Zobrazeno 1 - 10
of 21
pro vyhledávání: '"Lucian Soane"'
Publikováno v:
PLoS Biology, Vol 10, Iss 9, p e1001399 (2012)
Cell death by apoptosis is indispensable for proper development and tissue homeostasis in all multicellular organisms, and its deregulation plays a key role in cancer and many other diseases. A crucial event in apoptosis is the formation of protein-p
Externí odkaz:
https://doaj.org/article/d06e94dfc07a43579177eb136fbb76e8
Autor:
Lucian Soane, Loïc Lionnard, J. Marie Hardwick, Xinchen Teng, Abdel Aouacheria, Kyle Metz, Atsushi Kamiya
Publikováno v:
CNS Neuroscience & Therapeutics
CNS Neuroscience and Therapeutics
CNS Neuroscience and Therapeutics, 2019, 25 (7), pp.887-902. ⟨10.1111/cns.13156⟩
CNS Neuroscience and Therapeutics, Wiley, 2019, 25 (7), pp.887-902. ⟨10.1111/cns.13156⟩
CNS Neuroscience and Therapeutics
CNS Neuroscience and Therapeutics, 2019, 25 (7), pp.887-902. ⟨10.1111/cns.13156⟩
CNS Neuroscience and Therapeutics, Wiley, 2019, 25 (7), pp.887-902. ⟨10.1111/cns.13156⟩
International audience; The underlying molecular basis for neurodevelopmental or neuropsychiatric disorders is not known. In contrast, mechanistic understanding of other brain disorders including neurodegeneration has advanced considerably. Yet, thes
Publikováno v:
Journal of Neuroscience Research. 85:3407-3415
Altered mitochondrial energy metabolism contributes to the pathophysiology of acute brain injury caused by ischemia, trauma, and neurotoxins and by chronic neurodegenerative disorders such as Parkinson’s and Huntington’s diseases. Although much e
Autor:
Lucian Soane, Gary Fiskum
Publikováno v:
Journal of Neurochemistry. 95:230-243
Protein delivery mediated by protein transduction domains (PTD) such as the HIV-1 TAT-PTD has emerged as a promising approach for neuroprotection. The objective of this study was to generate and evaluate the neuroprotective potential of TAT fusion pr
Autor:
Lucian Soane, Gary Fiskum
Publikováno v:
Journal of Bioenergetics and Biomembranes. 37:179-190
Bcl-2 and other closely related members of the Bcl-2 family of proteins inhibit the death of neurons and many other cells in response to a wide variety of pathogenic stimuli. Bcl-2 inhibition of apoptosis is mediated by its binding to pro-apoptotic p
Autor:
Susanna Weerth, Teodora Niculescu, Florin Niculescu, Moon L. Shin, Lucian Soane, Cedric S. Raine, Violeta Rus, Horea Rus
Publikováno v:
Annals of the New York Academy of Sciences. 1010:530-533
Complement activation is involved in the initiation of inflammation and antibody-mediated demyelination in experimental autoimmune encephalomyelitis (EAE). We investigated the role of MAC in apoptosis in myelin-induced EAE in complement C5-deficient
Autor:
Teodora Niculescu, Moon L. Shin, Jae-Hyun Park, Lucian Soane, Tudor Badea, Horea Rus, Florin Niculescu
Publikováno v:
Journal of Neuroimmunology. 142:58-66
Sublytic C5b-9 alters the molecular phenotype of myotubes by inhibiting muscle-specific gene expression. Here, we showed that C5b-9 induced c-fos mRNA and transcription. Using c-fos promoter-CAT constructs and electrophoretic mobility shift assay (EM
Autor:
Florin Niculescu, Hila Sorana, Violeta Rus, Horea Rus, Lucian Soane, Matthew Fosbrink, Tudor C. Badea, Moon L. Shin
Publikováno v:
Journal of Biological Chemistry. 277:502-508
Proliferation of aortic smooth muscle cells contributes to atherogenesis and neointima formation. Sublytic activation of complement, particularly C5b-9, induces cell cycle progression in aortic smooth muscle cells. RGC-32 is a novel protein that may
Publikováno v:
The Journal of Immunology. 167:2305-2311
Apoptosis of oligodendrocytes is induced by serum growth factor deprivation. We showed that oligodendrocytes and progenitor cells respond to serum withdrawal by a rapid decline of Bcl-2 mRNA expression and caspase-3-dependent apoptotic death. Sublyti
Publikováno v:
Journal of Biological Chemistry. 273:26977-26981
Sublytic complement activation on oligodendrocytes (OLG) down-regulates expression of myelin genes and induces cell cycle in culture. Differential display (DD) was used to search for new genes whose expression is altered in response to complement and