Yu Tang

ORCID: 0000-0001-9709-9614
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About
Contact & Profiles
Research Areas
  • CRISPR and Genetic Engineering
  • Pluripotent Stem Cells Research
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Genetic Neurodegenerative Diseases
  • Parkinson's Disease Mechanisms and Treatments
  • Alzheimer's disease research and treatments
  • Neurological disorders and treatments
  • RNA and protein synthesis mechanisms
  • RNA regulation and disease
  • Neurogenesis and neuroplasticity mechanisms
  • 3D Printing in Biomedical Research
  • Epigenetics and DNA Methylation
  • Nuclear Receptors and Signaling
  • Advanced biosensing and bioanalysis techniques
  • Genetics and Neurodevelopmental Disorders
  • Amyotrophic Lateral Sclerosis Research
  • Biomedical Ethics and Regulation
  • RNA Research and Splicing
  • MicroRNA in disease regulation
  • Histone Deacetylase Inhibitors Research
  • Autophagy in Disease and Therapy
  • COVID-19 Clinical Research Studies
  • Neurogenetic and Muscular Disorders Research
  • Cellular transport and secretion
  • Lysosomal Storage Disorders Research

Zhengzhou Children's Hospital
2021-2025

Zhengzhou University
2021-2025

Xiangya Hospital Central South University
2018-2024

Central South University
2017-2024

The University of Texas Southwestern Medical Center
2016-2021

South China Agricultural University
2019-2020

National Clinical Research
2019

Tianjin University of Technology
2019

Shanghai Jiao Tong University
2010-2017

Shanghai Ninth People's Hospital
2001-2017

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder caused by selective motor neuron degeneration. Abnormal protein aggregation and impaired degradation pathways may contribute to the disease pathogenesis. Although it has been reported that autophagy altered in patients animal model of ALS, little known about role degeneration this disease. Our previous study shows rapamycin, an MTOR-dependent autophagic activator, accelerates progression SOD1G93A mouse ALS. In...

10.4161/auto.27710 article EN Autophagy 2014-01-15

Although it is well established that embryonic stem (ES) cells have the potential to differentiate into dopamine neurons, molecular basis of this process, particularly role microRNAs (miRNAs), remains largely unknown. Here we report miR-132 plays a key in differentiation neurons by directly regulating expression Nurr1 (also known as nuclear receptor subfamily 4 group A member 2; Nr4a2). We constructed mouse ES cell line CGR8, which stably expresses GFP under tyrosine hydroxylase (TH)...

10.1242/jcs.086421 article EN Journal of Cell Science 2012-01-01

In vitro generation of motor neurons (MNs) is a promising approach for modeling neuron diseases such as amyotrophic lateral sclerosis (ALS). As aging leading risk factor the development neurodegeneration, it important to recapitulate age-related characteristics by using MNs at pathogenic ages. So far, cell reprogramming through induced pluripotent stem cells (iPSCs) and direct from primary fibroblasts are two major strategies obtain populations MNs. While iPSC must go across epigenetic...

10.3389/fnmol.2017.00359 article EN cc-by Frontiers in Molecular Neuroscience 2017-11-02

Autophagy plays an important role in Alzheimer's disease (AD). It has been reported that autophagic flux is altered patients with AD, and application of the autophagy enhancer rapamycin may alleviate cognitive impairment amyloid-β (Aβ) neuropathology transgenic animal model AD. Since also immune suppressor, there a concern long-term use bring severe unwanted side effects. The aim this study to test if carbamazepine (CBZ), anti-epileptic drug potent enhancement effect, anti-AD effects...

10.2174/1567205011310040008 article EN Current Alzheimer Research 2013-04-01

Amyloid β-peptide (Aβ) accumulation leads to neurodegeneration and Alzheimer's disease (AD). Aβ metabolism is a dynamic process in the production clearance that requires neprilysin (NEP) other enzymes degrade Aβ. It has been reported NEP expression significantly decreased brain of AD patients. Previously we have documented hypoxia risk factor for generation vivo vitro through increasing by altering β-cleavage γ-cleavage APP down-regulating NEP, causing tau hyperphosphorylation. Here,...

10.1371/journal.pone.0019229 article EN cc-by PLoS ONE 2011-04-29

Induced pluripotent stem cell (iPSC) provides a promising seeding for regenerative medicine. However, iPSC has the potential to form teratomas after transplantation. Therefore, it is necessary evaluate tumorigenic risks of and all its differentiated derivates prior use in clinical setting. Here, murine iPSCs were transduced with dual reporter gene consisting monomeric red fluorescent protein (mRFP) firefly luciferase (Fluc). Undifferentiated iPSCs, from induced differentiation...

10.1111/jcmm.12062 article EN cc-by Journal of Cellular and Molecular Medicine 2013-05-26

De novo mutations (DNMs) significantly contribute to sporadic diseases, particularly in neuropsychiatric disorders. Whole-exome sequencing (WES) and whole-genome (WGS) provide effective methods for detecting DNMs prioritizing candidate genes. However, it remains a challenge scientists, clinicians, biologists conveniently access analyse data regarding genes from scattered publications. To fill the unmet need, we integrated 580 799 DNMs, including 30 060 coding detected by WES/WGS 23 951...

