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Broad kinase inhibition mitigates early neuronal dysfunction and cognitive deficits in tauopathy
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
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Visinin‐like protein‐1: Diagnostic and prognostic biomarker in Alzheimer disease
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PERK inhibition prevents tau-mediated neurodegeneration in a mouse model of frontotemporal dementia
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Changes in proteome solubility indicate widespread proteostatic disruption in mouse models of neurodegenerative disease
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Tau drives translational selectivity by interacting with ribosomal proteins
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Visinin-like proteins (VSNLs): interaction partners and emerging functions in signal transduction of a subfamily of neuronal Ca2+-sensor proteins
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Alterations in oligodendrocyte proteins, calcium homeostasis and new potential markers in schizophrenia anterior temporal lobe are revealed by shotgun proteome analysis
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Elevated connexin43 immunoreactivity at sites of amyloid plaques in alzheimer's disease
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Aberrant protein phosphorylation in Alzheimer disease brain disturbs pro-survival and cell death pathways
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Elevated levels of 3-nitrotyrosine in brain from subjects with amnestic mild cognitive impairment: Implications for the role of nitration in the progression of Alzheimer's disease
inferredcites →https://doi.org/10.1016/j.celrep.2016.04.045openalex-snapshot
Interaction of tau with the RNA-Binding Protein TIA1 Regulates tau Pathophysiology and Toxicity
inferredcites →https://doi.org/10.1016/j.cels.2016.11.006openalex-snapshot
A Multi-network Approach Identifies Protein-Specific Co-expression in Asymptomatic and Symptomatic Alzheimer’s Disease
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Therapeutic strategies for the treatment of tauopathies: Hopes and challenges
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Specific deletion connexin43 in astrocyte ameliorates cognitive dysfunction in APP/PS1 mice
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Identification of changes in neuronal function as a consequence of aging and tauopathic neurodegeneration using a novel and sensitive magnetic resonance imaging approach
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Astrocyte Unfolded Protein Response Induces a Specific Reactivity State that Causes Non-Cell-Autonomous Neuronal Degeneration
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Deep Multilayer Brain Proteomics Identifies Molecular Networks in Alzheimer’s Disease Progression
inferredcites →https://doi.org/10.1016/j.neuroscience.2010.08.001openalex-snapshot
Astroglial connexin immunoreactivity is specifically altered at β-amyloid plaques in β-amyloid precursor protein/presenilin1 mice
inferredcites →https://doi.org/10.1016/j.yexcr.2008.03.015openalex-snapshot
PACSIN proteins bind tubulin and promote microtubule assembly
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Davunetide in patients with progressive supranuclear palsy: a randomised, double-blind, placebo-controlled phase 2/3 trial
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Discovery of 7-Methyl-5-(1-{[3-(trifluoromethyl)phenyl]acetyl}-2,3-dihydro-1 H -indol-5-yl)-7 H -pyrrolo[2,3- d ]pyrimidin-4-amine (GSK2606414), a Potent and Selective First-in-Class Inhibitor of Protein Kinase R (PKR)-like Endoplasmic Reticulum Kinase (PERK)
inferredcites →https://doi.org/10.1021/pr400098ropenalex-snapshot
Measuring and Managing Ratio Compression for Accurate iTRAQ/TMT Quantification
inferredcites →https://doi.org/10.1038/cdd.2017.58openalex-snapshot
When PERK inhibitors turn out to be new potent RIPK1 inhibitors: critical issues on the specificity and use of GSK2606414 and GSK2656157
inferredcites →https://doi.org/10.1038/nn1695openalex-snapshot
Syndapin I is the phosphorylation-regulated dynamin I partner in synaptic vesicle endocytosis
inferredcites →https://doi.org/10.1038/nrm1072openalex-snapshot
Beyond the gap: functions of unpaired connexon channels
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Neuronal calcium sensor proteins: generating diversity in neuronal Ca2+ signalling
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Calcium dyshomeostasis and intracellular signalling in alzheimer's disease
inferredcites →https://doi.org/10.1038/s41419-019-1523-3openalex-snapshot
The unfolded protein response modulators GSK2606414 and KIRA6 are potent KIT inhibitors
inferredcites →https://doi.org/10.1038/s41467-019-10428-1openalex-snapshot
Factors other than hTau overexpression that contribute to tauopathy-like phenotype in rTg4510 mice
inferredcites →https://doi.org/10.1038/s41591-020-0815-6openalex-snapshot
Large-scale proteomic analysis of Alzheimer’s disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation
inferredcites →https://doi.org/10.1038/sdata.2018.36openalex-snapshot
Global quantitative analysis of the human brain proteome in Alzheimer’s and Parkinson’s Disease
inferredcites →https://doi.org/10.1038/tp.2011.20openalex-snapshot
Association of VSNL1 with schizophrenia, frontal cortical function, and biological significance for its gene product as a modulator of cAMP levels and neuronal morphology
inferredcites →https://doi.org/10.1042/bsr20193510openalex-snapshot
Astroglial connexins and cognition: memory formation or deterioration?
