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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 15 Apr 2016.

Microtubule-associated protein tau

MAPT, PHF-tau, FTDP-17
This gene encodes the microtubule-associated protein tau (MAPT) whose transcript undergoes complex, regulated alternative splicing, giving rise to several mRNA species. MAPT transcripts are differentially expressed in the nervous system, depending on stage of neuronal maturation and neuron type. MAPT gene mutations have been associated with several neurodegenerative disorders such as Alzheimer's disease, Pick's disease, frontotemporal dementia, cortico-basal degeneration and progressive supranuclear palsy. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: AGE, CAN, HAD, H1, APP
Papers using MAPT antibodies
PANTHER: a library of protein families and subfamilies indexed by function
Jackson George R. et al., In Human Molecular Genetics, 2002
... FTDP-17 mutations in tau transgenic mice provoke lysosomal abnormalities ...
Cortical amino acidergic pathways in Alzheimer's disease
DeFelipe Javier et al., In Frontiers in Neuroanatomy, 1986
... (VGLUT-1, 1:5,000, AB5905: Chemicon); parvalbumin (PV, 1:1,000, AB11427: Abcam, Cambridge, United Kingdom); and an anti-human PHF-tau monoclonal antibody (clone AT8, 1:100, MN1020: Thermo Scientific; Waltham, MA, USA) ...
Papers on MAPT
Cellular and molecular modifier pathways in tauopathies: the big picture from screening invertebrate models.
Jahn et al., Heidelberg, Germany. In J Neurochem, Feb 2016
UNASSIGNED: Abnormal tau accumulations were observed and documented in postmortem brains of patients affected by Alzheimer's disease (AD) long before the identification of mutations in the Microtubule associated protein tau (MAPT) gene, encoding the tau protein, in a different neurodegenerative disease called Frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17).
Enhanced genome editing in mammalian cells with a modified dual-fluorescent surrogate system.
Luo et al., Århus, Denmark. In Cell Mol Life Sci, Feb 2016
and 4.9 % when performing single- and double-gene targeting (MAPT and SORL1), respectively, in PPFs using C-Check-validated CRISPR/Cas9 vectors.
Identification of mutations in Korean patients with amyotrophic lateral sclerosis using multigene panel testing.
Kim et al., South Korea. In Neurobiol Aging, Jan 2016
Using this technique, we tried to identify mutations in 4 index patients with familial ALS and 148 sporadic ALS in Korean population and identified 4 known mutations in SOD1, ALS2, MAPT, and SQSTM1 genes, respectively, and 28 variants of uncertain significance in 9 genes.
Variants in the SNCA gene associate with motor progression while variants in the MAPT gene associate with the severity of Parkinson's disease.
Chen et al., Shanghai, China. In Parkinsonism Relat Disord, Jan 2016
INTRODUCTION: It is well known that α-synuclein (SNCA) and microtubule associated protein (MAPT) genes predispose individuals to develop Parkinson's disease (PD).
Biochemical and Behavioral Evaluation of Human MAPT Mutations in Transgenic Drosophila melanogaster.
Ramesh et al., Zābol, Iran. In Biochem Genet, Dec 2015
UNASSIGNED: Mutations in the human microtubule-associated protein tau (hMAPT) gene including R406W and V337M result in autosomal dominant neurodegenerative disorder.
Genome-wide Meta-analysis on the Sense of Smell Among US Older Adults.
Chen et al., New Caledonia. In Medicine (baltimore), Nov 2015
(rs199443 in NSF, P = 3.02 × 10; and rs2732614 in KIAA1267-LRRC37A, P = 6.65 × 10) exhibited cis effects on the expression of microtubule-associated protein tau (MAPT, 17q21.31) in 447 frontal-cortex samples obtained postmortem and profiled by RNA-seq (P < 1 × 10).
Pathways to Parkinsonism Redux: convergent pathobiological mechanisms in genetics of Parkinson's disease.
