A5058761500- Mitochondrial Function and Pathology
- HIV Research and Treatment
- Autophagy in Disease and Therapy
- Ubiquitin and proteasome pathways
- Neuroscience and Neuropharmacology Research
- Cellular transport and secretion
- ATP Synthase and ATPases Research
- HIV/AIDS drug development and treatment
- Adipose Tissue and Metabolism
- Neuroinflammation and Neurodegeneration Mechanisms
- Nerve injury and regeneration
- EEG and Brain-Computer Interfaces
- Lysosomal Storage Disorders Research
- Genetics and Neurodevelopmental Disorders
- Parkinson's Disease Mechanisms and Treatments
- Autism Spectrum Disorder Research
- Mechanisms of cancer metastasis
- Neurological Disease Mechanisms and Treatments
- Cardiomyopathy and Myosin Studies
- Extracellular vesicles in disease
- Viral Infections and Outbreaks Research
- Congenital heart defects research
- Pluripotent Stem Cells Research
- Sirtuins and Resveratrol in Medicine
- Immune cells in cancer
Harbin Veterinary Research Institute
2018-2025
Chinese Academy of Agricultural Sciences
2018-2025
National Institutes of Health
2016-2024
National Institute of Neurological Disorders and Stroke
2019-2023
Harbin University of Commerce
2023
East China University of Science and Technology
2017
Jilin University
2013-2016
University of Maryland, Baltimore
2012-2016
Jilin Medical University
2015-2016
Centre for Biomedical Engineering and Physics
2014
Accumulating evidence suggests that neuroinflammation plays an important role in the progression of Parkinson’s disease (PD). Excessively activated microglia produce several pro-inflammatory enzymes and cytokines, leading to damage surrounding neurons eventually inducing neurodegeneration. Therefore, inhibition microglial overactivation may be a potential therapeutic strategy prevent further PD. β-Hydroxybutyric acid (BHBA) has been shown suppress lipopolysaccharide (LPS)-induced...
In addition to established membrane remodeling roles in various cellular locations, actin has recently emerged as a participant mitochondrial fission. However, the underlying mechanisms of its participation remain largely unknown. We report that transient de novo F-actin assembly on mitochondria occurs upon induction fission and accumulates without forming detectable submitochondrial foci. Impairing division through Drp1 knockout or inhibition prolonged time accumulation also led abnormal...
Neurons face the challenge of maintaining cellular homeostasis through lysosomal degradation. While enzymatically active degradative lysosomes are enriched in soma, their axonal trafficking and positioning impact on physiology remain elusive. Here, we characterized axon-targeted delivery by applying fluorescent probes that selectively label forms cathepsins D, B, L, GCase. By time-lapse imaging cortical neurons microfluidic devices standard dishes, reveal soma-derived rapidly influx into...
Ubiquitin- and proteasome-dependent outer mitochondrial membrane (OMM)-associated degradation (OMMAD) is critical for cellular homeostasis. However, the scope molecular mechanisms of OMMAD pathways are still not well understood. We report that OMM-associated E3 ubiquitin ligase MARCH5 controls dynamin-related protein 1 (Drp1)-dependent fission cell sensitivity to stress-induced apoptosis. knockout selectively inhibited ubiquitination proteasomal MiD49, a receptor Drp1, consequently led...
β -Hydroxybutyric acid (BHBA) has neuroprotective effects, but the underlying molecular mechanisms are unclear. Microglial activation plays an important role in neurodegenerative diseases by producing several proinflammatory enzymes and cytokines. The current study investigates potential whereby BHBA affects expression of potentially proteins cultured murine microglial BV-2 cells stimulated with lipopolysaccharide (LPS). results showed that significantly reduced LPS-induced protein mRNA...
MARCH5, an OMM-associated E3 ubiquitin ligase, controls mitochondrial function. Despite its importance, the mechanism and factors controlling MARCH5 activity are largely unknown. Here we report that C-terminal domain plays a critical role in degradation of substrates, likely by facilitating release ubiquitinated proteins from OMM. We also found fission Drp1 Mff negatively regulate MARCH5’s toward MiD49 Mcl1. Knockouts either or led to reduced expression, shorter half-lives, increased...
