scholarly journals Tau Protein as a Fusion Tag for Recombinant Peptide/Protein Expression

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Yunfei Liu ◽  
Meng Gao ◽  
Yongqi Huang
Keyword(s):  
Protein Expression ◽  
Tau Protein ◽  
Fusion Tag ◽  
Recombinant Peptide

Flavonoids from Scutellaria baicalensis Georgi Stems and Leaves Regulate the Brain Tau Hyperphosphorylation at M|ultiple Sites Induced by Composited Aβ in Rats

2021 ◽  
Vol 20 ◽  
Author(s):  
Yazhen Shang ◽  
Shengkai Ding
Keyword(s):  
Cerebral Cortex ◽  
Protein Expression ◽  
Tau Protein ◽  
Drug Group ◽  
Scutellaria Baicalensis ◽  
Intracerebroventricular Injection ◽  
Model Group ◽  
Expression Levels ◽  
Scutellaria Baicalensis Georgi ◽  
Stems And Leaves

Background: Neurofibrillary tangles (NFTs), formed by hyperphosphorylation of Tau protein in Alzheimer's disease (AD) are the main pathomechanisms of neuronal degeneration, which can be used as a sign of brain disorder. It is positively correlated with the degree of cognitive impairment in AD. Objective: The objective of this study is to investigate the effect of Scutellaria baicalensis Georgi stems and leaves flavonoids (SSF) on the hyperphosphorylated expression levels at multiple sites of Tau protein induced by β-amyloid protein 25-35 (Aβ25-35) in combined with aluminum trichloride (AlCl3) and recombinant human transforming growth factor-β1 (RHTGF-β1) (composited Aβ) in rats. Methods: The model of rats for AD was established by intracerebroventricular injection of Aβ25-35 and AlCl3 combined with RHTGF-β1. On day 45 after the operation, the Morris water maze was used to screen the rats’ memory impairment model for AD. The successful model rats were randomly divided into the model group and three-dose of drug group. The drug group rats were daily and orally SSF administrated for 38 days. Western blotting was used to detect the protein expression of P-Tau (Thr181), P-Tau (Thr217), P-Tau (Thr231), P-Tau (Ser199), P-Tau (Ser235), P-Tau (Ser396) and P-Tau (Ser404) in the hippocampus and cerebral cortex of rats. Results: Compared with the sham group, the protein expression of P-Tau (Thr181), P-Tau (Thr217), P-Tau (Thr231), P-Tau (Ser199), P-Tau (Ser235), P-Tau (Ser396) and P-Tau (Ser404) was significantly increased in the hippocampus and cerebral cortex in the model group (P < 0.01). However, the three doses of 35, 70 and 140 mg/kg SSF regulated the expression of phosphorylated Tau protein at the above sites to varying degrees in the hippocampus and cerebral cortex (P < 0.01) induced by composited Aβ. Conclusion: SSF can significantly reduce the protein expression levels of P-Tau (Thr181), P-Tau (Thr217), P-Tau (Thr231), P-Tau (Ser199), P-Tau (Ser235), P-Tau (Ser396) and P-Tau (Ser404) in rats’ brain induced by the intracerebroventricular injection of composited Aβ. These results demonstrated that the neuro-protection and the impaired memory improvement of SSF were due to the inhibition for the hyperphosphorylation of Tau protein at multiple sites.

Relationship Between Gastric Cancer Tau Protein Expression and Paclitaxel Sensitivity

2013 ◽  
Vol 19 (3) ◽  
pp. 429-435 ◽  
Author(s):  
Qiong Wang ◽  
Nanyao Wang ◽  
Guoyi Shao ◽  
Jianzhong Qian ◽  
Dong Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Protein Expression ◽  
Tau Protein

scholarly journals Selective human tau protein expression in different clock circuits of the Drosophila brain disrupts different aspects of sleep and circadian rhythms

2020 ◽  
Author(s):  
David Jaciuch ◽  
Jack Munns ◽  
Sangeeta Chawla ◽  
Seth J. Davis ◽  
Mikko Juusola
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Locomotor Activity ◽  
Protein Expression ◽  
Tau Protein ◽  
Tau Proteins ◽  
Model Organisms ◽  
Neuron Network ◽  
Main Site ◽  
The Impact

AbstractCircadian behavioural deficits, such as increased daytime naps and reduced night-time sleep, are common in Alzheimer’s disease and other tauopathies. But it has remained unclear whether these circadian abnormalities arise from tau pathology in either the master pacemaker or downstream neurons. Here we study this question by selectively expressing different human tau proteins in specific Drosophila brain circuits and monitoring locomotor activity under light-dark (LD) and in “free-running” dark-dark (DD) conditions. We show that expressing human tau proteins in the fly brain recapitulates faithfully several behavioural changes found in tauopathies. We identify discrete neuronal subpopulations within the clock network as the primary target of distinct circadian behavioural disturbances in different environmental conditions. Specifically, we show that the PDF-positive pacemaker neurons are the main site for night-activity gain and -sleep loss, whereas the non-PDF clock-neurons are the main site of reduced intrinsic behavioural rhythmicity. Bioluminescence measurements revealed that the molecular clock is intact despite the behavioural arrhythmia. Our results establish that dysfunction in both the central clock- and afferent clock-neurons jointly contribute to the circadian locomotor activity rhythm disruption in Drosophila expressing human tau.Significance StatementThis study directly links in vivo human tau protein expression in region-specific Drosophila clock-neurons with the resulting sleep and circadian rhythm deficits to extract new knowledge of how Alzheimer’s disease and other tauopathies perturb the balance of activity and sleep. We anticipate that this novel approach will provide a useful general template for other studies of neurodegeneration in model organisms, seeking to dissect the impact of neurodegenerative disease on circadian behaviour, and further deepening our understanding of how the clock-neuron network works.

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