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Tau Expression (tau + expression)
Selected AbstractsNeurogenesis and cell cycle-reactivated neuronal death during pathogenic tau aggregationGENES, BRAIN AND BEHAVIOR, Issue 2008K. Schindowski The aim of the present study was to investigate the relation between neurogenesis, cell cycle reactivation and neuronal death during tau pathology in a novel tau transgenic mouse line THY-Tau22 with two frontotemporal dementia with parkinsonism linked to chromosome-17 mutations in a human tau isoform. This mouse displays all Alzheimer disease features of neurodegeneration and a broad timely resolution of tau pathology with hyperphosphorylation of tau at younger age (up to 6 months) and abnormal tau phosphorylation and tau aggregation in aged mice (by 10 months). Here, we present a follow-up of cell cycle markers with aging in control and transgenic mice from different ages. We show that there is an increased neurogenesis during tau hyperphosphorylation and cell cycle events during abnormal tau phosphorylation and tau aggregation preceding neuronal death and neurodegeneration. However, besides phosphorylation, other mechanisms including tau mutations and changes in tau expression and/or splicing may be also involved in these mechanisms of cell cycle reactivation. Altogether, these data suggest that cell cycle events in THY-Tau22 are resulting from neurogenesis in young animals and cell death in older ones. It suggests that neuronal cell death in such models is much more complex than believed. [source] Microtubule-associated protein tau in human prostate cancer cells: Isoforms, phosphorylation, and interactions,JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2009Skye Souter Abstract Tau is a microtubule-associated protein whose function has been investigated primarily in neurons. Recently, tau expression has been correlated with increased drug resistance in various cancers of non-neuronal tissues. In this report, we investigate the tau expressed in cancerous prostate lines ALVA-31, DU 145, and PC-3. Prostate cancer tau is heat-stable and highly phosphorylated, containing many of the modifications identified in Alzheimer's disease brain tau. RT-PCR and phosphatase treatment indicated that all six alternatively spliced adult brain tau isoforms are expressed in ALVA-31 cells, and isoforms containing exon 6 as well as high molecular weight tau isoforms containing either exon 4A or a larger splice variant of exon 4A are also present. Consistent with its hyperphosphorylated state, a large proportion of ALVA-31 tau does not bind to microtubules, as detected by confocal microscopy and biochemical tests. Finally, endogenous ALVA-31 tau can interact with the p85 subunit of phosphatidylinositol 3-kinase, as demonstrated by co-immunoprecipitations and in vitro protein-binding assays. Our results suggest that tau in prostate cancer cells does not resemble that from normal adult brain and support the hypothesis that tau is a multifunctional protein. J. Cell. Biochem. 108: 555,564, 2009. © 2009 Wiley-Liss, Inc. [source] HER2 and tau expression as potential markers for response and survival to first line taxane plus cisplatin therapy in non-small cell lung cancerASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Issue 4 2009Byoung Yong SHIM Abstract Aim: The aim of this study was to assess the role of various HER2, tau and bcl2 as prognostic markers of responsiveness to taxane and cisplatin therapy in patients with advanced NSCLC. Methods: Amplification of HER2 gene determined by chromogenic in situ hybridization (CISH) and HER2, tau and bcl2 protein expression determined by immunohistochemistry were assessed in 49 patients with NSCLC enrolled in our four clinical trials of taxane plus cisplatin chemotherapy. Results: The patients were classified as responders or non-responders, a negative tau expression was associated with a significantly higher rate of response compared to a positive tau expression (OR 3.33, 95% CI 1.01,10.97, P = 0.043). Patients with more than stable disease compared to those with progressive disease showed that negative amplification of the HER2 gene was associated with a significantly higher rate of disease control compared to positive amplification (OR 7.35, 95% CI 0.83,65.21, P = 0.048). Furthermore, HER2 gene amplification was strongly associated with the overall survival: 20 months (95% CI 9.007,30.993) in patients with negative amplification of the HER2 gene versus 12 months (95% CI 6.584,17.416) in patients with positive amplification of the HER2 gene (P = 0.040). A multivariate analysis with the Cox proportional hazards model confirmed that HER2 gene amplification was a significant independent prognostic factor with a hazard ratio of 2.334 (95% CI 1.060,5.142, P = 0.035). Conclusion: Tau protein expression and HER2 gene amplification are the prognostic factors in NSCLC patients treated with a taxane and cisplatin combination. [source] | ||||||||||