Zhijiao Xu

ORCID: 0000-0003-3888-0106
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About
Contact & Profiles
Research Areas
  • RNA regulation and disease
  • CRISPR and Genetic Engineering
  • Retinal Development and Disorders
  • RNA and protein synthesis mechanisms
  • Hearing, Cochlea, Tinnitus, Genetics
  • RNA Interference and Gene Delivery
  • Analytical Chemistry and Sensors
  • Analytical Chemistry and Chromatography
  • Genomics and Chromatin Dynamics
  • RNA Research and Splicing
  • Advanced Chemical Sensor Technologies

Eye & ENT Hospital of Fudan University
2021-2023

State Key Laboratory of Medical Neurobiology
2021-2023

Fudan University
2019-2022

The First Affiliated Hospital, Sun Yat-sen University
2019

Zhongshan Hospital
2019

Sun Yat-sen University
2019

Northwest A&F University
2017

Yangzhou Vocational University
2017

Programmable RNA editing tools enable the reversible correction of mutant transcripts, reducing potential risk associated with permanent genetic changes use DNA tools. However, these to treat disease remains unknown. Here, we evaluated therapy Cas13-based base editors in myosin VI p.C442Y heterozygous mutation (Myo6C442Y/+) mouse model that recapitulated phenotypes human dominant-inherited deafness. We first screened several variants and guide RNAs (gRNAs) targeting Myo6C442Y cultured cells...

10.1126/scitranslmed.abn0449 article EN Science Translational Medicine 2022-07-20

Abstract CRISPR/RfxCas13d (CasRx) editing system can specifically and precisely cleave single-strand RNAs, which is a promising treatment for various disorders by downregulation of related gene expression. Here, we tested this RNA-editing approach on Beethoven ( Bth ) mice, an animal model human DFNA36 due to point mutation in Tmc1 . We first screened 30 sgRNAs cell cultures found that CasRx with sgRNA3 reduced the transcript 90.8%, wild type + 44.3%. then injected newly developed AAV vector...

10.1038/s41392-022-00893-4 article EN cc-by Signal Transduction and Targeted Therapy 2022-03-14

Myosin VI(MYO6) is an unconventional myosin that vital for auditory and vestibular function. Pathogenic variants in the human MYO6 gene cause autosomal-dominant or -recessive forms of hearing loss. Effective treatments Myo6 mutation causing loss are limited. We studied whether adeno-associated virus (AAV)-PHP.eB vector-mediated vivo delivery Staphylococcus aureus Cas9 (SaCas9-KKH)-single-guide RNA (sgRNA) complexes could ameliorate a Myo6WT/C442Y mouse model recapitulated phenotypes...

10.1016/j.ymthe.2021.06.015 article EN cc-by-nc-nd Molecular Therapy 2021-06-24

Abstract Background Aging, noise, infection, and ototoxic drugs are the major causes of human acquired sensorineural hearing loss, but treatment options limited. CRISPR/Cas9 technology has tremendous potential to become a new therapeutic modality for non-inherited loss. Here, we develop strategies prevent aminoglycoside-induced deafness, common type via disrupting Htra2 gene in inner ear which is involved apoptosis not been investigated cochlear hair cell protection. Results The results...

10.1186/s13059-021-02311-4 article EN cc-by Genome biology 2021-03-22

The architecture and function of chromatin are largely regulated by local interacting molecules, such as transcription factors noncoding RNAs.However, our understanding these regulatory molecules at a given locus is limited because technical difficulties.Here, we describe the use Clustered Regularly Interspaced Short Palindromic Repeats an engineered ascorbate peroxidase 2 (APEX2) system to investigate interactions (CAPLOCUS).We showed that with specific small-guide RNA targets, CAPLOCUS...

10.1093/nar/gkz134 article EN cc-by Nucleic Acids Research 2019-02-19

An electronic nose (PEN3) containing 10 metal oxide semiconductor type chemical sensors was used to discriminate between eight varieties of apple juice.

10.1039/c6ay02610a article EN Analytical Methods 2017-01-01

A wide spectrum of SLC26A4 mutations causes Pendred syndrome and enlarged vestibular aqueduct, both associated with sensorineural hearing loss (SNHL). splice-site mutation, c.919-2A>G (A-2G), which is common in Asian populations, impairs the 3′ splice site intron 7, resulting exon 8 skipping during pre-mRNA splicing a subsequent frameshift that creates premature termination codon following exon. Currently, there no effective drug treatment for SHNL. For A-2G-triggered SNHL, molecules correct...

10.1016/j.omtn.2022.03.015 article EN cc-by-nc-nd Molecular Therapy — Nucleic Acids 2022-03-20
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