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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 02 Oct 2014.

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: CAN, AGE, 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
Molecular dynamics simulation of the phosphorylation-induced conformational changes of a tau peptide fragment.
Mancera et al., Perth, Australia. In Proteins, 30 Sep 2014
Aggregation of the microtubule associated protein tau (MAPT) within neurons of the brain is the leading cause of tauopathies such as Alzheimer's disease.
Dysregulated expression of lipid storage and membrane dynamics factors in Tia1 knockout mouse nervous tissue.
Auburger et al., In Neurogenetics, May 2014
Because other stress granule components such as TDP-43, FUS, ATXN2,SMN, MAPT, HNRNPA2B1, and HNRNPA1 are crucial for the motor neuron diseases amyotrophic lateral sclerosis (ALS)/spinal muscular atrophy (SMA) and for the frontotemporal dementia(FTD), here we studied mouse nervous tissue to identify mRNAs with selective dependence on Tia1 deletion.
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.
[Synergistic interaction between melittin and chemotherapeutic agents and their possible mechanisms: an experimental research].
Zou et al., In Zhongguo Zhong Xi Yi Jie He Za Zhi, Feb 2014
(3) After treatment suppressed were the expressions of chemotherapeutic agent-associated genes of BGC-823 cells such as thymidylate synthetase (TS), excision repair cross-complementing gene 1 (ERCC1), breast cancer susceptibility gene 1 (BRCA1), beta-tubulin III (TUBB3), and microtubule-associated protein tau (MAPT).
Neuronal-specific deficiency of the splicing factor Tra2b causes apoptosis in neurogenic areas of the developing mouse brain.
Wirth et al., Köln, Germany. In Plos One, Dec 2013
TRA2B has been shown to be involved in splicing processes of Nasp (nuclear autoantigenic sperm protein), MAPT (microtubule associated protein tau) and SMN (survival motor neuron), and is therefore implicated in spermatogenesis and neurological diseases like Alzheimer's disease, dementia, Parkinson's disease and spinal muscular atrophy.
Brain pathology in myotonic dystrophy: when tauopathy meets spliceopathy and RNAopathy.
Sergeant et al., Lille, France. In Front Mol Neurosci, Dec 2013
Tauopathies are a group of nearly 30 neurodegenerative diseases that are characterized by intraneuronal protein aggregates of the microtubule-associated protein Tau (MAPT) in patient brains.
Frontotemporal lobar degeneration: current perspectives.
Diehl-Schmid et al., München, Germany. In Neuropsychiatr Dis Treat, Dec 2013
Of these, the microtubule-associated protein tau (MAPT), the transactive response DNA-binding protein, and the fused in sarcoma protein are most important.
A case of 17q21.31 microduplication and 7q31.33 microdeletion, associated with developmental delay, microcephaly, and mild dysmorphic features.
George et al., Auckland, New Zealand. In Case Rep Genet, Dec 2013
which encompasses the CRHR1, MAPT, and KANSL1 genes, as well as a microdeletion in chromosome 7q31.33
Vaccination with Sarkosyl insoluble PHF-tau decrease neurofibrillary tangles formation in aged tau transgenic mouse model: a pilot study.
Brion et al., Paris, France. In J Alzheimers Dis, Dec 2013
This immunization protocol with fibrillar PHF-tau was well tolerated and did not induce an inflammatory reaction in the brain or adverse effect in these aged mice.
Tau oligomers as potential targets for early diagnosis of tauopathy.
Higuchi et al., Gainesville, United States. In J Alzheimers Dis, Dec 2013
The rTg4510 mouse line expressing human tau with P301L FTDP-17-tau mutation has been established to understand the role of tau in neurodegeneration.
Tau pathology and neurodegeneration.
Goedert et al., Cambridge, United Kingdom. In Lancet Neurol, Jun 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.
The role of tau in neurodegenerative diseases and its potential as a therapeutic target.
Wolfe, Boston, United States. In Scientifica (cairo), 2011
The discovery that dominant mutations in the MAPT gene encoding tau are associated with familial frontotemporal dementia strongly supports abnormal tau protein as directly involved in disease pathogenesis.
Neuropathologically defined subtypes of Alzheimer's disease with distinct clinical characteristics: a retrospective study.
Dickson et al., Jacksonville, United States. In Lancet Neurol, 2011
Microtubule-associated protein tau (MAPT) H1H1 genotype was more common in limbic-predominant AD (54 [70%]) than in hippocampal sparing AD (24 [46%]; p=0.011), but did not differ significantly between limbic-predominant and typical AD (204 [59%]; p=0.11).
Identification of common variants influencing risk of the tauopathy progressive supranuclear palsy.
Schellenberg et al., Marburg an der Lahn, Germany. In Nat Genet, 2011
Variation in MAPT gene is associated with tauopathy progressive supranuclear palsy.
Common genetic variation in the HLA region is associated with late-onset sporadic Parkinson's disease.
Payami et al., Albany, United States. In Nat Genet, 2010
We confirmed associations with SNCA and MAPT, replicated an association with GAK (using data from the NGRC and a previous study, P = 3.2 x 10(-9)) and detected a new association with the HLA region (using data from the NGRC only, P = 2.9 x 10(-8)), which replicated in two datasets (meta-analysis P = 1.9 x 10(-10)).
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