FAT4 Fine-Tunes Kidney Development by Regulating RET Signaling

Hongtao Zhang, Mazdak Bagherie-Lachidan, Caroline Badouel, Leonie Enderle, Philippos Peidis, Rod Bremner, Satu Kuure, Sanjay Jain, Helen McNeill

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

FAT4 mutations occur in humans with kidney disease. Controlling RET tyrosine kinase activity is critical for normal kidney development. Zhang et al. show that FAT4 restricts RET signaling activity by binding to RET and reducing RET interactions with its ligand GDNF-GFRA1. Thus, FAT4 loss leads to hyperactive RET signaling and disease.

Original languageEnglish
Pages (from-to)780-792.e4
JournalDevelopmental cell
Volume48
Issue number6
DOIs
StatePublished - Mar 25 2019

Keywords

  • CAKUT
  • FAT4
  • RET
  • Van Maldergem syndrome
  • cadherin
  • kidney development
  • non-autonomous

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  • Cite this

    Zhang, H., Bagherie-Lachidan, M., Badouel, C., Enderle, L., Peidis, P., Bremner, R., Kuure, S., Jain, S., & McNeill, H. (2019). FAT4 Fine-Tunes Kidney Development by Regulating RET Signaling. Developmental cell, 48(6), 780-792.e4. https://doi.org/10.1016/j.devcel.2019.02.004