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EphA7 is required for otic epithelial homeostasis by modulating Claudin6 in Xenopus

  1. Author:
    Wang, Xiaolei
    Sun,Jian
    Wang, Zhaobao
    Li, Chaocui
    Mao, Bingyu
  2. Author Address

    Medical College, Qingdao University, Qingdao, 266071, China; State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China., State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China; Cancer and Developmental Biology Laboratory, National Cancer Institute, National Institute of Health, Frederick, MD, 21702, USA., School of Control Science and Engineering, Shandong University, Jinan, 250061, China; Energy-rich Compounds Production by Photosynthetic Carbon Fixation Research Center, College of Life Sciences, Qingdao Agricultural University, Qingdao, 266109, China., State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China. Electronic address: mao@mail.kiz.ac.cn.,
    1. Year: 2020
    2. Date: May 28
    3. Epub Date: 2020 03 25
  1. Journal: Biochemical and biophysical research communications
    1. 526
    2. 2
    3. Pages: 375-380
  2. Type of Article: Article
  3. ISSN: 0006-291X
  1. Abstract:

    Receptor tyrosine kinase EphA7 is specifically expressed in otic region in Xenopus early development. However, its role in otocyst development remains unknown. Knockdown of EphA7 by a specific morpholino oligonucleotide (MO) reduced the size of the otocyst and triggered otic epithelial cell extrusion. Interestingly, EphA7 depletion attenuated the membrane level of the tight junction protein Claudin6 (CLDN6). Utilizing the Cldn6 MO, we further confirmed that CLDN6 attenuation also led to otic epithelial cell extrusion. Our work suggested that EphA7 modulates the otic epithelial homeostasis through stabilizing the CLDN6 membrane level. Copyright © 2020 Elsevier Inc. All rights reserved.

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External Sources

  1. DOI: 10.1016/j.bbrc.2020.03.099
  2. PMID: 32222280
  3. WOS: 000530031800015
  4. PII : S0006-291X(20)30590-8

Library Notes

  1. Fiscal Year: FY2019-2020
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