Auswahl der wissenschaftlichen Literatur zum Thema „Alpha-secretases“
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Zeitschriftenartikel zum Thema "Alpha-secretases"
Nunan, Janelle, und David H. Small. „Proteolytic processing of the amyloid-beta protein precursor of Alzheimer's disease“. Essays in Biochemistry 38 (01.10.2002): 37–49. http://dx.doi.org/10.1042/bse0380037.
Der volle Inhalt der QuelleLuca, Monica Di. „Alpha beta-and gamma-secretases in alzheimer s disease“. Frontiers in Bioscience S4, Nr. 3 (2012): 1126–50. http://dx.doi.org/10.2741/s322.
Der volle Inhalt der QuelleMezyk, Renata, Monika Bzowska und Joanna Bereta. „Structure and functions of tumor necrosis factor-alpha converting enzyme.“ Acta Biochimica Polonica 50, Nr. 3 (30.09.2003): 625–45. http://dx.doi.org/10.18388/abp.2003_3656.
Der volle Inhalt der QuelleKiesel, Violet A., und Silvia D. Stan. „Diallyl trisulfide, a chemopreventive agent from Allium vegetables, inhibits alpha-secretases in breast cancer cells“. Biochemical and Biophysical Research Communications 484, Nr. 4 (März 2017): 833–38. http://dx.doi.org/10.1016/j.bbrc.2017.01.184.
Der volle Inhalt der QuelleSingh, Som, Felix Yang, Andy Sivils, Victoria Cegielski und Xiang-Ping Chu. „Amylin and Secretases in the Pathology and Treatment of Alzheimer’s Disease“. Biomolecules 12, Nr. 7 (17.07.2022): 996. http://dx.doi.org/10.3390/biom12070996.
Der volle Inhalt der QuelleAssaf, Naglaa, Marwa E. El-Shamarka, Neveen A. Salem, Yasser A. Khadrawy und Nesrine S. El Sayed. „Neuroprotective effect of PPAR alpha and gamma agonists in a mouse model of amyloidogenesis through modulation of the Wnt/beta catenin pathway via targeting alpha- and beta-secretases“. Progress in Neuro-Psychopharmacology and Biological Psychiatry 97 (März 2020): 109793. http://dx.doi.org/10.1016/j.pnpbp.2019.109793.
Der volle Inhalt der QuelleKim, Doo Yeon, Laura A. MacKenzie Ingano, Bryce W. Carey, Warren Pettingell und Dora M. Kovacs. „P4-290 Voltage-gated sodium channel beta2 subunit is processed by alpha-, beta- and gamma-secretases, generating fragments elevated in AD brains“. Neurobiology of Aging 25 (Juli 2004): S557—S558. http://dx.doi.org/10.1016/s0197-4580(04)81848-7.
Der volle Inhalt der QuelleKron, Nicholas S., und Lynne A. Fieber. „Aplysia Neurons as a Model of Alzheimer’s Disease: Shared Genes and Differential Expression“. Journal of Molecular Neuroscience 72, Nr. 2 (18.10.2021): 287–302. http://dx.doi.org/10.1007/s12031-021-01918-3.
Der volle Inhalt der QuelleLopez Lloreda, Claudia, Sarah Chowdhury, Shivesh Ghura, Elena Alvarez-Periel und Kelly Jordan-Sciutto. „HIV-Associated Insults Modulate ADAM10 and Its Regulator Sirtuin1 in an NMDA Receptor-Dependent Manner“. Cells 11, Nr. 19 (22.09.2022): 2962. http://dx.doi.org/10.3390/cells11192962.
Der volle Inhalt der QuelleYanagino, Kaori, und Naoyuki Miyashita. „Structure Prediction of the Transmembrane Region of Alpha- and Beta- Secretases using Replica-Exchange Molecular Dynamics Simulations, and the Interaction between Amyloid Precursor Protein and Them“. Biophysical Journal 120, Nr. 3 (Februar 2021): 25a. http://dx.doi.org/10.1016/j.bpj.2020.11.414.
Der volle Inhalt der QuelleDissertationen zum Thema "Alpha-secretases"
Cochet, Maud. „Implication du complexe récepteur 5-HT4/APP/ADAM10 dans la voie non-amyloïdogénique de la maladie d’Alzheimer“. Thesis, Montpellier 1, 2011. http://www.theses.fr/2011MON1T005.
