular role of HMGB1 derived from macrophages during acute inflammatory shock. This work has demonstrated in vitro and in vivo that, as an alarmine HMGB1 derived from macrophages, does not influence the occurrence of fibrosis following chronic inflammation. Moreover, we demonstrated in vitro and in vivo that as a nuclear factor HMGB1 exerts a potent anti-inflammatory action on macrophages by regulating lysosome biogenesis and function and skewing towards a M2 profile. All these results taken together helped to better characterize and understand the biological functions of HMGB1 proteins during the inflammatory reaction. Boosting these anti-inflammatory functions of HMGB1 may constitute a potential therapeutic approach to counteract the deleterious effect of hyper-inflammation in patients with acute/chronic inflammatory diseases
Kågedal, Katarina. "Cathepsin D released from lysosomes mediates apoptosis /". Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med771s.pdf.
Selmi, Samia. "Études biochimiques et fonctionnelles des lysosomes thyroïdiens". Lyon 1, 1989. http://www.theses.fr/1989LYO1T049.
Jakhria, Toral Chandulal. "Amyloid fibrils are nanoparticles that target lysosomes". Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7628/.
Atakpa, Peace. "Ca2+ signalling between the endoplasmic reticulum and lysosomes". Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288002.
Książki na temat "Lysosomes":
Holtzman, Eric. Lysosomes. New York: Plenum Press, 1989.
Öllinger, Karin, i Hanna Appelqvist, red. Lysosomes. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6934-0.
Holtzman, Eric. Lysosomes. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4.
Holtzman, Eric. Lysosomes. New York: Plenum Press, 1989.
Mehta, Atul B., i Bryan Winchester. Lysosomal storage disorders: A practical guide. Chichester, West Sussex: Wiley-Blackwell, 2013.
Maxfield, Frederick R., James M. Willard i Shuyan Lu, red. Lysosomes: Biology, Diseases, and Therapeutics. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118978320.
Reunov, A. V. Liticheskai︠a︡ funkt︠s︡ii︠a︡ kletki. Moskva: Nauka, 2008.
Panin, L. E. Lizosomy: Rolʹ v adaptat͡s︡ii i vosstanovlenii. Novosibirsk: Izd-vo "Nauka," Sibirskoe otd-nie, 1987.
G, Thoene Jess, red. Pathophysiology of lysosomal transport. Boca Raton: CRC Press, 1992.
H, Glaumann, i Ballard F. J, red. Lysosomes: Their role in protein breakdown. London: Academic Press, 1987.
Części książek na temat "Lysosomes":
Holtzman, Eric. "Historical Fragments; Methods; Some Terminology". W Lysosomes, 1–24. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_1.
Holtzman, Eric. "Endocytosis and Heterophagy". W Lysosomes, 25–92. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_2.
Holtzman, Eric. "Acidification; Membrane Properties; Permeability and Transport". W Lysosomes, 93–160. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_3.
Holtzman, Eric. "Uses and Abuses of Endocytotic and Heterophagic Pathways". W Lysosomes, 161–241. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_4.
Holtzman, Eric. "Autophagy and Related Phenomena". W Lysosomes, 243–318. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_5.
Holtzman, Eric. "Extensive Release. Excessive Storage". W Lysosomes, 319–61. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_6.
Holtzman, Eric. "Genesis". W Lysosomes, 363–418. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4899-2540-4_7.
Valk, Jacob, i Marjo S. van der Knaap. "Lysosomes and Lysosomal Disorders". W Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 66–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_6.
Wevers, R. A., i V. Gieselmann. "Lysosomes and Lysosomal Disorders". W Magnetic Resonance of Myelination and Myelin Disorders, 66–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-27660-2_5.
van der Knaap, Marjo S., i Jacob Valk. "Lysosomes and Lysosomal Disorders". W Magnetic Resonance of Myelin, Myelination, and Myelin Disorders, 53–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03078-3_5.
