Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome. - Wikidata - wikimedia - TriplyDB

Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

http://www.wikidata.org/entity/Q36841753

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Down syndrome: searching for the genetic culprits Dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) modulates serine/arginine-rich protein 55 (SRp55)-promoted Tau exon 10 inclusion MicroRNA: Implications for Alzheimer Disease and other Human CNS Disorders DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome Dissecting Alzheimer disease in Down syndrome using mouse models A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome Tangles, Toxicity, and Tau Secretion in AD - New Approaches to a Vexing Problem Tau and tauopathies Structures of Down Syndrome Kinases, DYRKs, Reveal Mechanisms of Kinase Activation and Substrate Recognition The structure of a dual-specificity tyrosine phosphorylation-regulated kinase 1A-PKC412 complex reveals disulfide-bridge formation with the anomalous catalytic loop HRD(HCD) cysteine Design and synthesis of a library of lead-like 2,4-bisheterocyclic substituted thiophenes as selective Dyrk/Clk inhibitors Selective inhibition of the kinase DYRK1A by targeting its folding process Personality and risk of Alzheimer's disease: new data and meta-analysis.DYRK1A genetic variants are not linked to Alzheimer's disease in a Spanish case-control cohort.Dyrk1A overexpression leads to increase of 3R-tau expression and cognitive deficits in Ts65Dn Down syndrome mice Neuropathological role of PI3K/Akt/mTOR axis in Down syndrome brain.Mechanisms of tau-induced neurodegeneration.Plasma DYRK1A as a novel risk factor for Alzheimer's disease.Phosphorylation of tau at Thr212, Thr231, and Ser262 combined causes neurodegeneration The role of DYRK1A in neurodegenerative diseases.REST regulates DYRK1A transcription in a negative feedback loop.Link between DYRK1A overexpression and several-fold enhancement of neurofibrillary degeneration with 3-repeat tau protein in Down syndrome Regulation of alternative splicing of tau exon 10 by 9G8 and Dyrk1A Down syndrome--recent progress and future prospects.Alzheimer's disease neurofibrillary degeneration: pivotal and multifactorial Truncation and activation of GSK-3β by calpain I: a molecular mechanism links to tau hyperphosphorylation in Alzheimer's disease.Screening Dyrk1A inhibitors by MALDI-QqQ mass spectrometry: systematic comparison to established radiometric, luminescence, and LC-UV-MS assays.Truncation and Activation of Dual Specificity Tyrosine Phosphorylation-regulated Kinase 1A by Calpain I: A MOLECULAR MECHANISM LINKED TO TAU PATHOLOGY IN ALZHEIMER DISEASE.Opportunities and Limitations of Modelling Alzheimer's Disease with Induced Pluripotent Stem Cells Altered regulation of tau phosphorylation in a mouse model of down syndrome aging Antioxidants in Down syndrome.Hypocellularity in the Murine Model for Down Syndrome Ts65Dn Is Not Affected by Adult Neurogenesis.Down syndrome and the molecular pathogenesis resulting from trisomy of human chromosome 21.Down syndrome and Alzheimer's disease: Common pathways, common goals.The genomically mosaic brain: aneuploidy and more in neural diversity and disease.The role of overexpressed DYRK1A protein in the early onset of neurofibrillary degeneration in Down syndrome.Developmental regulation of tau phosphorylation, tau kinases, and tau phosphatases.Interactions between GSK3β and amyloid genes explain variance in amyloid burden.Dysregulation of insulin signaling, glucose transporters, O-GlcNAcylation, and phosphorylation of tau and neurofilaments in the brain: Implication for Alzheimer's disease.New Perspectives of Dyrk1A Role in Neurogenesis and Neuropathologic Features of Down Syndrome

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

http://www.wikidata.org/entity/Q36841753

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

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Overexpression of Dyrk1A contributes to neurofibrillary degeneration in Down syndrome.

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Jerzy Wegiel

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Khalid Iqbal

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Narayan Ramakrishna

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Yu-Wen Hwang

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Zhihou Liang

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P2860

The kinase DYRK phosphorylates protein-synthesis initiation factor eIF2Bepsilon at Ser539 and the microtubule-associated protein tau at Thr212: potential role for DYRK as a glycogen synthase kinase 3-priming kinase

A genome-wide Drosophila RNAi screen identifies DYRK-family kinases as regulators of NFAT

Isolation of human and murine homologues of the Drosophila minibrain gene: human homologue maps to 21q22.2 in the Down syndrome "critical region"

Sequence characteristics, subcellular localization, and substrate specificity of DYRK-related kinases, a novel family of dual specificity protein kinases

Hyperphosphorylation induces self-assembly of tau into tangles of paired helical filaments/straight filaments

DSCR1, overexpressed in Down syndrome, is an inhibitor of calcineurin-mediated signaling pathways

Human minibrain homologue (MNBH/DYRK1): characterization, alternative splicing, differential tissue expression, and overexpression in Down syndrome

Dynamin is a minibrain kinase/dual specificity Yak1-related kinase 1A substrate

Dyrk1A expression pattern supports specific roles of this kinase in the adult central nervous system

Aberrant glycosylation modulates phosphorylation of tau by protein kinase A and dephosphorylation of tau by protein phosphatase 2A and 5

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