A5103224136- RNA Research and Splicing
- Hepatitis Viruses Studies and Epidemiology
- Liver Disease Diagnosis and Treatment
- Alzheimer's disease research and treatments
- Inflammasome and immune disorders
- RNA regulation and disease
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Structure and Function
- Nematode management and characterization studies
- HIV-related health complications and treatments
- Cytomegalovirus and herpesvirus research
- Liver Diseases and Immunity
- Amoebic Infections and Treatments
- HIV/AIDS drug development and treatment
- Pediatric Urology and Nephrology Studies
- Bioinformatics and Genomic Networks
- interferon and immune responses
- RNA modifications and cancer
- Insects and Parasite Interactions
- Urinary Tract Infections Management
- Advanced Glycation End Products research
- Genetic Neurodegenerative Diseases
- Pesticide Exposure and Toxicity
- DNA Repair Mechanisms
- Cardiac Fibrosis and Remodeling
Tokyo Medical and Dental University
2021-2024
Huzhou University
2024
Yanbian University
2015
Brain inflammation generally accompanies and accelerates neurodegeneration. Here we report a microglial mechanism in which polyglutamine binding protein 1 (PQBP1) senses extrinsic tau 3R/4R proteins by direct interaction triggers an innate immune response activating cyclic GMP-AMP synthase (cGAS)-Stimulator of interferon genes (STING) pathway. Tamoxifen-inducible microglia-specific depletion PQBP1 primary culture vitro mouse brain vivo shows that is essential for sensing-tau to induce...
Polyglutamine binding protein 5 (PQBP5), also called nucleolar 10 (NOL10), binds to polyglutamine tract sequences and is expressed in the nucleolus. Using dynamic imaging of high-speed atomic force microscopy, we show that PQBP5/NOL10 an intrinsically disordered protein. Super-resolution microscopy correlative light electron method makes up skeletal structure nucleolus, constituting granule meshwork granular component area, which distinct from other substructures, such as fibrillar center...
Viral fulminant hepatitis (FH) is a severe disease with high mortality resulting from excessive inflammation in the infected liver. Clinical interventions have been inefficient due to lack of knowledge for inflammatory pathogenesis virus-infected We show that wild-type mice murine virus strain-3 (MHV-3), model viral FH, manifest and association significant elevation IL-1β expression serum Whereas, infection receptor-I deficient (IL-1R1-/-) or IL-1R antagonist (IL-1Ra) treated mice,...
DNA damage is increased in Alzheimer's disease (AD), while the underlying mechanisms are unknown. Here, we employ comprehensive phosphoproteome analysis, and identify abnormal phosphorylation of 70 kDa subunit Ku antigen (Ku70) at Ser77/78, which prevents Ku70-DNA interaction, human AD postmortem brains. The inhibits accumulation Ku70 to foci double strand break (DSB), impairs repair eventually causes transcriptional repression-induced atypical cell death (TRIAD). Cells under TRIAD necrosis...
Prion-like protein propagation is considered a common pathogenic mechanism in neurodegenerative diseases. Here we investigate the vivo pattern and aggregation state of mutant α-synuclein by injecting adeno-associated viral (AAV)-α-synuclein-A53T-EGFP into mouse olfactory cortex. Comparison states various brain regions at multiple time points after injection using western blot analyses shows that monomeric mutant/misfolded propagates to remote 2 weeks propagated proteins aggregate situ being...
Objective To analyse the HIV-1 subtypes and molecular transmission characteristics of HIV-infected older individuals aged 50 above in Huzhou City, provide a scientific basis for prevention treatment strategies them. Design A cross-sectional study with clustered network cases was performed, basic epidemiological information retrieved from Chinese Centres Disease Prevention Control (CDC) Information System. Setting participants conducted 899 newly diagnosed January 2019 March 2023 city,...
The early-stage pathologies of frontotemporal lobal degeneration (FTLD) remain largely unknown. In VCPT262A-KI mice carrying VCP gene mutation linked to FTLD, insufficient DNA damage repair in neural stem/progenitor cells (NSCs) activated DNA-PK and CDK1 that disabled MCM3 essential for the G1/S cell cycle transition. Abnormal exit produced neurons over unrepaired induced transcriptional repression-induced atypical death (TRIAD) necrosis accompanied by specific markers pSer46-MARCKS YAP....
Abstract Multiple gene mutations cause familial frontotemporal lobar degeneration (FTLD) while no single exists in sporadic FTLD. Various proteins aggregate variable regions of the brain, leading to multiple pathological and clinical prototypes. The heterogeneity FTLD could be one reasons preventing development disease-modifying therapy. We newly develop a mathematical method analyze chronological changes PPI networks with sequential big data from comprehensive phosphoproteome four knock-in...