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Human Polyclonal MAPT Primary Antibody for WB - ABIN3043190
Tu, Pang, Chen, Zhang, Zhang, Lu, Wang: Effects of surface charges of graphene oxide on neuronal outgrowth and branching. in The Analyst 2013
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Cow (Bovine) Monoclonal MAPT Primary Antibody for IHC (p), WB - ABIN3043669
Li, Li, Li, Quan, Wang: Cellular and molecular mechanisms underlying the action of ginsenoside Rg1 against Alzheimer's disease. in Neural regeneration research 2014
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Human Polyclonal MAPT Primary Antibody for IHC, WB - ABIN362074
Giasson, Sampathu, Wilson, Vogelsberg-Ragaglia, Mushynski, Lee: The environmental toxin arsenite induces tau hyperphosphorylation. in Biochemistry 2002
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Human Polyclonal MAPT Primary Antibody for IHC - ABIN967154
Nacharaju, Ko, Yen: Characterization of in vitro glycation sites of tau. in Journal of neurochemistry 1997
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Human Polyclonal MAPT Primary Antibody for IHC - ABIN967158
Gustin, Ozes, Akca, Pincheira, Mayo, Li, Guzman, Korgaonkar, Donner: Cell type-specific expression of the IkappaB kinases determines the significance of phosphatidylinositol 3-kinase/Akt signaling to NF-kappa B activation. in The Journal of biological chemistry 2004
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Human MAPT Primary Antibody for IHC - ABIN967144
Lalonde, Kim, Fukuchi: Exploratory activity, anxiety, and motor coordination in bigenic APPswe + PS1/DeltaE9 mice. in Neuroscience letters 2004
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Human Polyclonal MAPT Primary Antibody for IHC - ABIN967152
Alonso, Mederlyova, Novak, Grundke-Iqbal, Iqbal: Promotion of hyperphosphorylation by frontotemporal dementia tau mutations. in The Journal of biological chemistry 2004
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Human MAPT Primary Antibody for IHC - ABIN967147
Andreadis, Brown, Kosik: Structure and novel exons of the human tau gene. in Biochemistry 1992
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Human Polyclonal MAPT Primary Antibody for IHC, WB - ABIN362062
Puig, Rey, Ferrer: Individual and regional variations of phospho-tau species in progressive supranuclear palsy. in Acta neuropathologica 2005
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Human Polyclonal MAPT Primary Antibody for IHC (p), ELISA - ABIN544823
Gamblin, Chen, Zambrano, Abraha, Lagalwar, Guillozet, Lu, Fu, Garcia-Sierra, LaPointe, Miller, Berry, Binder, Cryns: Caspase cleavage of tau: linking amyloid and neurofibrillary tangles in Alzheimer's disease. in Proceedings of the National Academy of Sciences of the United States of America 2003
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EPR analysis indicated that fibrils seeded with truncated and mutated Tau, but not htau40, are structurally disordered in the second half of repeat four and onward. These findings suggest that the disorder in this region diminishes the ability of 4R Tau fibrils to recruit 3R Tau monomers, revealing a new mechanism for Tau cross-seeding barriers.
data suggest that H1/H2 MAPT haplotype is not a risk factor to Parkinson Disease in Mexican mestizo population.
Seed competent tau monomer thus adopts multiple, stable seed-competent conformations, each of which encodes a limited number of strains.
Abeta and tau may be considered as novel biomarkers of sleep disorder in AD pathology, and that they function by regulating the expression levels of orexin A and adenosine A1R.
A decrease in CDK5 and MAPT gene expression was found in Alzheimer's disease (AD) patients' brains, significant differences were found in CDK5 expression in the hippocampus and the entorhinal cortex. In both cases, mRNA was lower in the AD group); however, the same analysis using the MAPT gene revealed no significant statistical differences.