inferredcites →https://doi.org/10.1074/jbc.m112.403451openalex-snapshot
PACSIN1, a Tau-interacting Protein, Regulates Axonal Elongation and Branching by Facilitating Microtubule Instability
inferredcites →https://doi.org/10.1083/jcb.93.1.97openalex-snapshot
Isolation of intracellular membranes by means of sodium carbonate treatment: application to endoplasmic reticulum.
inferredcites →https://doi.org/10.1091/mbc.e05-01-0076openalex-snapshot
EHD Proteins Associate with Syndapin I and II and Such Interactions Play a Crucial Role in Endosomal Recycling
inferredcites →https://doi.org/10.1093/jnen/nlv018openalex-snapshot
Altered Levels of Visinin-Like Protein 1 Correspond to Regional Neuronal Loss in Alzheimer Disease and Frontotemporal Lobar Degeneration
inferredcites →https://doi.org/10.1093/jnen/nly037openalex-snapshot
Gene Expression Profile in Frontal Cortex in Sporadic Frontotemporal Lobar Degeneration-TDP
inferredcites →https://doi.org/10.1093/nar/gkz1031openalex-snapshot
The reactome pathway knowledgebase
inferredcites →https://doi.org/10.1093/nar/gkz369openalex-snapshot
g:Profiler: a web server for functional enrichment analysis and conversions of gene lists (2019 update)
inferredcites →https://doi.org/10.1097/jes.0b013e3182798a95openalex-snapshot
Measuring Protein Synthesis With SUnSET
inferredcites →https://doi.org/10.1101/gr.1239303openalex-snapshot
Cytoscape: A Software Environment for Integrated Models of Biomolecular Interaction Networks
inferredcites →https://doi.org/10.1101/gr.233866.117openalex-snapshot
Large-scale discovery of mouse transgenic integration sites reveals frequent structural variation and insertional mutagenesis
inferredcites →https://doi.org/10.1111/j.1471-4159.2007.05194.xopenalex-snapshot
The GSK3 hypothesis of Alzheimer’s disease
inferredcites →https://doi.org/10.1126/science.1113694openalex-snapshot
Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function
inferredcites →https://doi.org/10.1126/science.aau0437openalex-snapshot
Alzheimer's disease: The right drug, the right time
inferredcites →https://doi.org/10.1126/scitranslmed.3006767openalex-snapshot
Oral Treatment Targeting the Unfolded Protein Response Prevents Neurodegeneration and Clinical Disease in Prion-Infected Mice
inferredcites →https://doi.org/10.1126/scitranslmed.aaw8412openalex-snapshot
Off-target toxicity is a common mechanism of action of cancer drugs undergoing clinical trials
inferredcites →https://doi.org/10.1128/mcb.23.20.7198-7209.2003openalex-snapshot
Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival
inferredcites →https://doi.org/10.1186/1750-1326-9-8openalex-snapshot
Effects of the C57BL/6 strain background on tauopathy progression in the rTg4510 mouse model
inferredcites →https://doi.org/10.1186/s12929-019-0609-7openalex-snapshot
Clinical trials of new drugs for Alzheimer disease
inferredcites →https://doi.org/10.1186/s13024-018-0282-4openalex-snapshot
Deep proteomic network analysis of Alzheimer’s disease brain reveals alterations in RNA binding proteins and RNA splicing associated with disease
inferredcites →https://doi.org/10.1186/s40169-017-0181-2openalex-snapshot
A perspective on multi‐target drug discovery and design for complex diseases
inferredcites →https://doi.org/10.1186/s40478-018-0642-xopenalex-snapshot
GJA1 (connexin43) is a key regulator of Alzheimer’s disease pathogenesis
inferredcites →https://doi.org/10.1186/s40478-019-0664-zopenalex-snapshot
A walk through tau therapeutic strategies
inferredcites →https://doi.org/10.1186/s40478-020-00950-5openalex-snapshot