10.1093/nar/gkz923 article EN cc-by-nc Nucleic Acids Research 2019-10-08

DYT1 dystonia is a hereditary neurologic movement disorder characterized by uncontrollable muscle contractions. It caused heterozygous mutation in Torsin A ( TOR1A ), gene encoding membrane-embedded ATPase. While animal models provide insights into disease mechanisms, significant species-dependent differences exist since animals with the identical fail to show pathology. Here, we model using human patient-specific cholinergic motor neurons (MNs) that are generated through either direct...

10.1523/jneurosci.2507-20.2020 article EN cc-by-nc-sa Journal of Neuroscience 2021-01-19

Alzheimer's disease (AD) is the most common age-related dementia characterized by progressive neuronal loss. However, molecular mechanisms for loss still debated. Here, we used induced pluripotent stem cells (iPSCs) derived from somatic of familial AD patients carrying PSEN1 mutations to study early pathogenic event AD. We found that premature differentiation with decreased proliferation and increased apoptosis occured in AD-iPSC-derived neural progenitor (AD-NPCs) once was initiated,...

10.18632/oncotarget.13776 article EN Oncotarget 2016-12-02

Summary Aims Previously, we have documented that prenatal hypoxia can aggravate the cognitive impairment and A lzheimer's disease ( AD ) neuropathology in APP Swe / PS 1 A246E 1) transgenic mice, valproic acid VPA prevent hypoxia‐induced down‐regulation of β‐amyloid (Aβ) degradation enzyme neprilysin NEP primary neurons. In this study, investigated molecular mechanisms VPA's anti‐AD effects found reduce neuritic plaque formation improve learning deficits mouse model. Methods The pregnant...

10.1111/cns.12186 article EN other-oa CNS Neuroscience & Therapeutics 2013-12-02

Emerging studies of human pluripotent stem cells (hPSCs) raise new prospects for neurodegenerative disease modeling and cell replacement therapies. Therefore, understanding the mechanisms underlying commitment neural progenitor (NPCs) is important application hPSCs in It has been reported that epigenetic modifications histones play roles differentiation, but exact regulating hPSC differentiation towards NPCs are not fully elucidated. We demonstrated suppression histone deacetylases (HDACs)...

10.1186/s12915-014-0095-z article EN cc-by BMC Biology 2014-11-19

Abstract Common polygenic diseases result from compounded risk contributed by multiple genetic variants, meaning that simultaneous correction or introduction of single nucleotide variants is required for disease modeling and gene therapy. Here, we show precise, efficient, multiplex base editing up to three target sites across 11 genes/loci in cynomolgus monkey embryos using CRISPR-based cytidine- adenine-base editors. Unbiased whole genome sequencing demonstrates high specificity embryos....

10.1038/s41467-020-16173-0 article EN cc-by Nature Communications 2020-05-11

GGC repeat expansions within NOTCH2NLC have been identified as the genetic cause of neuronal intranuclear inclusion disease (NIID). To understand molecular pathogenesis NIID, here, we established both a transgenic mouse model and human neural progenitor cells (hNPCs) model. Expression with expanded repeats produced widespread perinuclear polyglycine (polyG), polyalanine (polyA), polyarginine (polyR) inclusions, leading to behavioral deficits severe neurodegeneration, which faithfully...

10.1126/sciadv.add6391 article EN cc-by-nc Science Advances 2022-11-23

Transfer RNAs (tRNAs) are products of RNA polymerase III (Pol III) and essential for mRNA translation ultimately cell growth proliferation. Whether how individual tRNA genes specifically regulated is not clear. Here, we report that SOX4, a well-known Pol II-dependent transcription factor critical neurogenesis reprogramming somatic cells, also directly controls, unexpectedly, the expression subset therefore protein synthesis proliferation human glioblastoma cells. Genome-wide location...

10.1073/pnas.1920200117 article EN Proceedings of the National Academy of Sciences 2020-03-02

Abstract Background Intracardiac thrombus (ICT) is the rarest yet most severe complication of Mycoplasma pneumoniae pneumonia (SMPP) in children. This study aims to elucidate clinical characteristics patients with SMPP-related ICT. Methods We retrospectively enrolled 68 children SMPP (18 cases ICT, 50 non-ICT) who were admitted from January 2014 2024. compared their demographic data, symptoms, laboratory tests, imaging findings, treatment strategies, and prognoses. Additionally, we...

10.1186/s13052-025-01890-3 article EN cc-by ˜The œItalian Journal of Pediatrics/Italian journal of pediatrics 2025-02-11

Programmed death ligand 1 (PD-L1) functions as a key immune inhibitory factor by binding with its receptor, programmed (PD-1), to induce cell dysfunction and escape of the system. However, mechanisms PD-L1 expression under growth stimulation are not well characterized. Here, we demonstrate novel role for glial line-derived neurotrophic (GDNF) in upregulating head neck squamous carcinoma (HNSCC). The correlation PD-L1, GDNF perineural invasion (PNI) status were evaluated bioinformatics...

10.1080/2162402x.2017.1353860 article EN OncoImmunology 2017-07-20
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