Xingsen Zhao

ORCID: 0000-0003-1721-0859
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About
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Research Areas
  • RNA modifications and cancer
  • Glycosylation and Glycoproteins Research
  • Galectins and Cancer Biology
  • Medicinal Plant Pharmacodynamics Research
  • Williams Syndrome Research
  • Cancer-related molecular mechanisms research
  • Cancer-related gene regulation
  • Epigenetics and DNA Methylation
  • Congenital heart defects research
  • Peptidase Inhibition and Analysis
  • Genetics and Neurodevelopmental Disorders
  • Carbohydrate Chemistry and Synthesis
  • Circular RNAs in diseases
  • RNA regulation and disease
  • Microbial bioremediation and biosurfactants
  • Education, Achievement, and Giftedness
  • Motivation and Self-Concept in Sports
  • Enhanced Oil Recovery Techniques
  • Creativity in Education and Neuroscience
  • CRISPR and Genetic Engineering
  • Cardiac Structural Anomalies and Repair
  • Algal biology and biofuel production
  • Alzheimer's disease research and treatments
  • Metabolomics and Mass Spectrometry Studies
  • Cholesterol and Lipid Metabolism

Zhejiang University
2019-2025

Children's Hospital of Zhejiang University
2019-2025

Sun Yat-sen University
2025

National Clinical Research
2024

Peking University
2007

Abstract A genome-wide differential expression of long noncoding RNAs (lncRNAs) was identified in blood specimens autism spectrum disorder (ASD). total 3929 lncRNAs were found to be differentially expressed ASD peripheral leukocytes, including 2407 that upregulated and 1522 downregulated. Simultaneously, 2591 messenger (mRNAs), 1789 821 downregulated, also leukocytes. Functional pathway analysis these revealed neurological pathways the synaptic vesicle cycling, long-term depression...

10.1038/tp.2015.144 article EN cc-by Translational Psychiatry 2015-10-20

Previous studies have shown that Ogt-mediated O-GlcNAcylation is essential for neuronal development and function. However, the function of O-GlcNAc transferase (Ogt) in astrocytes remains largely unknown. Here we show Ogt deficiency induces inflammatory activation vivo vitro, impairs cognitive mice. The restoration via GlcNAc supplementation inhibits astrocytes, inflammation improves impaired deficient Mechanistically, interacts with NF-κB p65 catalyzes astrocytes. signaling pathway by...

10.1186/s12974-023-02824-8 article EN cc-by Journal of Neuroinflammation 2023-06-22

Ogt-mediated O-GlcNAcylation is enriched in the nervous system and involves neuronal development, brain function neurological diseases. However, roles of Ogt embryonic neurogenesis have remained largely unknown. Here, we show that highly expressed brain, depletion reduces proliferation neural stem cells migration new born neurons. cultured hippocampal neurons impairs maturation, including reduced dendritic numbers length, immature development spines. Mechanistically, decreases activity...

10.1093/hmg/ddab223 article EN Human Molecular Genetics 2021-07-30

The L2 Motivational Self System (L2MSS) determines an individual's motivation in second language learning and influences the experience intended effort. Although physical activity (PA) has been shown to enhance academic efficacy, role of PA whether it promotes efficacy not elucidated. Therefore, present study examined as a mediator explored its ameliorative effects L2MSS. A total 981 international students from different countries were selected 8 universities Beijing research subjects...

10.1038/s41598-025-86517-7 article EN cc-by-nc-nd Scientific Reports 2025-01-26

Abstract Sleep behavior is regulated by diverse mechanisms including genetics, neuromodulation and environmental signals. However, it remains completely unknown regarding the roles of epitranscriptomics in regulating sleep behavior. In present study, we showed that deficiency RNA m 6 A methyltransferase Mettl3 excitatory neurons specifically induces microglia activation, neuroinflammation neuronal loss thalamus mice. remarkably disrupts rhythm reduces amount non-rapid eye movement sleep. We...