Transcriptional profiling of multiple system atrophy cerebellar tissue highlights differences between the parkinsonian and cerebellar sub-types of the disease
inferredcites →https://doi.org/10.1212/wnl.0b013e318248e568openalex-snapshot
CSF VILIP-1 predicts rates of cognitive decline in early Alzheimer disease
inferredcites →https://doi.org/10.1242/jcs.02376openalex-snapshot
Neuronal Ca2+ sensor protein VILIP-1 affects cGMP signalling of guanylyl cyclase B by regulating clathrin-dependent receptor recycling in hippocampal neurons
inferredcites →https://doi.org/10.1242/jcs.113.24.4511openalex-snapshot
All three PACSIN isoforms bind to endocytic proteins and inhibit endocytosis
inferredcites →https://doi.org/10.1373/clinchem.2006.070912openalex-snapshot
Identification of Novel Brain Biomarkers
inferredcites →https://doi.org/10.1373/clinchem.2008.104497openalex-snapshot
The Brain Injury Biomarker VLP-1 Is Increased in the Cerebrospinal Fluid of Alzheimer Disease Patients
inferredcites →https://doi.org/10.1523/jneurosci.0587-07.2007openalex-snapshot
Accumulation of Pathological Tau Species and Memory Loss in a Conditional Model of Tauopathy
inferredcites →https://doi.org/10.1523/jneurosci.0628-17.2017openalex-snapshot
Local Inhibition of PERK Enhances Memory and Reverses Age-Related Deterioration of Cognitive and Neuronal Properties
inferredcites →https://doi.org/10.1523/jneurosci.0984-06.2006openalex-snapshot
Parkinson's Disease Brain Mitochondrial Complex I Has Oxidatively Damaged Subunits and Is Functionally Impaired and Misassembled
inferredcites →https://doi.org/10.1523/jneurosci.3029-15.2016openalex-snapshot
Pathological Tau Promotes Neuronal Damage by Impairing Ribosomal Function and Decreasing Protein Synthesis
inferredcites →https://doi.org/10.1523/jneurosci.5397-12.2013openalex-snapshot
Tau Accumulation Activates the Unfolded Protein Response by Impairing Endoplasmic Reticulum-Associated Degradation
inferredcites →https://doi.org/10.2174/1567205013666151218145431openalex-snapshot
PERK-opathies: An Endoplasmic Reticulum Stress Mechanism Underlying Neurodegeneration
inferredcites →https://doi.org/10.3109/10715762.2010.520014openalex-snapshot
Roles of 3-nitrotyrosine- and 4-hydroxynonenal-modified brain proteins in the progression and pathogenesis of Alzheimer's disease
inferredcites →https://doi.org/10.3233/jad-150060openalex-snapshot
The Role of Visinin-Like Protein-1 in the Pathophysiology of Alzheimer’s Disease
inferredcites →https://doi.org/10.3389/fnagi.2019.00083openalex-snapshot
Identification of Temporal Characteristic Networks of Peripheral Blood Changes in Alzheimer’s Disease Based on Weighted Gene Co-expression Network Analysis
inferredcites →https://doi.org/10.3389/fnins.2018.00111openalex-snapshot
PERK Pathway Activation Promotes Intracerebral Hemorrhage Induced Secondary Brain Injury by Inducing Neuronal Apoptosis Both in Vivo and in Vitro
inferredcites →https://doi.org/10.3389/fnmol.2018.00118openalex-snapshot
Connexin-Mediated Functional and Metabolic Coupling Between Astrocytes and Neurons
inferredcites →https://doi.org/10.3892/etm.2017.4905openalex-snapshot
Dynamical differential networks and modules inferring disrupted genes associated with the progression of Alzheimer's disease
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Incoming claims: where this work appears in other papers’ reference lists and arguments.
inferred← citeshttps://doi.org/10.3389/fnagi.2021.791679openalex-snapshot
Magnetic Resonance Imaging in Tauopathy Animal Models
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