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anti-Human MAPT Antibodies:
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Human Polyclonal MAPT Primary Antibody for IHC (p), WB - ABIN6652127
Puig, Rey, Ferrer: Individual and regional variations of phospho-tau species in progressive supranuclear palsy. in Acta neuropathologica 2005
Show all 15 Pubmed References
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
Show all 7 Pubmed References
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
Show all 7 Pubmed References
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
Show all 9 Pubmed References
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
Show all 4 Pubmed References
Human Polyclonal MAPT Primary Antibody for IHC, WB - ABIN362062
DeGiorgis, Jaffe, Moreira, Carlotti, Leite, Pant, Dosemeci: Phosphoproteomic analysis of synaptosomes from human cerebral cortex. in Journal of proteome research 2005
Show all 6 Pubmed References
Human Polyclonal MAPT Primary Antibody for WB - ABIN546569
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 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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Human Polyclonal MAPT Primary Antibody for IF, IHC - ABIN6711924
Peng, He, Tang, Tao, Chen, Gao, Zhang, He, Dai, Zhu, Lv, Zhang, Qiao, Zhao, Gao, Zhu: Trio is a key guanine nucleotide exchange factor coordinating regulation of the migration and morphogenesis of granule cells in the developing cerebellum. in The Journal of biological chemistry 2010
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The MAPT mutation of Frontotemporal Dementia, the main significant areas were in the temporo-parietal and frontal lobes as well as bilateral cuneus.
Review of recent advances on tau in the dendritic compartments, with implications for understanding and treatment of AD and related neurological conditions. [Review Article]
oligomeric Abeta strongly increased AT8 and AT180 phosphorylation of tau and caused a loss of dendritic spines.
This study demonstrated that the Presymptomatic MAPT carriers showed greater atrophy in the medial temporal region in patient with Frontotemporal Dementia than control subjects.
BDNF and Tau as biomarkers of severity in multiple sclerosis
These results indicate that MAPT haplotype-tagging polymorphisms and MAPT haplotypes should be further tested as potential genetic biomarkers of AD.
This study showed that the MAPT mutation in Frontotemporal Dementia had the most atrophic hippocampi, with the subfields showing the largest difference from controls.
Relationship between baseline CSF Abeta1-42 and tau accumulation was strongest in APOEepsilon4 carriers.
CSF tau is associated with impaired cortical plasticity, cognitive decline and astrocyte survival only in APOE4-positive Alzheimer's disease
Data show that the formation of early heterotypic oligomeric complex of alpha-syn and tau K18 can promote maturation into fibrils through binding-induced misfolding and aggregation. These results suggest that the alpha-syn:tau ratio critically governs the rate of the amyloid formation. alpha-Syn and tau K18 together aggregate at a much faster rate with a much shorter lag phase compared to the individual proteins.
These data suggest that CK1epsilon is involved in the regulation of tau phosphorylation, the alternative splicing of tau exon 10, and cognitive performance. Up-regulation of CK1epsilon might contribute to tau pathology by hyperphosphorylating tau and by dysregulating the alternative splicing of tau exon 10 in AD.
We suggest that these new MAPT isoforms can be translated into normal or amino-terminal-truncated tau proteins. We further suggest that activation of MAPT's alternative promoter under pathological conditions leads to the production of truncated proteins, changes in protein localization and function, and thus neurodegeneration.
although chronic and abundant expression of TAU(P301L) starting from early embryonic development led to hyperphosphorylation, TAU(P301L) did not form oligomers and neurofibrillary tangles, and did not cause elevated apoptosis and microglial activation.
Bred hemizygous mice that express P301L tau (TauP301L) and detected hyper-phosphorylated tau (p-tau) predominantly in the hippocampus, cortex, brainstem and thalamus. (13)C/(1)H MRS reveals astrocytic dysfunction via reduced glial aspartate and impaired glutamate-glutamine cycle. An increase in glutamate and GABA and decrease in glutamine were observed in homozygous mice compared to hemizygous and control littermates.
Results indicate that the trans isomer of microtubule associated protein tau (Tau) peptide is aggregation-prone and that the WW domain of peptidyl-prolyl-isomerase Pin1 (Pin1) effectively inhibits its aggregation.
Study shows that phosphorylation of serine 305 in tau inhibits aggregation.
Patients with diffuse Lewy body disease had more severe pathology of each type and a shorter duration of illness than individuals with transitional Lewy body disease. The three pathologies accounted for 25% of the total variance of duration of illness, with 19% accounted for by alpha-synuclein alone or in combination with tau and Abeta.
High Levels of Phosphorylated Tau is associated with Neurocognitive Sequelae in Adult Childhood Leukemia Survivors.
This study showed that Pathogenic mutations in the microtubule-associated protein tau gene were not found using two single nucleotide polymorphisms in patient with chronic progressive degenerative parietal ataxia.
Study found that FTDP-17 mutations enhance tau oligomer formation and that P301L tau oligomers form smaller tau oligomers than wilt type, V337M, and R406W oligomers.
This work identified Synaptogyrin-3 as the binding partner of Tau on synaptic vesicles, revealing a new presynapse-specific Tau interactor.
Ischemia-induced brain injury and motor deficit in asparagine endopeptidase (AEP)-knockout mice are reduced, probably because ischemia activates AEP. AEP cleaves inhibitor 2 of protein phosphatase 2A (I2PP2A), which translocates from the neuronal nucleus to the cytoplasm and produces hyperphosphorylation of tau through inhibition of PP2A.
Wild-type mice were exposed to multiple regimens of repetitive mild traumatic brain injury. There was a highly significant main effect of impact energy, frequency, and duration of exposure on Abeta1-42, tau, and alpha-synuclein levels (P < .001), and a significant interaction between impact energy and duration of exposure for Abeta1-42 and tau (P < .001), but not for alpha-synuclein.
These results suggest that deleterious effects from TRIM28 depletion are limited to development and that its inhibition adulthood provides a potential path for modulating alpha-Syn and tau levels.
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.
defects in MAPT lead to aberrant mitotic spindle function, abnormal chromosome segregation, and apoptosis
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.
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.
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.
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