Among hip fracture patients, 88.6% of the cognitively normal (Clinical Dementia Rating-CDR 0; n = 70) and 98.8% with mild cognitive impairment (CDR 0.5; n = 81) fell in the abnormal biomarker categories by CSF Abeta42/40 ratio, p-tau, and t-tau measures.
findings show how tau can adopt distinct folds in the human brain in different diseases, an essential step for understanding the formation and propagation of molecular conformers
we show that important downstream pathways, including autophagy and the unfolded protein response, are coregulated with neurotoxicity and actin cytoskeletal stabilization in brains of flies expressing wild-type human and various FTDP-17 tau mutants, supporting a conserved mechanism of neurotoxicity of wild-type tau and FTDP-17 mutant tau in disease pathogenesis
Frontotemporal dementia patients manifest significant reduction of the GluR3 subunit in the postsynaptic fraction due to autoantibodies along with increased levels of neuronal Tau.
P301L and S320F mutation of Tau showed robust protein aggregation.
Inhibition of galectin-8- and NDP52-dependent autophagy increased seeded tau aggregation.
Microtubule associated protein tau (tau) is shown to prefer binding to AT-rich sequence.
defects in MAPT lead to aberrant mitotic spindle function, abnormal chromosome segregation, and apoptosis
The study reviewed two congenital myotonic dystrophy type 1 patients, with a case showing severe cognitive dysfunction and atypical pathology associated with predominant 4-repeat tauopathy. The exact mechanism of 4-repeat tau dominancy is not yet known.
Full-length Tau when cross-seeded in the presence of polyglutamate with amyloid seeds obtained de novo from its two fragments: K18 and K18DeltaK280 converts into daughter fibrils whose only initial generations are controlled by the conformational memory effect. In the following rounds of seeding, the phenotypes carried by mother seeds "lose" to the phenotype that emerges spontaneously in FL Tau fibrils self-assembling ...
In an survey of South African rugby players, the tau rs2435200 AA genotype was significantly associated with reduced susceptibility to concussion, while the rs2435200 AG genotype was associated with increased susceptibility of sustaining multiple concussions.
Results found the expression of the exogenous mutant tau protein restricted in medial entorhinal cortex (MEC) at one month in mouse. Its expression induces endogenous tau hyperphosphorylation and accumulation in hippocampus and cortex and inhibits neuronal activity, leading to hippocampus-dependent memory deficit. These data suggest a novel mechanism of early Alzheimer's disease initiated by tau accumulation in MEC.
Abnormal filamentous aggregates that are formed by tangled tau protein turn out to be classic amyloid fibrils, meeting all the criteria defined under the fuzzy oil drop model in the context of amyloid characterization. The model recognizes amyloids as linear structures where local hydrophobicity minima and maxima propagate in an alternating manner along the fibril's long axis.
Data suggest that an eleven-amino acid sequence (18-28) unique to extreme N-terminus of TAU from humans and non-human primates is linked to differential interactions of TAU with a small subset of partners in cortical nerve tissue (here, cell lysates from Tau knockout mice).
It was revealed that Al2O3 NPs bind to tau protein and form a static complex and fold the structure of tau toward a more packed structure. Molecular docking and molecular dynamic investigations revealed that NPs bind to the hydrophilic residues of the tau segments and promote some marginal structural folding of tau segment
TauKO mice were hyperglycemic and glucose intolerant at an early age. Islet insulin content was reduced and proinsulin levels were significantly elevated in tauKO mice, resulting in impaired glucose-stimulated insulin secretion. Loss of tau also resulted in increased epididymal fat mass and leptin levels, reduced glucose production, and insulin resistance at later ages, leading to complete onset of diabetes.
MeCP2-Transgenic mice display elevated GFAP and Tau expression within the hippocampus and cortex followed by neuronal loss in these brain regions.
Phosphorylation of Tau protein is associated with reduced hippocampal excitability in Alzheimer's disease.
that tau modulates motility in a motor-specific manner to direct intracellular transport
the AD-like tau accumulation induces anxiety through disrupting miR92a-vGAT-GABA signaling, which reveals molecular mechanisms underlying the anxiety behavior in AD patients and potentially leads to the development of new therapeutics for tauopathies.
These results show for the first time that the phosphorylation and isoform alteration of tau are regulated differently during mouse development.
In adult and aged tau(+/+), tau(+/-), tau(-/-) mice tau deficiency could not induce significant motor disorders. However, found lower expression levels of transcription factors Orthodenticle homeobox 2 (OTX2) of midbrain dopaminergic neurons in older aged mice. Results suggested that tau deficiency alone might not be enough to mimic the pathology of Parkinson's disease.
