Yanjie Sun

ORCID: 0000-0001-9382-4401
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Prion Diseases and Protein Misfolding
  • Chromium effects and bioremediation
  • Cholinesterase and Neurodegenerative Diseases
  • Viral Infections and Vectors
  • Mosquito-borne diseases and control
  • Immune Response and Inflammation
  • Neuroendocrine regulation and behavior
  • Protein Tyrosine Phosphatases
  • 14-3-3 protein interactions
  • Computational Drug Discovery Methods
  • Neurotransmitter Receptor Influence on Behavior
  • Biochemical and Molecular Research
  • Nuclear Receptors and Signaling
  • Cell death mechanisms and regulation
  • biodegradable polymer synthesis and properties
  • Parvovirus B19 Infection Studies
  • Functional Brain Connectivity Studies
  • Medicinal Plants and Neuroprotection
  • Cancer Mechanisms and Therapy
  • Metal complexes synthesis and properties
  • Corrosion Behavior and Inhibition
  • Adenosine and Purinergic Signaling
  • Viral Infections and Outbreaks Research

Suihua University
2025

University of Duisburg-Essen
2023-2024

West German Heart and Vascular Center Essen
2023

Shandong First Medical University
2023

Jinan City People's Hospital
2023

Wuhan Institute of Technology
2023

Hebei Medical University
2017-2020

Second Hospital of Hebei Medical University
2017-2020

New York University
2008-2019

Xinxiang Medical University
2018-2019

Alzheimer's Disease (AD) is the most common of conformational neurodegenerative disorders characterized by conversion a normal biological protein into β-sheet-rich pathological isoform. In AD soluble Aβ (sAβ) forms oligomers and fibrils which assemble neuritic plaques. The toxic form thought to be oligomeric. A recent study reveals cellular prion protein, PrPC, receptor for oligomers. suppress LTP signal in murine hippocampal slices but activity remains when pretreated with PrP monoclonal...

10.1186/1471-2202-11-130 article EN cc-by BMC Neuroscience 2010-10-14

Amyloid plaques are a key pathological hallmark of Alzheimer's disease (AD). The detection amyloid in the brain is important for diagnosis AD, as well following potential targeting therapeutic interventions. Our group has developed several contrast agents to detect vivo using magnetic resonance microimaging (µMRI) AD transgenic mice, where we used mannitol enhance blood barrier (BBB) permeability. In present study, bifunctional ultrasmall superparamagnetic iron oxide (USPIO) nanoparticles,...

10.1371/journal.pone.0057097 article EN cc-by PLoS ONE 2013-02-27

Alzheimer's disease (AD) is the most common cause of dementia, and currently, there no effective treatment. The major neuropathological lesions in AD are accumulation amyloid β (Aβ) as plaques congophilic angiopathy, well aggregated tau form neurofibrillary tangles (NFTs). In addition, inflammation microglia/macrophage function play an important role pathogenesis. We have hypothesized that stimulation innate immune system via Toll-like receptor 9 (TLR9) agonists, such type B CpG...

10.1186/s40478-014-0101-2 article EN cc-by Acta Neuropathologica Communications 2014-09-01

Alzheimer's disease (AD) is characterized by the presence of parenchymal amyloid-β (Aβ) plaques, cerebral amyloid angiopathy (CAA) and neurofibrillary tangles. Currently there are no effective treatments for AD. Immunotherapeutic approaches under development hampered complications related to ineffectual clearance CAA. Genome-wide association studies have demonstrated importance microglia in AD pathogenesis. Microglia primary innate immune cells brain. Depending on their activation state...

10.1523/jneurosci.1967-16.2016 article EN cc-by-nc-sa Journal of Neuroscience 2016-12-15

Abstract Inheritance of the apolipoprotein E4 (apoE4) genotype has been identified as major genetic risk factor for late onset Alzheimer’s disease (AD). Studies have shown that apoE, apoE4 in particular, binds to amyloid- β (A ) peptides at residues 12-28 A and this binding modulates accumulation progression. We previously several AD transgenic mice lines blocking apoE/A interaction with P reduced tau-related pathology, leading cognitive improvements treated mice. Recently, we designed a...

10.1038/s41598-017-08604-8 article EN cc-by Scientific Reports 2017-08-08

Inheritance of the apolipoprotein E4 (apoE4) genotype has been identified as major genetic risk factor for late-onset Alzheimer's disease (AD). Studies have shown that binding between apoE and amyloid-β (Aβ) peptides occurs at residues 244-272 12-28 Aβ. ApoE4 implicated in promoting Aβ deposition impairing clearance We hypothesized blocking apoE/Aβ interaction would serve an effective new approach to AD therapy. previously treatment with Aβ12-28P can reduce amyloid plaques APP/PS1 transgenic...

10.1111/jnc.12484 article EN Journal of Neurochemistry 2013-10-12

The accumulation of amyloid-β (Aβ) peptides as toxic oligomers, amyloid plaques, and cerebral angiopathy (CAA) is critical in the pathogenesis Alzheimer's disease (AD). binding Aβ to apolipoprotein E (ApoE) plays an important role modulation deposition clearance. We have shown that blocking Aβ/ApoE interaction with Aβ(12-28P), a nontoxic blood-brain-barrier permeable non-fibrillogenic synthetic peptide, constitutes novel therapeutic approach for AD by reducing parenchymal deposition. In...

