A5082478573- Alzheimer's disease research and treatments
- 14-3-3 protein interactions
- Down syndrome and intellectual disability research
- RNA Research and Splicing
- Neuroscience and Neuropharmacology Research
- Genetics and Neurodevelopmental Disorders
- Cancer-related gene regulation
- Cholinesterase and Neurodegenerative Diseases
- Sirtuins and Resveratrol in Medicine
- Endoplasmic Reticulum Stress and Disease
- Signaling Pathways in Disease
- Calcium signaling and nucleotide metabolism
- Biochemical effects in animals
- Calpain Protease Function and Regulation
- RNA modifications and cancer
- Autophagy in Disease and Therapy
- Glycosylation and Glycoproteins Research
- Diet and metabolism studies
- Mitochondrial Function and Pathology
- Nuclear Receptors and Signaling
- Peptidase Inhibition and Analysis
- Cancer Mechanisms and Therapy
- Congenital heart defects research
- Osteomyelitis and Bone Disorders Research
- GDF15 and Related Biomarkers
Nantong University
2013-2025
Chinese PLA General Hospital
2021
Hebei North University
2021
State Grid Corporation of China (China)
2020
Central South University
2003-2018
Xiangya Hospital Central South University
2003-2018
Capital Medical University
2014-2018
New York State Office for People With Developmental Disabilities
2010-2017
China Agricultural University
2012
Massachusetts General Hospital
2012
Abnormal hyperphosphorylation of tau appears to be crucial in neurofibrillary degeneration Alzheimer's disease (AD). Previous studies suggest that a down-regulation protein phosphatase 2A (PP2A), the major human brain, contri
Abstract Abnormal hyperphosphorylation of tau is pivotally involved in the pathogenesis Alzheimer's disease (AD) and related tauopathies. Glycogen synthase kinase 3β (GSK-3β) a primary that most implicated pathology AD. However, exact molecular nature GSK-3β AD unclear. In present study, we found was truncated at C-terminus correlated with over-activation calpain I brain. Truncation positively hyperphosphorylation, tangles score Braak stage human Calpain proteolyzed vitro C-terminus, leading...
<i>Tau</i> exon 10, which encodes the second microtubule-binding repeat, is regulated by alternative splicing. Its splicing generates Tau isoforms with three- or four-microtubule-binding repeats, named 3R-tau and 4R-tau. Adult human brain expresses equal levels of Imbalance 4R-tau causes aggregation neurofibrillary degeneration. In present study, we found that factor SRp55 (serine/arginine-rich protein 55) promoted 10 inclusion. Knockdown significantly exclusion. The promotion inclusion...
Alternative splicing of tau exon 10 generates isoforms with three or four microtubule-binding repeats, 3R-tau and 4R-tau, which is equally expressed in adult human brain. Imbalanced expression 4R-tau has been found several sporadic inherited tauopathies, suggesting that dysregulation sufficient to cause neurodegenerative diseases. We previously reported Dyrk1A, overexpressed Down syndrome brains, regulates alternative exogenous 10. In the present study, we investigated regulation endogenous...
Hyperphosphorylation and dysregulation of exon 10 splicing Tau are pivotally involved in pathogenesis Alzheimer disease (AD) and/or other tauopathies. Alternative 10, which encodes the second microtubule-binding repeat, generates isoforms containing three four repeats, termed 3R-Taus 4R-Taus, respectively. Dual specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A) lies at Down syndrome critical region chromosome 21. Overexpression this may contribute to early pathology via...
Interferon Regulatory Factors (IRFs) are critical modulators of immune and inflammatory responses, yet their roles in Alzheimer’s disease (AD) other neurodegenerative disorders remain incompletely understood. While IRFs recognized for regulatory functions neuroinflammation, microglial activation, neuronal survival, dual as both drivers pathological inflammation mediators neuroprotective pathways underscore a sophisticated paradox disorders. This review aims to synthesize current evidence on...
