Development of small-molecule Tau-SH3 interaction inhibitors that prevent amyloid-β toxicity and network hyperexcitability
暂无分享,去创建一个
Jonathan R Roth | J. Day | Hunter B. Dean | C. Augelli-Szafran | N. Boyle | Pedro Ruiz | Samantha J. Thompson | Adam R. Aldaher | Jacob S. Mesina | Mark J. Suto | Erik D. Roberson | Travis Rush | Trae B. Dunn | J. N. Cochran | Zhengrong Yang | Vibha Pathak | Mousheng Wu | Jeremy J. Day | J. R. Bostwick
[1] T. Ali,et al. Peptide aptamer targeting Aβ–PrP–Fyn axis reduces Alzheimer’s disease pathologies in 5XFAD transgenic mouse model , 2023, Cellular and Molecular Life Sciences.
[2] C. Mummery,et al. Tau-targeting antisense oligonucleotide MAPTRx in mild Alzheimer’s disease: a phase 1b, randomized, placebo-controlled trial , 2023, Nature Medicine.
[3] L. Ittner,et al. Treatment of epilepsy using a targeted p38γ kinase gene therapy. , 2022, Science advances.
[4] J. Sibarita,et al. Fyn nanoclustering requires switching to an open conformation and is enhanced by FTLD-Tau biomolecular condensates , 2022, Molecular Psychiatry.
[5] Yiyun Huang,et al. Reversal of synapse loss in Alzheimer mouse models by targeting mGluR5 to prevent synaptic tagging by C1Q , 2022, Science Translational Medicine.
[6] T. Thippeswamy,et al. Fyn-tau Ablation Modifies PTZ-Induced Seizures and Post-seizure Hallmarks of Early Epileptogenesis , 2020, Frontiers in Cellular Neuroscience.
[7] A. Ittner,et al. Reduction of advanced tau-mediated memory deficits by the MAP kinase p38γ , 2020, Acta Neuropathologica.
[8] S. Strittmatter,et al. Fyn kinase inhibition reduces protein aggregation, increases synapse density and improves memory in transgenic and traumatic Tauopathy , 2020, Acta Neuropathologica Communications.
[9] Jonathan R Roth,et al. Alzheimer’s disease risk gene BIN1 induces Tau-dependent network hyperexcitability , 2020, bioRxiv.
[10] L. Mucke,et al. Tau Reduction Prevents Key Features of Autism in Mouse Models , 2020, Neuron.
[11] Jonathan R Roth,et al. A peptide inhibitor of Tau-SH3 interactions ameliorates amyloid-β toxicity , 2019, Neurobiology of Disease.
[12] A. Andreotti,et al. The SH3 domains of the protein kinases ITK and LCK compete for adjacent sites on T cell–specific adapter protein , 2019, The Journal of Biological Chemistry.
[13] Eric M Reiman,et al. Effect of AZD0530 on Cerebral Metabolic Decline in Alzheimer Disease , 2019, JAMA neurology.
[14] Dongxue Wang,et al. Systematic profiling of SH3-mediated Tau-Partner interaction network in Alzheimer's disease by integrating in silico analysis and in vitro assay. , 2019, Journal of molecular graphics & modelling.
[15] A. Araque,et al. Tau is required for progressive synaptic and memory deficits in a transgenic mouse model of α-synucleinopathy , 2019, Acta Neuropathologica.
[16] S. Strittmatter,et al. Anti‐PrPC antibody rescues cognition and synapses in transgenic alzheimer mice , 2019, Annals of clinical and translational neurology.
[17] S. Strittmatter,et al. Rescue of Transgenic Alzheimer’s Pathophysiology by Polymeric Cellular Prion Protein Antagonists , 2019, Cell reports.
[18] J. Lambert,et al. Structural Basis of Tau Interaction With BIN1 and Regulation by Tau Phosphorylation , 2018, Front. Mol. Neurosci..
[19] H. Nygaard. Targeting Fyn Kinase in Alzheimer’s Disease , 2018, Biological Psychiatry.
[20] Timothy A. Miller,et al. Tau reduction prevents neuronal loss and reverses pathological tau deposition and seeding in mice with tauopathy , 2017, Science Translational Medicine.
[21] A. Ittner. SITE-SPECIFIC PHOSPHORYLATION OF TAU INHIBITS AMYLOID-β TOXICITY IN ALZHEIMER’S MICE , 2016, Alzheimer's & Dementia.
[22] L. Mucke,et al. Network abnormalities and interneuron dysfunction in Alzheimer disease , 2016, Nature Reviews Neuroscience.
[23] C. Simmerling,et al. ff14SB: Improving the Accuracy of Protein Side Chain and Backbone Parameters from ff99SB. , 2015, Journal of chemical theory and computation.
[24] E. Roberson,et al. Seizure resistance without parkinsonism in aged mice after tau reduction , 2014, Neurobiology of Aging.
[25] J. Wells,et al. Small-molecule inhibitors of protein-protein interactions: progressing toward the reality. , 2014, Chemistry & biology.
[26] R. Bostwick,et al. AlphaScreen HTS and Live-Cell Bioluminescence Resonance Energy Transfer (BRET) Assays for Identification of Tau–Fyn SH3 Interaction Inhibitors for Alzheimer Disease , 2014, Journal of biomolecular screening.
[27] A. Bush,et al. Motor and cognitive deficits in aged tau knockout mice in two background strains , 2014, Molecular Neurodegeneration.
[28] L. Mucke,et al. Tau Reduction Prevents Disease in a Mouse Model of Dravet Syndrome , 2014, Annals of neurology.
