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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 10 Nov 2015.

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
Genetic Disorders with Tau Pathology: A Review of the Literature and Report of Two Patients with Tauopathy and Positive Family Histories.
Wszolek et al., Jacksonville, United States. In Neurodegener Dis, 10 Dec 2015
Mutations in the microtubule-associated protein tau gene (MAPT) cause a small subset of primary tauopathies.
Biochemical classification of tauopathies by immunoblot, protein sequence and mass spectrometric analyses of sarkosyl-insoluble and trypsin-resistant tau.
Hasegawa et al., Tokyo, Japan. In Acta Neuropathol, 04 Dec 2015
We have analyzed pathological tau in Alzheimer's disease, and in frontotemporal lobar degeneration associated with tauopathy to include cases with Pick bodies, corticobasal degeneration, progressive supranuclear palsy, and ones due to intronic mutations in MAPT.
The Direction of the Acceleration and Rotational Forces Associated with Mild Traumatic Brain Injury in Rodents Effect Behavioural and Molecular Outcomes.
Esser et al., Calgary, Canada. In J Neurosci Methods, 17 Nov 2015
Male and female rats underwent a behavioural test battery followed by analysis of 5 TBI-associated biomarkers (BDNF, Eno2, GFAP, MAPT, TERT) from the prefrontal cortex and hippocampus.
Pathways to Parkinsonism Redux: convergent pathobiological mechanisms in genetics of Parkinson's disease.
Cookson et al., Bethesda, United States. In Hum Mol Genet, 15 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).
Association of APOE with tau-tangle pathology with and without β-amyloid.
Bennett et al., São Paulo, Brazil. In Neurobiol Aging, 28 Oct 2015
UNASSIGNED: This study tested the hypothesis that the association of apolipoprotein E (APOE) with paired helical filament tau (PHF-tau) tangle pathology differs in brains with and without β-amyloid.
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.
Studying Tauopathies in Drosophila: A Fruitful Model.
Chen et al., Baltimore, United States. In Exp Neurol, May 2015
UNASSIGNED: Tauopathies are a group of neurodegenerative disorders that include hereditary frontotemporal dementias (FTDs) such as FTD with parkinsonism linked to chromosome 17 (FTDP-17), as well as sporadic variants of FTDs like progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Pick's disease.
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).
Invited review: Frontotemporal dementia caused by microtubule-associated protein tau gene (MAPT) mutations: a chameleon for neuropathology and neuroimaging.
Goedert et al., Indianapolis, United States. In Neuropathol Appl Neurobiol, Feb 2015
Hereditary frontotemporal dementia associated with mutations in the microtubule-associated protein tau gene (MAPT) is a protean disorder.
Analysis of in vivo turnover of tau in a mouse model of tauopathy.
Holtzman et al., Tokyo, Japan. In Mol Neurodegener, Dec 2014
To examine the effect of a tauopathy-associated mutation on tau clearance, half-lives of various tau species were compared between the mice with a FTDP-17 mutation that induces β-sheet formation, ΔK280 mutation (pro-aggregant mice) and control mice with additional β-sheet breaking mutations (anti-aggregant mice).
Huntington's disease is a four-repeat tauopathy with tau nuclear rods.
Lucas et al., Madrid, Spain. In Nat Med, Aug 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, Jul 2014
Mutations in three genes-MAPT, GRN, and C9orf72--have been associated with FTD.
Genetics of dementia.
Kwok et al., Sydney, Australia. In Lancet, Apr 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.
Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism.
Baekelandt et al., Leuven, Belgium. In Front Genet, 2013
Another gene, microtubule associated protein tau (MAPT), has been genetically linked to a dominant form of frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) and genome-wide association studies report a strong association between MAPT and sporadic PD.
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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