Global ETD Search

1	Role of P70 S6 kinase in the formation of tau pathologies in Alzheimer's disease / An, Wen-Lin, January 2005 (has links) Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 4 uppsatser.
2	The role of protein phosphatases in regulation of Drosophila S6 by nutrient signaling pathways Bielinski, Vincent Anthony. January 2006 (has links) Thesis (Ph. D.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Embargoed. Vita. Bibliography: 104-116.
3	The regulation of G protein-coupled receptor (GPCR) signal transduction by p90 Ribosomal S6 Kinase 2 (RSK2) / Sheffler, Douglas James. January 2006 (has links) Thesis (Ph. D.)--Case Western Reserve University, 2006. / [School of Medicine] Department of Biochemistry. Includes bibliographical references. Available online via OhioLINK's ETD Center.
4	MSK1 regulates homeostatic and experience-dependent synaptic plasticity Corrêa, Sonia A.L., Hunter, C.J., Palygin, O., Wauters, S.C., Martin, K.J., McKenzie, C., McKelvey, K., Morris, R.G., Pankratov, Y., Arthur, J.S., Frenguelli, B.G. January 2012 (has links) No / The ability of neurons to modulate synaptic strength underpins synaptic plasticity, learning and memory, and adaptation to sensory experience. Despite the importance of synaptic adaptation in directing, reinforcing, and revising the behavioral response to environmental influences, the cellular and molecular mechanisms underlying synaptic adaptation are far from clear. Brain-derived neurotrophic factor (BDNF) is a prime initiator of structural and functional synaptic adaptation. However, the signaling cascade activated by BDNF to initiate these adaptive changes has not been elucidated. We have previously shown that BDNF activates mitogen- and stress-activated kinase 1 (MSK1), which regulates gene transcription via the phosphorylation of both CREB and histone H3. Using mice with a kinase-dead knock-in mutation of MSK1, we now show that MSK1 is necessary for the upregulation of synaptic strength in response to environmental enrichment in vivo. Furthermore, neurons from MSK1 kinase-dead mice failed to show scaling of synaptic transmission in response to activity deprivation in vitro, a deficit that could be rescued by reintroduction of wild-type MSK1. We also show that MSK1 forms part of a BDNF- and MAPK-dependent signaling cascade required for homeostatic synaptic scaling, which likely resides in the ability of MSK1 to regulate cell surface GluA1 expression via the induction of Arc/Arg3.1. These results demonstrate that MSK1 is an integral part of a signaling pathway that underlies the adaptive response to synaptic and environmental experience. MSK1 may thus act as a key homeostat in the activity- and experience-dependent regulation of synaptic strength. Analysis of Variance Animals Brain-derived neurotrophic factor Cells Cytoskeletal proteins Dendritic spines Environment Enzyme inhibitors Excitatory postsynaptic potentials Female Gene expression regulation Green fluorescent proteins Hippocampus Homeostasis Male Mice Inbred C57BL Transgenic Nerve tissue proteins Neuronal plasticity Neurons Patch-clamp techniques Point mutation Receptors AMPA Ribosomal protein S6 kinases Signal transduction Sodium channel blockers Synapses Tetrodotoxin Time factors REF 2014

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