[29] A. Vortmeyer,et al. Metabotropic Glutamate Receptor 5 Is a Coreceptor for Alzheimer Aβ Oligomer Bound to Cellular Prion Protein , 2013, Neuron.
[30] D. Holtzman,et al. Antisense Reduction of Tau in Adult Mice Protects against Seizures , 2013, The Journal of Neuroscience.
[31] Daniel R Roe,et al. PTRAJ and CPPTRAJ: Software for Processing and Analysis of Molecular Dynamics Trajectory Data. , 2013, Journal of chemical theory and computation.
[32] S. Younkin,et al. Tau Loss Attenuates Neuronal Network Hyperexcitability in Mouse and Drosophila Genetic Models of Epilepsy , 2013, The Journal of Neuroscience.
[33] V. Laporte,et al. Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice. , 2012, The American journal of pathology.
[34] N. Leclerc,et al. Interaction of Endogenous Tau Protein with Synaptic Proteins Is Regulated by N-Methyl-d-aspartate Receptor-dependent Tau Phosphorylation* , 2012, The Journal of Biological Chemistry.
[35] A. Vortmeyer,et al. Alzheimer Amyloid-β Oligomer Bound to Post-Synaptic Prion Protein Activates Fyn to Impair Neurons , 2012, Nature Neuroscience.
[36] Hans-Ulrich Demuth,et al. Prion-Like Behavior and Tau-dependent Cytotoxicity of Pyroglutamylated β-Amyloid , 2012, Nature.
[37] W. Noble,et al. Tyrosine phosphorylation of tau regulates its interactions with Fyn SH2 domains, but not SH3 domains, altering the cellular localization of tau , 2011, The FEBS journal.
[38] L. Mucke,et al. Amyloid-β/Fyn–Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer's Disease , 2011, The Journal of Neuroscience.
[39] Jürgen Götz,et al. Dendritic Function of Tau Mediates Amyloid-β Toxicity in Alzheimer's Disease Mouse Models , 2010, Cell.
[40] E. Mandelkow,et al. Proline-directed Pseudo-phosphorylation at AT8 and PHF1 Epitopes Induces a Compaction of the Paperclip Folding of Tau and Generates a Pathological (MC-1) Conformation* , 2008, Journal of Biological Chemistry.
[41] M. Zvelebil,et al. Phosphorylation Regulates Tau Interactions with Src Homology 3 Domains of Phosphatidylinositol 3-Kinase, Phospholipase Cγ1, Grb2, and Src Family Kinases* , 2008, Journal of Biological Chemistry.
[42] L. Mucke,et al. Enkephalin Elevations Contribute to Neuronal and Behavioral Impairments in a Transgenic Mouse Model of Alzheimer's Disease , 2008, The Journal of Neuroscience.
[43] Anatol C. Kreitzer,et al. Aberrant Excitatory Neuronal Activity and Compensatory Remodeling of Inhibitory Hippocampal Circuits in Mouse Models of Alzheimer's Disease , 2007, Neuron.
[44] L. Mucke,et al. Reducing Endogenous Tau Ameliorates Amyloid ß-Induced Deficits in an Alzheimer's Disease Mouse Model , 2007, Science.
[45] F. Studier,et al. Protein production by auto-induction in high density shaking cultures. , 2005, Protein expression and purification.
[46] L. Thal,et al. Altered p59Fyn kinase expression accompanies disease progression in Alzheimer's disease: implications for its functional role , 2005, Neurobiology of Aging.
[47] Junmei Wang,et al. Development and testing of a general amber force field , 2004, J. Comput. Chem..
[48] L. Mucke,et al. Fyn Kinase Modulates Synaptotoxicity, But Not Aberrant Sprouting, in Human Amyloid Precursor Protein Transgenic Mice , 2004, The Journal of Neuroscience.
[49] Yitao Liu,et al. Treatment of Ischemic Brain Damage by Perturbing NMDA Receptor- PSD-95 Protein Interactions , 2002, Science.
[50] M. Vitek,et al. Tau is essential to β-amyloid-induced neurotoxicity , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[51] Sreenath V. Sharma,et al. UCS15A, a novel small molecule, SH3 domain-mediated protein–protein interaction blocking drug , 2002, Oncogene.
[52] J. Trotter,et al. Process Outgrowth of Oligodendrocytes Is Promoted by Interaction of Fyn Kinase with the Cytoskeletal Protein Tau , 2002, The Journal of Neuroscience.
[53] I. Campbell,et al. The Role of the Src Homology 3-Src Homology 2 Interface in the Regulation of Src Kinases* , 2001, The Journal of Biological Chemistry.
[54] Sreenath V. Sharma,et al. UCS15A, a non-kinase inhibitor of Src signal transduction , 2001, Oncogene.
[55] N. Hirokawa,et al. Muscle weakness, hyperactivity, and impairment in fear conditioning in tau-deficient mice , 2000, Neuroscience Letters.
[56] S. Nakanishi,et al. PSD-95 promotes Fyn-mediated tyrosine phosphorylation of the N-methyl-D-aspartate receptor subunit NR2A. , 1999, Proceedings of the National Academy of Sciences of the United States of America.
[57] H. Band,et al. Tau interacts with src-family non-receptor tyrosine kinases. , 1998, Journal of cell science.
[58] T. Morgan,et al. Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[59] J. Wood,et al. The protein tyrosine kinase, fyn, in Alzheimer's disease pathology , 1993, Neuroreport.
[60] Guoqiang Dong,et al. Overview of Protein-Protein Interactions and Small-Molecule Inhibitors Under Clinical Development , 2018 .