Expression of tau exon 8 in different species

Chen, Wei Ta; Liu, Wan Kyng; Yen, Shu Hui

doi:10.1016/0304-3940(94)90688-2

Cited by 17 publications

(9 citation statements)

References 13 publications

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“…In addition to the canonical exon 6, two alternative splice sites result in frameshifts and the introduction of stop codons and thus encode tau variants (6p and 6d) that cannot bind microtubules (Andreadis, 2005;Luo et al, 2004). Exon 8 was reported to be expressed in bovine tau (Chen et al, 1994;Himmler, 1989). Exons 9,10,11 and 12 span the microtubule binding domains of tau.…”

Section: Expression and Distribution Of Taumentioning

confidence: 99%

It’s all about tau

Tapia-Rojas

Cabezas-Opazo

Deaton

et al. 2019

Progress in Neurobiology

140

123

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Tau is a protein that is highly enriched in neurons and was originally defined by its ability to bind and stabilize microtubules. However, it is now becoming evident that the functions of tau extend beyond its ability to modulate microtubule dynamics. Tau plays a role in mediating axonal transport, synaptic structure and function, and neuronal signaling pathways. Although tau plays important physiological roles in neurons, its involvement in neurodegenerative diseases, and most prominently in the pathogenesis of Alzheimer disease (AD), has directed the majority of tau studies. However, a thorough knowledge of the physiological functions of tau and its posttranslational modifications under normal conditions are necessary to provide the foundation for understanding its role in pathological settings. In this review, we will focus on human tau, summarizing tau structure and organization, as well as its posttranslational modifications associated with physiological processes. We will highlight possible mechanisms involved in mediating the turnover of tau and finally discuss newly elucidated tau functions in a physiological context.

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Section: Expression and Distribution Of Taumentioning

confidence: 99%

It’s all about tau

Tapia-Rojas

Cabezas-Opazo

Deaton

et al. 2019

Progress in Neurobiology

140

123

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“…Thus far, exon 8 has not been observed in human MAPT transcripts. Expression studies in different species identified exon 8 containing transcripts in rhesus monkey and in small amounts in cow [Chen et al, 1994;Nelson et al, 1996].…”

Section: Introductionmentioning

confidence: 99%

The role of tau (MAPT) in frontotemporal dementia and related tauopathies

2004

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Tau is a multifunctional protein that was originally identified as a microtubule-associated protein. In patients diagnosed with frontotemporal dementia and parkinsonism linked to chromosome 17, mutations in the gene encoding tau (MAPT) have been identified that disrupt the normal binding of tau to tubulin resulting in pathological deposits of hyperphosphorylated tau. Abnormal filamentous tau deposits have been reported as a pathological characteristic in several other neurodegenerative diseases, including frontotemporal dementia, Pick Disease, Alzheimer disease, argyrophilic grain disease, progressive supranuclear palsy, and corticobasal degeneration. In the last five years, extensive research has identified 34 different pathogenic MAPT mutations in 101 families worldwide. In vitro, cell-free and transfected cell studies have provided valuable information on tau dysfunction and transgenic mice carrying human MAPT mutations are being generated to study the influence of MAPT mutations in vivo. This mutation update describes the considerable differences in clinical and pathological presentation of patients with MAPT mutations and summarizes the effect of the different mutations on tau functioning. In addition, the role of tau as a genetic susceptibility factor is discussed, together with the genetic evidence for additional causal genes for tau-positive as well as tau-negative dementia.

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“…Included were exons 6 and 8 that are not expressed in human brain, 29,30 and exon 4A encoding 'big tau' in the peripheral nervous system. [31][32][33] In addition we analysed exon 0 and 1 kb of 5Ј regulatory sequence comprising different neuronal promoter elements, 34 and intron 13 that is retained in human MAPT transcripts.…”

Section: Mutation Analysis Of Maptmentioning

confidence: 99%

“…Monoclonal (MC) and polyclonal (PC) antibodies raised against tau, both phosphorylation dependent (AT8, MC, 1:40, Innogenetics, Gent, Belgium; AT180, MC, 1:500, Innogenetics; AT270, MC, 1:500, Innogenetics; PHF1, MC, 1:500, gift from Peter Davies, Albert Einstein College of Medicine, New York, NY, USA; MC1, MC, 1:25, also a gift by Peter Davies), and phosphorylation independent (BR01, MC, 1:500, Innogenetics; Tau2, MC, 1:100, Sigma, St Louis, MO, USA) were used, as well as antibodies against ubiquitin (PC, 1:500, Dako, Glostrup, Denmark), polyglutamine (1C2, MC, 1:1000, Chemicon, Temecula, CA, USA), Human Leucocyte Antigen-DR (HLA-DR, MC, 1:100, Dako), ␣-BCrystallin (PC, 1:500, Novocastra Laboratories, Newcastle upon Tyne, UK), amyloid-␤ (␤A4, MC, 1:100, Dako), ␣-synuclein (PC, 1:500, Chemicon), ␤-tubulin (TUB 2.1, MC, 1:500, Sigma), glial fibrillary acidic protein (GFAP, MC, 1:500, Dako), synaptophysin (1:100, PC, Dako), microtubule associated protein (MAP2, MC, 1:100, Boehringer, Mannheim, Germany), neurofilament (SMI-32, 1:1000, Sternberger Monoclonals, Lutherville, MD, USA) and the prion protein (PrP [27][28][29][30] , PC, 1:200, Chemicon). Heat-induced antigen retrieval was performed by heating slides at 80°C for 30 min in 0.1 M sodium citrate buffer at pH 7.7 for several antibodies (polyglutamine, HLA-DR, ␤-tubuline, synaptophysin, MAP2, GFAP, BR01, and Tau2).…”

Section: Neuropathologymentioning

confidence: 99%

Tau negative frontal lobe dementia at 17q21: significant finemapping of the candidate region to a 4.8 cM interval

Rademakers¹,

Cruts²,

Dermaut³

et al. 2002

Mol Psychiatry

102

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We report the results of a genome-wide search in a four-generation pedigree with autosomal dominant early-onset dementia (mean onset age: 64.9 years, range 53-79 years). In this family we previously excluded the known Alzheimer's disease genes based on linkage analysis and mutation screening of the amyloid precursor protein gene (exons 16 and 17) and the presenilin 1 and 2 genes. In addition we excluded mutations in the prion protein gene and exons 9-13 of the microtubule associated protein tau (MAPT) gene. We obtained conclusive linkage with chromosome 17q21 markers with a maximum multi-point LOD score of 5.51 at D17S951 and identified a candidate region of 4.8 cM between D17S1787 and D17S958 containing MAPT. Recent clinical and neuropathological follow-up of the family showed that the phenotype most closely resembled frontotemporal dementia (FTD) characterized by dense ubiquitin-positive neuronal inclusions that were tau negative. Extensive mutation analysis of MAPT identified 38 sequence variations in exons, introns, untranslated regions and the 5Ј regulatory sequence, however none was comprised within the disease haplotype. Although our findings do not entirely exclude a mutation in a yet unanalyzed region of MAPT, the apparent absence of MAPT mutations combined with the lack of tau pathology is highly suggestive for another defective gene at 17q21 responsible for FTD in this family.

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Expression of tau exon 8 in different species

Cited by 17 publications

References 13 publications

It’s all about tau

It’s all about tau

The role of tau (MAPT) in frontotemporal dementia and related tauopathies

Tau negative frontal lobe dementia at 17q21: significant finemapping of the candidate region to a 4.8 cM interval

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