Der volle Inhalt der QuelleIn addition to the amyloidogenic pathway of Alzheimer's disease whereby Amyloid Precursor Protein (APP) is cleaved by β- et γ-secretases, the substrate can also be cleaved by α secretases, producing soluble APP alpha (sAPPα)(non-amyloidogenic pathway) and thus preventing the generation of pathogenic Amyloid-beta peptides. Despite, intensive research, the mechanisms regulating APP cleavage by α-secretases remain poorly understood. In this study, we tried to elucidate how 5-HT4Rs stimulate the release of sAPPα. We show that expression of serotonin type 4 receptors (5-HT4Rs) constitutively induces APP cleavage by the α-secretase ADAM10 and release of non-amyloidogenic fragments, sAPPα, in HEK-293 cells and cortical neurons. This effect is fully independent of cAMP production and relies on the transport of the 5-HT4R/APP/mature ADAM10 complex to the plasma membrane. Indeed, 5-HT4Rs but not other G protein-coupled receptors (GPCRs) known to activate sAPPα release, physically interact, directly or indirectly, with ADAM10 and APP to promote their targeting to the plasma membrane. Stimulation of 5 HT4Rs by an agonist further increases sAPPα fragments release and this effect is mediated through cAMP/Epac signalling. These findings describe a new mechanism whereby a GPCR stimulates the cleavage of APP by α-secretases and provide novel insights into the regulation of APP and α-secretase sorting
Padilla, Ferrer Aïda. „ADAM10 in myelination of the central nervous system : study of ADAM10 localization and development of an inducible oligodendroglial ADAM10 knock out (KOOLA10) mouse strain“. Electronic Thesis or Diss., Université Paris Cité, 2022. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=4270&f=41801.
Der volle Inhalt der QuelleIn the central nervous system (CNS), oligodendrocytes (OL) envelop the axons with their membrane extensions, forming the myelin sheath. The OL death and the loss of myelin (demyelination) occur in demyelinating diseases such as multiple sclerosis, for which there is no specific cure nowadays. Our goal is to enhance an endogenous repair process via the ADAM10/sAPPa pathway. The Amyloid Precursor Protein (APP) can be cleaved by a-secretases, members of the ADAM (A Desintegrin And Metalloprotease) family such as ADAM10, the main a-secretase in the CNS. The enzymatic cleavage of APP generates a neuroprotective soluble peptide called sAPPa. Our previous results showed that the pharmacological activation of a-secretases was able to enhance OL differentiation in vitro, to promote myelin protection from demyelination, to enhance remyelination ex vivo and in vivo and to improve the locomotor function. The aim of my thesis was, thus, to further investigate the role of oligodendroglial ADAM10 in myelin formation and maintenance. Three lines of investigation have been pursued. The first aim was to investigate the regional and cellular expression of ADAM10 in the CNS by immunolabeling of ADAM10 protein in adult mice and in primary neuronal and glial cultures. ADAM10 was widely expressed in brain, cerebellum and spinal cord with high expression in the hippocampus and piriform cortex. Neurons expressed much more ADAM10 than glial cells in CNS tissues and in vitro we were able to detect ADAM10 in neurons, OL, astrocytes and microglia. The second aim was to investigate the role of oligodendroglial ADAM10 in myelination. Therefore, we have created a novel mouse strain (KOOLA10) that allows the deletion of OL ADAM10 at specific time points related to the process of oligodendrogenesis and myelination. In this mouse strain, the deficiency is induced by the excision of the exon 3 of Adam10 gene flanked by 2 loxP sequences by the Cre recombinase, which is under the control of the PLP (Proteolipid Protein) promoter. When ADAM10 deficiency was induced at birth during oligodendrogenesis, an impairment in exploratory activity was observed at P21 but it was compensated later on. When ADAM10 deficiency was induced during myelin maintenance in adult mice, the aforementioned behavior worsened over time. Further analysis is still required to explain the behavioral changes observed in KO mice. Surprisingly, the level of MBP (Myelin Basic Protein), assessed by western blot and immunohistological studies, did not show an apparent change in KO mice. The third aim was to investigate the role of ADAM10 in OL development and functionality. The ADAM10 knock-down using siRNA in the 158N OL cell line did not modify cell morphology, proliferation or migration but it induced a decrease in myelin gene expression. To validate these results, we set up a new OL primary cell isolation and culture protocol. Preliminary results also pointed to a reduction of myelin genes expression in ADAM10-deficient OL. Finally, we used organotypic culture of cerebellum, highly rich in myelin, to address the effect of ADAM10 deficiency. We set up a transfection protocol to knock down ADAM10 in cerebellar slices and further focused on the study of myelination in KOOLA10. A significant decrease in the number of myelinated axons was observed in cerebellar slices from KO mice after demyelination, suggesting a beneficial effect of OL ADAM10 in myelin protection or repair. In conclusion, I have shown the distribution of ADAM10 in the CNS, generated the KOOLA10 mouse strain and set up different protocols and tools that allow the investigation of the role of oligodendroglial ADAM10 in myelination. I have obtained evidence suggesting that OL ADAM10 affects exploratory behavior and myelin and is necessary for myelin protection and/or repair. Further investigation is required to better decipher the role of OL ADAM10 in myelin maintenance, and CNS re/myelination
Woodard-Grice, Alencia V. „Hyposialylation regulates [alpha]4[beta]1 integrin binding to VCAM-1“. Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/woodard.pdf.
Der volle Inhalt der QuelleBuchteile zum Thema "Alpha-secretases"
Anand, Abhinav, Neha Sharma, Monica Gulati und Navneet Khurana. „Amyloid Beta“. In Research Anthology on Diagnosing and Treating Neurocognitive Disorders, 1–17. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-3441-0.ch001.
Der volle Inhalt der QuelleAnand, Abhinav, Neha Sharma, Monica Gulati und Navneet Khurana. „Amyloid Beta“. In Advances in Medical Diagnosis, Treatment, and Care, 235–51. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-5282-6.ch011.
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