A5069780960- Alzheimer's disease research and treatments
- RNA Research and Splicing
- Genetics and Neurodevelopmental Disorders
- Mitochondrial Function and Pathology
- Cholinesterase and Neurodegenerative Diseases
- Protein Structure and Dynamics
- Metal complexes synthesis and properties
- Histone Deacetylase Inhibitors Research
- Signaling Pathways in Disease
- RNA modifications and cancer
- Connective Tissue Growth Factor Research
- Parkinson's Disease Mechanisms and Treatments
- Epigenetics and DNA Methylation
- Crystal structures of chemical compounds
- Metal-Organic Frameworks: Synthesis and Applications
- Biomarkers in Disease Mechanisms
- Autophagy in Disease and Therapy
- Cellular transport and secretion
- Drug Transport and Resistance Mechanisms
- RNA regulation and disease
- Mesenchymal stem cell research
- Endoplasmic Reticulum Stress and Disease
- Redox biology and oxidative stress
- Cancer-related gene regulation
- Peptidase Inhibition and Analysis
The Affiliated Yongchuan Hospital of Chongqing Medical University
2020-2024
Chongqing Medical University
2020-2024
Southwest University
2013
Abstract It is long been suggested that one‐carbon metabolism (OCM) associated with Alzheimer's disease (AD), whereas the potential mechanisms remain poorly understood. Taking advantage of chemical biology, mitochondrial serine hydroxymethyltransferase (SHMT2) directly regulated translation ADAM metallopeptidase domain 10 (ADAM10), a therapeutic target for AD reported. That small‐molecule kenpaullone (KEN) promoted ADAM10 via 5′ untranslated region (5′UTR) and improved cognitive functions in...
Exploring the potential lead compounds for Alzheimer’s disease (AD) remains one of challenging tasks. Here, we report that plant extract conophylline (CNP) impeded amyloidogenesis by preferentially inhibiting BACE1 translation via 5′ untranslated region (5′UTR) and rescued cognitive decline in an animal model APP/PS1 mice. ADP-ribosylation factor–like protein 6–interacting 1 (ARL6IP1) was then found to mediate effect CNP on translation, amyloidogenesis, glial activation, function. Through...
Mitochondrial Tu translation elongation factor (TUFM or EF-Tu) is part of the mitochondrial machinery. It reported that TUFM expression reduced in brain Alzheimer's disease (AD), suggesting might play a role pathophysiology. In this study, we found protein level was decreased hippocampus and cortex especially aged APP/PS1 mice, an animal model AD. HEK cells stably express full-length human amyloid-β precursor (HEK-APP), knockdown overexpression increased levels β-amyloid (Aβ) converting...
Abstract Aims Amyloid beta (Aβ) is an important pathological feature of Alzheimer's disease (AD). A disintegrin and metalloproteinase 10 (ADAM10) can reduce the production toxic Aβ by activating nonamyloidogenic pathway amyloid precursor protein (APP). We previously found that apicidin, which a histone deacetylase (HDAC) inhibitor, promote expression ADAM10 in vitro. This study was designed to determine potential apicidin treatment reverse learning memory impairments AD mouse model possible...
Amyloidogenesis is one of the key pathophysiological changes in Alzheimer's disease (AD). Accumulation toxic Aβ results from catalytic processing β-amyloid precursor protein (APP) associated converting enzyme 1 (BACE1) activity. It reported that dead-box helicase 17 (DDX17) controls RNA metabolism and involved development multiple diseases. However, whether DDX17 might play a role amyloidogenesis has not been documented. In present study, we found level was significantly increased HEK...
Background: Accumulation of hyperphosphorylated Tau (pTau) contributes to the formation neurofibrillary tangles in Alzheimer’s disease (AD), and targeting Tau/pTau metabolism has emerged as a therapeutic approach. We have previously reported that mitochondrial 3-hydroxy-3-methylglutaryl-COA synthase 2 (HMGCS2) is involved AD by promoting autophagic clearance amyloid-β protein precursor via ketone body-associated mechanism, whether HMGCS2 may also regulate remains elusive. Objective: The...
AP2S1 is the sigma 2 subunit of adaptor protein (AP2) that essential for endocytosis. In this study, we investigated potential role in intracellular processing amyloid precursor (APP), which contributes to pathogenesis Alzheimer disease (AD) by generating toxic β-amyloid peptide (Aβ). We found knockdown or overexpression decreased increased levels APP and Aβ cells stably expressing human full-length APP695, respectively. This effect was unrelated endocytosis but involved lysosomal...
Abstract Thioredoxin‐2 (TXN2) is a mitochondrial protein and represents one of the intrinsic antioxidant enzymes. It has long been recognized that dysfunction oxidative stress contribute to pathogenesis Alzheimer's disease (AD). We hypothesized TXN2 might play role in AD‐like pathology. In this study, we found SH‐SY5Y HEK cells stably express full‐length human amyloid‐β precursor (HEK‐APP), silencing or over‐expression selectively increased decreased transcription beta‐site amyloid cleaving...
Sulfuretin is a flavonoid that protects cell from damage induced by reactive oxygen species and inflammation. In this study, we investigated the role of sulfuretin in processing amyloid precursor protein (APP), association with two catalytic enzymes α-secretase disintegrin metalloproteinase (ADAM10), beta-site APP cleaving enzyme 1 (BACE1) play important roles generation β (Aβ) Alzheimer's disease (AD). We found increased levels immature but not mature form ADAM10 protein. The enhanced...
TNFAIP3-interacting protein 2 (TNIP2) is known as a negative regulator of NF-κB signaling and inhibit inflammatory response apoptosis, also involved in RNA metabolism. In this study, we investigated the potential role TNIP2 amyloidogenesis critically associated with Alzheimer’s disease (AD). We found significant decline level both mouse cell model AD. SH-SY5Y HEK cells that stably express human full-length APP695 (SY5Y-APP HEK-APP), overexpression decreased levels β-secretase (BACE1) C99,...
目的 探讨铅在人肾小管上皮细胞表型转化中的作用及对纤维化相关因子的影响.方法 体外培养人类近端肾小管上皮细胞系(HK-2)细胞,以2.5、5.0、10.0μmol/L醋酸铅剂量染毒,以Oμmol/L醋酸铅剂量组为对照组,应用形态学、间接免疫荧光-流式细胞术、反转录-聚合酶链反应(RT-PCR)观察醋酸铅染毒72 h HK-2细胞形态、α-平滑肌肌动蛋白(α-SMA)和纤维连接蛋白(FN)表达的改变,以及对纤维化相关因子转化生长因子(TGF-β1)、结缔组织生长因子(CTGF)的影响.结果...