10.1038/s41421-024-00756-y article EN cc-by Cell Discovery 2025-02-04

Abstract Alzheimer’s disease is the most common cause of dementia. Although increasing evidence suggests that disruptions in lipid metabolism are closely associated with disease, overall profile and sterol changes occur brain during remains unclear. In this study, we compared tissues extracted from 32-week-old male wild-type mice 5×FAD transgenic model mice, which carry mutations amyloid precursor protein ( APP ) presenilin 1 PS1 genes. Using untargeted lipidomics sterolomics techniques,...

10.4103/nrr.nrr-d-24-00975 article EN cc-by-nc-sa Neural Regeneration Research 2025-02-24

Arginine methylation of histones plays a critical role in regulating gene expression. The writers (methyltransferases) and readers methylarginine marks are well-known, but the erasers–arginine demethylases–remain mysterious. Here we identify Myc-induced nuclear antigen 53 (Mina53), jumonji C domain containing protein, as an arginine demethylase for removing asymmetric di-methylation at 3 histone H4 (H4R3me2a). Using photoaffinity capture method, first Mina53 interactor H4R3me2a. Biochemical...

10.1038/s41467-024-54680-6 article EN cc-by-nc-nd Nature Communications 2024-11-26

Specific mutations within the replication foci targeting sequence (RFTS) domain of human DNMT1 are causative two types adult-onset neurodegenerative diseases, HSAN1E and ADCA-DN, but underlying mechanisms largely unknown. We generated

10.1126/sciadv.abe8511 article EN cc-by-nc Science Advances 2021-09-03

Although previous studies have shown that an enriched environment (EE) promotes neurogenesis and alters DNA histone modifications, it remains largely unknown whether EE affects epitranscriptome in the context of neuronal development. Here, we showed exposure enhanced pool adult neural stem/progenitor cells (aNSPCs) promoted differentiation aNSPCs. also improved cognitive capabilities altered expression genes relating to development, neurogenesis, memory. N 6 -Methyladenosine (m A)...

10.3389/fcell.2022.903179 article EN cc-by Frontiers in Cell and Developmental Biology 2022-06-02

Abstract Williams Syndrome (WS; OMIM#194050) is a rare disorder, which caused by the microdeletion of one copy 25-27 genes, and WS patients display diverse neuronal deficits. Although remarkable progresses have been achieved, mechanisms for these distinct deficits are still largely unknown. Here, we shown that neural progenitor cells (NPCs) in forebrain organoids abnormal proliferation differentiation capabilities, synapse formation. Genes with altered expression related to development...

10.1101/2024.04.25.591131 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-04-25

Williams syndrome (WS; OMIM#194050) is a rare disorder, which caused by the microdeletion of one copy 25–27 genes, and WS patients display diverse neuronal deficits. Although remarkable progresses have been achieved, mechanisms for these distinct deficits are still largely unknown. Here, we shown that neural progenitor cells (NPCs) in forebrain organoids abnormal proliferation differentiation capabilities, synapse formation. Genes with altered expression related to development neurogenesis....

10.7554/elife.98081 article EN cc-by eLife 2024-08-19

Williams Syndrome (WS; OMIM#194050) is a rare disorder, which caused by the microdeletion of one copy 25-27 genes, and WS patients display diverse neuronal deficits. Although remarkable progresses have been achieved, mechanisms for these distinct deficits are still largely unknown. Here, we shown that neural progenitor cells (NPCs) in forebrain organoids abnormal proliferation differentiation capabilities, synapse formation. Genes with altered expression related to development neurogenesis....

10.7554/elife.98081.1 preprint EN 2024-08-19

Williams syndrome (WS; OMIM#194050) is a rare disorder, which caused by the microdeletion of one copy 25–27 genes, and WS patients display diverse neuronal deficits. Although remarkable progresses have been achieved, mechanisms for these distinct deficits are still largely unknown. Here, we shown that neural progenitor cells (NPCs) in forebrain organoids abnormal proliferation differentiation capabilities, synapse formation. Genes with altered expression related to development neurogenesis....

10.7554/elife.98081.2 article EN cc-by eLife 2024-12-13
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