gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Mar 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
Supplier
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
Supplier
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
Lack of exacerbation of neurodegeneration in a double transgenic mouse model of mutant LRRK2 and tau.
New
Beal et al., New York City, United States. In Hum Mol Genet, 24 Apr 2015
Microtubule associated-protein tau (MAPT) mutations cause a group of neurodegenerative diseases termed tauopathies.
Impaired retrograde transport by the Dynein/Dynactin complex contributes to Tau-induced toxicity.
New
Voigt et al., Hannover, Germany. In Hum Mol Genet, 20 Apr 2015
UNASSIGNED: The gene mapt codes for the microtuble-associated protein Tau.
A novel Alzheimer disease locus located near the gene encoding tau protein.
New
Farrer et al., Boston, United States. In Mol Psychiatry, 17 Apr 2015
Among APOE ɛ4- subjects, novel genome-wide significant (GWS) association was observed with 17 SNPs (all between KANSL1 and LRRC37A on chromosome 17 near MAPT) in a meta-analysis of the stage 1 and stage 2 data sets (best SNP, rs2732703, P=5·8 × 10(-9)).
Lovastatin suppresses the aberrant tau phosphorylation from FTDP-17 mutation and okadaic acid-induction in rat primary neurons.
New
Ma et al., Wuxi, China. In Neuroscience, 11 Apr 2015
Here we demonstrated that lovastatin suppressed the aberrant tau phosphorylation both from FTDP-17 mutation and okadaic acid induction in cultured rat primary neurons.
Presymptomatic cognitive and neuroanatomical changes in genetic frontotemporal dementia in the Genetic Frontotemporal dementia Initiative (GENFI) study: a cross-sectional analysis.
New
Impact
Rossor et al., London, United Kingdom. In Lancet Neurol, 31 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).
Frontotemporal dementia parkinsonism: Clinical findings in a large Iranian family.
New
Meamar et al., Eşfahān, Iran. In Adv Biomed Res, Dec 2014
FTD and parkinsonism linked to chromosome 17 (FTDP-17) was defined during the International Consensus Conference in Ann Arbor, Michigan in 1996.
Huntington's disease is a four-repeat tauopathy with tau nuclear rods.
New
Impact
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.
New
Impact
Momeni et al., Lubbock, United States. In Lancet Neurol, Jul 2014
Mutations in three genes-MAPT, GRN, and C9orf72--have been associated with FTD.
Frontotemporal lobar degeneration: a clinical approach.
Review
New
Miller et al., San Francisco, United States. In Semin Neurol, Apr 2014
Parkinsonism presents in all syndromes, especially cases with tau pathology and MAPT or GRN mutations.
Genetics of dementia.
Review
New
Impact
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.
Physiological and pathological phosphorylation of tau by Cdk5.
Review
Hisanaga et al., Hachiōji, Japan. In Front Mol Neurosci, 2013
Hyperphosphorylation of microtubule-associated protein tau is one of the major pathological events in Alzheimer's disease (AD) and other related neurodegenerative diseases, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17).
Genetics and genomics of Parkinson's disease.
Review
Farrer et al., Vancouver, Canada. In Genome Med, 2013
Recent discoveries in sporadic, Mendelian and more complex forms of parkinsonism provide novel insight into disease etiology; 28 genes, including those encoding alpha-synuclein (SNCA), leucine-rich repeat kinase 2 (LRRK2) and microtubule-associated protein tau (MAPT), have been linked and/or associated with PD.
Phosphatases of α-synuclein, LRRK2, and tau: important players in the phosphorylation-dependent pathology of Parkinsonism.
Review
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.
Review
Impact
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.
New perspective on parkinsonism in frontotemporal lobar degeneration.
Review
Chung et al., South Korea. In J Mov Disord, 2013
The genes associated with parkinsonism are microtubule associated protein tau (MAPT), progranulin (GRN or PGRN), and chromosome 9 open reading frame 72 (C9ORF72) repeat expansion.
Dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) modulates serine/arginine-rich protein 55 (SRp55)-promoted Tau exon 10 inclusion.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
share on facebooktweetadd +1mail to friends