Cookson et al., Bethesda, United States. In Hum Mol Genet, Nov 2015
Here, we will focus on those genes nominated by genome-wide association studies (GWAS) in sporadic PD, with a particular emphasis on genes that overlap between familial and sporadic disease such as those encoding a-synuclein (SNCA), tau (MAPT), and leucine-rich repeat kinase 2 (LRRK2).
Genetics of Progressive Supranuclear Palsy.
Kim et al., Anyang, South Korea. In J Mov Disord, Sep 2015
Pathologically, diagnosis of PSP is based on characteristic features, such as neurofibrillary tangles, neutrophil threads, tau-positive astrocytes and their processes in basal ganglia and brainstem, and the accumulation of 4 repeat tau protein.
Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: a cross-sectional analysis.
Rossor et al., London, United Kingdom. In Lancet Neurol, Mar 2015
In about a third of patients, the disease is caused by autosomal dominant genetic mutations usually in one of three genes: progranulin (GRN), microtubule-associated protein tau (MAPT), or chromosome 9 open reading frame 72 (C9orf72).
Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies?
Soussi-Yanicostas et al., Paris, France. In Oxid Med Cell Longev, 2014
Hyperphosphorylation and aggregation of the microtubule-associated protein tau in brain, are pathological hallmarks of a large family of neurodegenerative disorders, named tauopathies, which include Alzheimer's disease.
Regulation of human MAPT gene expression.
Lefebvre et al., Lille, France. In Mol Neurodegener, 2014
The number of known pathologies involving deregulated Tau expression/metabolism is increasing.
Huntington's disease is a four-repeat tauopathy with tau nuclear rods.
Lucas et al., Madrid, Spain. In Nat Med, 2014
An imbalance of tau isoforms containing either three or four microtubule-binding repeats causes frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) in families with intronic mutations in the MAPT gene.
Frontotemporal dementia and its subtypes: a genome-wide association study.
Momeni et al., Lubbock, United States. In Lancet Neurol, 2014
Mutations in three genes-MAPT, GRN, and C9orf72--have been associated with FTD.
Genetics of dementia.
Kwok et al., Sydney, Australia. In Lancet, 2014
In this Review, we focus on the evidence for, and the approach to, genetic testing in Alzheimer's disease (APP, PSEN1, and PSEN2 genes), frontotemporal dementia (MAPT, GRN, C9ORF72, and other genes), and other familial dementias.
Tau pathology and neurodegeneration.
Goedert et al., Cambridge, United Kingdom. In Lancet Neurol, 2013
The pathway leading from soluble and monomeric to hyperphosphorylated, insoluble and filamentous tau protein is at the centre of many human neurodegenerative diseases, collectively referred to as tauopathies.
Dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) modulates serine/arginine-rich protein 55 (SRp55)-promoted Tau exon 10 inclusion.
Liu et al., Nantong, China. In J Biol Chem, 2012
Phosphorylation of SRp55 by Dyrk1A suppressed its ability to promote Tau exon 10 inclusion.
Loss of fused in sarcoma (FUS) promotes pathological Tau splicing.
Edbauer et al., München, Germany. In Embo Rep, 2012
Tau mRNA is identified as a physiological splicing target of FUS.
Cyclic AMP-dependent protein kinase regulates 9G8-mediated alternative splicing of tau exon 10.
Liu et al., China. In Febs Lett, 2012
Cyclic AMP-dependent protein kinase regulates 9G8-mediated alternative splicing of tau exon 10
Acute administration of L-DOPA induces changes in methylation metabolites, reduced protein phosphatase 2A methylation, and hyperphosphorylation of Tau protein in mouse brain.
Sontag et al., Dallas, United States. In J Neurosci, 2012
These findings reveal a novel mechanism involving methylation-dependent pathways in L-dopa induces PP2A hypomethylation and increases Tau phosphorylation, which may be potentially detrimental to neuronal cells.
Fibril-forming motifs are essential and sufficient for the fibrillization of human Tau.
Liang et al., Wuhan, China. In Plos One, 2011
Fibril-forming motifs play a key role in the fibrillization of human Tau protein and could be the determinants of amyloidogenic proteins tending to misfold.
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