Streszczenia konferencji na temat "Lysosomes":
Zhu, X. "Relationship Between Autophagy-Lysosomes Pathway and Ventilator-Induced Diaphragmatic Dysfunction". W American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2622.
Perera, Rushika M. "Abstract I22: New players and unique features of cancer lysosomes". W Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-i22.
Bakhit, C., D. Lewis, R. Billings i B. Malfroy. "CELLULAR CATABOLISM OF RECOMBINANT TISSUE-TYPE PLASMINOGEN ACTIVATOR: IDENTIFICATION AND CHARACTERIZATION OF A NOVEL HIGH AFFINITY UPTAKE SYSTEM ON RAT HEPATOCYTES". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644400.
Hung, Hsin-I., Geraldine Quiogue, John J. Lemasters i Anna-Liisa Nieminen. "Signaling from lysosomes to mitochondria sensitizes cancer cells to photodynamic treatment". W SPIE BiOS, redaktorzy David H. Kessel i Tayyaba Hasan. SPIE, 2011. http://dx.doi.org/10.1117/12.878306.
Quiogue, Geraldine, Shalini Saggu, Hsin-I. Hung, Malcolm E. Kenney, Nancy L. Oleinick, John J. Lemasters i Anna-Liisa Nieminen. "Signaling from lysosomes enhances mitochondria-mediated photodynamic therapy in cancer cells". W 12th World Congress of the International Photodynamic Association, redaktor David H. Kessel. SPIE, 2009. http://dx.doi.org/10.1117/12.823752.
Joncour, Vadim Le, Pauliina Filppu, Minna Holopainen, Maija Hyvönen, S. Pauliina Turunen, Harri Sihto, Isabel Burghardt i in. "Abstract LB-055: Novel therapeutic option targeting the tumor cell lysosomes". W 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-lb-055.
Tang, Hao-yang, Meng Qian, Cong Song i Yi-chao Zhang. "Lysosomes Computational Labeling Method Based on Feature Map Slice of Deeplabv3+". W 2019 IEEE Symposium Series on Computational Intelligence (SSCI). IEEE, 2019. http://dx.doi.org/10.1109/ssci44817.2019.9002802.
Nieminen, Anna-Liisa, Kashif Azizuddin, Ping Zhang, Malcolm E. Kenney, Peter Pediaditakis, John J. Lemasters i Nancy L. Oleinick. "Contribution of mitochondria and lysosomes to photodynamic therapy-induced death in cancer cells". W Biomedical Optics (BiOS) 2008, redaktor David Kessel. SPIE, 2008. http://dx.doi.org/10.1117/12.767356.
Metelitsina, Irina P., i N. F. Leus. "Action of low-energy monochromatic coherent light on the stability of retinal lysosomes". W Photonics West '95, redaktor Steven L. Jacques. SPIE, 1995. http://dx.doi.org/10.1117/12.209925.
Noguchi, Masayuki, Noriyuki Hirata i Futoshi Suizu. "Abstract A04: Interaction of VRK2 with Akt at lysosomes controls induction of autophagy". W Abstracts: AACR Special Conference on Targeting PI3K/mTOR Signaling; November 30-December 8, 2018; Boston, MA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.pi3k-mtor18-a04.
Raporty organizacyjne na temat "Lysosomes":
Levenson, Victor V. Lysosome-mediated Cell Death and Autophagy-Dependent Multidrug Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, październik 2008. http://dx.doi.org/10.21236/ada495800.
Shiio, Yuzuru. Targeting Androgen Receptor by Lysosomal Degradation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2014. http://dx.doi.org/10.21236/ada612607.
Shiio, Yuzuru. Targeting Androgen Receptor by Lysosomal Degradation in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, listopad 2015. http://dx.doi.org/10.21236/ada621824.
Palmer, Guy, Varda Shkap, Wendy Brown i Thea Molad. Control of bovine anaplasmosis: cytokine enhancement of vaccine efficacy. United States Department of Agriculture, marzec 2007. http://dx.doi.org/10.32747/2007.7695879.bard.