Tau deletion increased ATP production and improved the recognition memory and attentive capacity of juvenile mice.
MAPT variant interaction with mutant amyloid protein precursor causes frontotemporal dementia.
These results establish that in addition to the neuritic plaque, a second determinant is required to drive the conversion of wild-type tau.
miR-322 promotes Tau phosphorylation via negatively controlling BDNF-TrkB receptor activation
High tau expression is associated with blood vessel abnormalities and angiogenesis in Alzheimer's disease.
Disinhibiation of Gas6 binding to Tyro3 due to PGRN reduction results in activation of PKCalpha via PLCgamma, inducing tau phosphorylation at Ser203, mislocalization of tau to dendritic spines, and spine loss.
frontotemporal dementia and parkinsonism linked to chromosome 17 tau with a mutation in the C-terminal region had different banding patterns, indicating a different phosphorylation pattern.
For the three conditions, FRAP analysis revealed a similar mobility in dendrites compared with axons; however, Tau-mEOS2 was less mobile than hWT-Tau and hP301L-Tau and the mobile fraction was smaller, possibly reflecting less efficient microtubule binding of Tau when over-expressed. Together, our study presents Tau-mEOS2 mice as a novel tool for the study of Tau in a physiological and a pathological context.
Chronic Dyrk1 inhibition reversed cognitive deficits in Alzheimer's disease transgenic mice via reduction of APP and phosphorylated tau pathology.
Results suggest the importance of the autophagosome for the low-frequency stimulation-induced oligomerization of tau and suggest a reason for its age dependency. Interestingly, the lysosomal disturbance promoted the formation of the fibrillar form of aggregates consisting of hyper-phosphorylated tau.
the energy landscape of Tau-mediated, GTP-dependent 'active' microtubule bundles, is reported.
Findings suggest that the endothelin-1-induced down-regulation of NaV1.7 (SCN9A) diminishes NaV1.7-related catecholamine secretion and dephosphorylation of tau.
The protein phosphatase PP2A/Balpha binds to the microtubule-associated proteins Tau and MAP2 at a motif also recognized by the kinase Fyn.
show that cathepsin D cleaves both tau and beta-amyloid precursor protein (APP). Both tau and APP are involved in the pathogenesis of Alzheimer's disease
results suggest that Nav1.7-Ca2+ influx-protein kinase C-alpha pathway activated ERK1/ERK2 and p38, which increased phosphorylation of glycogen synthase kinase-3beta, decreasing tau phosphorylation
We conclude that GSK3beta phosphorylates tau directly at S(202) but requires the previous phosphorylation on S(235) to phosphorylate T(231). Phosphorylation of S(396), on the other hand, occurs sequentially.
hyperphosphorylated-tau specific local phosphorylation patterns at Thr212/Ser214 and Thr231/Ser235 using monoclonal antibodies (mAb) generated against correspondingly modified peptides
Suppressing the expression of all tau isoforms disrupted only those neuronal microtubules containing class II beta-tubulin, and that boosting the expression of the largest 'big', but not the smallest, tau isoform enhanced neurite outgrowth.
We found that inversion of the MAPT region is similarly polymorphic in other great ape species, and we present evidence that the inversions occurred independently in chimpanzees and humans
age-related increase in cAMP-dependent protein kinase (PKA) phosphorylation of tau at serine 214 (pS214-tau) in monkey dorsolateral prefrontal association cortex specifically targets spine synapses and the Ca(2+)-storing spine apparatus.
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.
G protein beta1/gamma2 subunit-interacting factor 1
, neurofibrillary tangle protein
, paired helical filament-tau
, Tau microtubule-associated protein
, microtubule associated protein tau
, tau-like protein
, tau-like protein-2
, microtubule-associated protein tau
, Microtubule-associated protein tau
, Neurofibrillary tangle protein
, Paired helical filament-tau
, sodium- and chloride-dependent taurine transporter
, solute carrier family 6 (neurotransmitter transporter, taurine), member 6
, solute carrier family 6 (neurotransmitter transporter, taurine), member 6b
, taurine transporter