Abstract SARS-CoV-2 and filovirus enter cells via the cell surface angiotensin-converting enzyme 2 (ACE2) or late-endosome Niemann-Pick C1 (NPC1) as a receptor. Here, we screened 974 natural compounds identified Tubeimosides I, II, III pan-coronavirus entry inhibitors that target NPC1. Using in-silico, biochemical, genomic approaches, provide evidence NPC1 also binds spike (S) protein on receptor-binding domain (RBD), which is blocked by Tubeimosides. Importantly, strongly promotes...
The pathogenesis of Parkinson’s disease (PD) often involves the over-activation microglia. Over-activated microglia could produce several inflammatory mediators, which trigger excessive inflammation and ultimately cause dopaminergic neuron damage. Anti-inflammatory effects glucagon-like peptide-2 (GLP-2) in periphery have been shown. Nonetheless, it has not illustrated brain. Thus, this study, we aimed to understand role GLP-2 activation elucidate underlying mechanisms. BV-2 cells were...
ABSTRACT Ser ine inc orporator 5 ( SER INC5, SER5) suppresses viral cell-free infection. However, its antiviral potency under cell-cell infection is not examined yet. Here, we established the in vitro systems to assess SER5’s activity on HIV-1 and bovine leukemia virus (BLV). Our results showed SER5 from different mammalian species, including Homo sapiens , Bos taurus Felis catus was capable of significantly inhibiting these SER5s were unable restrict Intriguingly, Ebola...
Serine incorporator 5 (SERINC5) is a host restriction factor that targets certain enveloped viruses, including human immunodeficiency virus type 1 (HIV-1) and murine leukemia (MLV). It integrates into the viral envelope from cell surface, inhibiting entry. SERINC5 transported to surface via polyubiquitination, while single K130R mutation retains it in cytoplasm. Both HIV-1 Nef MLV glycoGag proteins antagonize by reducing its expression producer cells. Here, we report employs selective...
The aim of this study was to investigate the anti-inflammatory effect IL-21 on LPS-induced mouse peritoneal macrophages. results showed that significantly inhibited mRNA expression IL-1 β , TNF- α and IL-6 in macrophages, but not IFN- γ IL-10, CCL5, or CXCL2. ELISA analysis also suppressed production culture supernatants. Western blot clearly ERK I κ B phosphorylation NF- translocation LPS-stimulated it increased STAT3 phosphorylation. Flow cytometric decreased M1 macrophages surface markers...
Glycosylated Gag (glycoGag) is an accessory protein expressed by most gammaretroviruses, including murine leukemia virus (MLV). MLV glycoGag not only enhances replication and disease progression but also increases human immunodeficiency type 1 (HIV-1) infectivity as Nef does. Recently, SERINC5 (Ser5) was identified the target for Nef, Nef-like activity has been attributed to Ser5 antagonism. Here, we investigated how antagonizes using glycoMA proteins. We confirm previous observations that...
Mycophenolate mofetil (MMF) is an alternative immunosuppressive agent that has been reported to be effective and well tolerated for the treatment of refractory inflammatory bowel disease (IBD). The aim this study was investigate therapeutic effect MMF on intestinal injury tissue inflammation, which were caused by Crohn’s (CD). Here, trinitrobenzene sulfonic acid-relapsing (TNBS) colitis induced in mice; then, we measured differentiation Th1/Th2 cells mouse splenocytes flow cytometry...
Abstract HIV-1 must counteract various host restrictions to establish productive infection. SERINC5 is a potent restriction factor that blocks entry from virions, but its activity counteracted by Nef. The and Nef activities are both initiated the plasma membrane, where packaged into virions for viral inhibition or downregulated via lysosomal degradation. However, it still unclear how localized expression regulated on membrane. We now report Cullin 3-KLHL20, trans -Golgi network...
HIV-1-negative factor (Nef) protein antagonizes serine incorporator 5 (SERINC5) by redirecting this potent restriction to the endosomes and lysosomes for degradation. However, precise mechanism remains unclear. Using affinity purification/mass spectrometry, we identify cyclin K (CycK) cyclin-dependent kinase 13 (CDK13) as a Nef-associated complex. CycK/CDK13 phosphorylates at position 360 (S360) in SERINC5, which is required Nef downregulation of SERINC5 from cell surface its counteractivity...