10.3233/jad-2011-101401 article EN Journal of Alzheimer s Disease 2011-04-11

Epithelial-mesenchymal transition (EMT) involves metastasis and drug resistance; thus, a new EMT reversing agent is required. It has shown that wild-type p53 can reverse back to epithelial characteristics, iron chelator acting as inducer been demonstrated. Moreover, recent study revealed etoposide could also inhibit EMT. Therefore, combination of with might achieve better inhibition To this end, we prepared di-2-pyridineketone hydrazone dithiocarbamate S-propionate podophyllotoxin ester...

10.1155/2019/2531493 article EN cc-by Oxidative Medicine and Cellular Longevity 2019-05-05

The biologically active form of the essential trace element chromium is believed to be oligopeptide chromodulin. Chromodulin binds four chromic ions before binding at or near site activating insulin receptor and subsequently potentiating tyrosine kinase activity receptor. Charge balance arguments preliminary spectroscopic studies suggested that centers might part a multinuclear assembly. Using combination X-ray absorption electron paramagnetic resonance spectroscopies variable-temperature...

10.1021/ja0202661 article EN Journal of the American Chemical Society 2002-12-24

Ventricular tachycardia is a common heart rhythm disorder and frequent cause of sudden cardiac death. Aberrant cell–cell coupling through gap junction channels, process termed remodeling, observed in many the major forms human disease associated with increased arrhythmic risk both humans animal models. Genetically engineered mice cardiac-restricted knockout Connexin43 , junctional protein, uniformly develop death, although detailed electrophysiological understanding their profound propensity...

10.1073/pnas.0500881102 article EN Proceedings of the National Academy of Sciences 2005-03-07

The broad spectrum of antiviral activity ribavirin (RBV) lies in its ability to inhibit IMP dehydrogenase, which lowers cellular GTP. However, RBV can act as a potent mutagen for some RNA viruses. Previously we have shown lack correlation between and GTP repression Hantaan virus (HTNV) evidence RBV's promote error-prone replication. To further explore the mechanism RBV, levels, specific infectivity, and/or mutation frequency was measured presence mycophenolic acid (MPA), selenazofurin, or...

10.1128/jvi.00874-07 article EN Journal of Virology 2007-08-16

Many neurodegenerative diseases are characterized by the conformational change of normal self-proteins into amyloidogenic, pathological conformers, which share structural properties such as high β-sheet content and resistance to degradation. The most common is Alzheimer's disease (AD) where soluble amyloid β (sAβ) peptide converted highly toxic oligomeric Aβ fibrillar that deposits neuritic plaques congophilic angiopathy. Currently, there no effective treatment for AD, but immunotherapy...

10.1371/journal.pone.0013391 article EN cc-by PLoS ONE 2010-10-13

Central to the pathogenesis of Alzheimer's disease (AD) and many other neurodegenerative diseases is conformational change a normal self-protein into toxic oligomeric species amyloid deposits. None these disorders have an effective therapy, but immunization approaches hold great promise. We previously shown that active with novel peptide when polymerized stable conformation, pBri, induced humoral immune response Aβ in AD model, APP/PS1 transgenic (Tg) mice, reducing plaque pBri...

10.1186/1742-2094-10-150 article EN cc-by Journal of Neuroinflammation 2013-12-01

Sorcin is a penta-EF hand Ca2+-binding protein that associates with both cardiac ryanodine receptors and L-type Ca2+ channels has been implicated in the regulation of intracellular cycling. To better define function sorcin, we characterized transgenic mice which sorcin was overexpressed heart. Transgenic developed normally no evidence hypertrophy change expression other calcium regulatory proteins. In vivo hemodynamics revealed significant reductions global indices contraction relaxation....

10.1074/jbc.m302009200 article EN cc-by Journal of Biological Chemistry 2003-07-25

Ribavirin (RBV) is a broad-spectrum antiviral agent that inhibits the production of infectious Hantaan virus (HTNV). Although mechanism action RBV against HTNV not understood, metabolized in human cells to both RBV-5'-monophosphate, which IMP dehydrogenase, resulting decrease intracellular GTP levels, and RBV-5'-triphosphate (RBV-TP), could selectively interact with viral RNA polymerase. To elucidate activity was most important its anti-HTNV activity, studied Vero E6 cells. Incubation 10 40...

10.1128/aac.00790-06 article EN Antimicrobial Agents and Chemotherapy 2006-12-20

Some iron chelators display significant anticancer activity that may involve ferritin degradation either in proteasomes or lysosomes, and the latter might ferritinophagy with a period. However, correlation of chelator was not fully determined. Revealing underlying link therefore is required. Di-2-pyridylketone dithiocarbamate (DpdtC), novel chelator, could mobilize from displayed excellent antitumor against hepatoma carcinoma cell lines (IC50s = 0.4 ± 0.2 for HepG2 3.5 0.3 μM Bel-7402,...

10.1155/2018/4928703 article EN cc-by Oxidative Medicine and Cellular Longevity 2018-01-01
Coming Soon ...