Protein phosphatase 2B (PP2B) is one of the major brain phosphatases and can dephosphorylate tau at several phosphorylation sites in vitro. Previous studies that measured PP2B activity human crude extracts showed was eithe
Microtubule-associated protein tau is found to be accumulated and aggregated in the brains of individuals with Alzheimer's disease related tauopathies. Dual-specificity tyrosine-phosphorylation regulated kinase 1A (Dyrk1A) overexpressed Down syndrome may play a critical role early onset pathology this disease. To investigate effect Dyrk1A on expression, we co-expressed different isoforms HEK-293FT cells measured mRNA levels using RT-PCR Western blots, respectively. We further investigated...
Tau is modified with O-GlcNAcylation extensively in human brain. The levels of tau are decreased Alzheimer's disease (AD) Sirtuin type 1 (SIRT1) an enzyme that deacetylates proteins including transcriptional factors and associates neurodegenerative diseases, such as AD. Aberrant SIRT1 expression AD brain parallel the accumulation tau. cAMP response element binding protein (CREB), a cellular transcription factor, plays critical role learning memory. In this present study, we found CREB...
Hyperphosphorylation of tau is pivotally involved in the pathogenesis Alzheimer’s disease (AD) and related tauopathies. Glycogen synthase kinase-3β (GSK-3β) protein phosphate 2A (PP2A) are crucial enzymes to regulate phosphorylation. GSK-3β activity regulated by its inhibitory phosphorylation at Ser9. We previously reported cross-talk between PP2A signaling showed that could dephosphorylate Here, we investigated dephosphorylation brain extracts presence phosphatase inhibitors found a...
Accumulated and abnormally hyperphosphorylated tau aggregates into neurofibrillary tangles in the brains of patients with Alzheimer's disease (AD). cAMP response binding protein (CREB), a constitutively expressed nuclear transcription factor, is critical component neuroprotective transcrip tional network. Numerous studies have shown that cAMP-dependent kinase (PKA)-CREB signaling down-regulated AD brain. In present study, we studied regulation expression by PKA-CREB signaling. We found...
Amyloid plaques and neurofibrillary tangles are two pathological hallmarks of Alzheimer's disease (AD). However, synaptic deficits occur much earlier correlate stronger with cognitive decline than amyloid tangles. Mislocalization tau is an early hallmark neurodegeneration precedes aggregations. Sirtuin type 1 (SIRT1) a deacetylase which acts on proteins including transcriptional factors associates closely AD.The present study investigated the association between SIRT1 expression/tau...
Ca2+/calmodulin-dependent protein kinase (CaMK) IIδ is predominantly expressed in the heart. There are three isoforms of CaMKIIδ resulting from alternative splicing exons 14, 15, and 16 its pre-mRNA, which regulated by factor SF2/ASF. Inclusion 15 or exon 14 generates δA δB isoform. The exclusion all gives rise to δC isoform, selectively increased pressure-overload-induced hypertrophy. Overexpression either induces hypertrophy heart failure, suggesting their specific role pathogenesis...
Approximately equal amounts of 3R-tau and 4R-tau resulting from alternative splicing tau exon 10 is necessary to maintain normal brain function. Dysregulation the imbalance 3R-tau/4R-tau have been seen in inherited sporadic tauopathies. Splicing factor SC35 (also name as SRSF2) plays an important role promoting inclusion. post-translationally modified by phosphorylation acetylation, but acetylation SC35-medicated inclusion unknown. Sirtuin type 1 (SIRT1) enzyme that deacetylates proteins...
With the availability of data and improvement computation ability, deep learning methods are promising in many areas. Due to wide deployment sensors smart meters distribution network, abundant can be obtained, which provides potential for application network. In this paper, concept typical structures networks discussed. Meanwhile, several applications network summarized. Finally, challenges prospects proposed.
Microglial activation is a characteristic feature of the pathogenesis prion diseases.The molecular mechanisms that underlie prion-induced microglial are not very well understood.In present study, we investigated role class B scavenger receptor CD36 in induced by neurotoxic protein (PrP) fragment 106-126 (PrP ).We first examined time course mRNA expression upon exposure to PrP BV2 microglia.We then analyzed different parameters -treated cells presence or anti-CD36 monoclonal antibody...