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anti-Human MAPT Antikörper:
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Cow (Bovine) Monoclonal MAPT Primary Antibody für IHC (p), WB - ABIN3043669
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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Human Polyclonal MAPT Primary Antibody für WB - ABIN3043190
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 für 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 Polyclonal MAPT Primary Antibody für 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 für 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 MAPT Primary Antibody für IHC - ABIN967143
Smet, Wieruszeski, Buée, Landrieu, Lippens: Regulation of Pin1 peptidyl-prolyl cis/trans isomerase activity by its WW binding module on a multi-phosphorylated peptide of Tau protein. in FEBS letters 2005
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Human MAPT Primary Antibody für 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 für 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 für 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 für WB - ABIN546569
Puig, Rey, Ferrer: Individual and regional variations of phospho-tau species in progressive supranuclear palsy. in Acta neuropathologica 2005
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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
genetic manipulation of Sirt3 revealed that amyloid-beta increased levels of total tau acetylated tau through its modulation of Sirt3.
Data suggest that both the small heat shock protein HspB1/Hsp27 and the constitutive chaperone Hsc70/HspA8 interact with tau to prevent tau-fibril/amyloid formation. Chaperones from different families play distinct but complementary roles in prevention of tau-fibril/amyloid formation. (HspB1 = heat shock protein family B small member 1; Hsc70 = heat shock protein family A Hsp70)
a 2.0-kDa peptide which biochemically and immunologically resembles the injected amino terminal tau 26-44 was endogenously detected in vivo, being present in hippocampal synaptosomal preparations from Alzheimer's disease subjects.
Study reports the identification of new bona fide human brain circular RNAs produced from the MAPT locus.
TAU attaches to brain lipid membranes where it self-assembles in a cation-dependent manner.
Microtubule hyperacetylation enhances KL1-dependent micronucleation under a Tau deficiency in mammary epithelial cells.
This article presents key studies of tau in oligodendrocytes and select important studies of tau in neurons. The extensive work on tau in neurons has considerably advanced the understanding of how tau promotes either health or disease. [review]
Zn2 + enhances Tau aggregation-induced apoptosis and toxicity in neuronal cells.
Tau binds to synaptic vesicles via its N-terminal domain and interferes with presynaptic functions.
Study identifies a potential "two-hit" mechanism in which tau acetylation disengages tau from microtubules (MT) and also promotes tau aggregation. Thus, therapeutic approaches to limit tau K280/K281 acetylation could simultaneously restore MT stability and ameliorate tau pathology in Alzheimer's disease and related tauopathies.
In vitro neuroprotective effects of naringenin nanoemulsion against beta-amyloid toxicity through the regulation of amyloidogenesis and tau phosphorylation.
To confirm the neuroprotective role of 24-OH, in vivo experiments were run on mice that express human tau without spontaneously developing tau pathology (hTau mice), by means of the intracerebroventricular injection of 24-OH.
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.
deletion or inhibition of the cytoplasmic shuttling factor HDAC6 suppressed neuritic tau bead formation in neurons.
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