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Related Experiment Videos

The RET receptor: function in development and dysfunction in congenital malformation.

S Manié1, M Santoro, A Fusco

  • 1Laboratoire de Génétique, CNRS UMR 5641, Domaine Rockefeller, 8 avenue Rockefeller, 69373 Cedex 08, Lyon, France.

Trends in Genetics : TIG
|October 5, 2001
PubMed
Summary

Germline mutations in the RET gene cause Hirschsprung disease and MEN2. This review details RET signaling, crucial for development, and its role in these disorders.

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Area of Science:

  • Genetics
  • Developmental Biology
  • Oncology

Background:

  • The RET proto-oncogene is implicated in neural crest disorders and cancer.
  • RET encodes a receptor tyrosine kinase vital for neural and kidney development.
  • Dysregulation of RET signaling contributes to disease pathogenesis.

Purpose of the Study:

  • To review the molecular mechanisms of RET activation.
  • To elucidate the role of RET signaling in development.
  • To connect RET signaling dysfunction to Hirschsprung disease.

Main Methods:

  • Review of existing literature on RET gene mutations and signaling pathways.
  • Analysis of RET's role in neural crest development.
  • Examination of RET's involvement in Hirschsprung disease and MEN2.

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Main Results:

  • Germline RET mutations cause Hirschsprung disease and multiple endocrine neoplasia type 2 (MEN2).
  • Somatic RET rearrangements are involved in papillary thyroid carcinoma.
  • RET signaling is essential for neural and kidney development.

Conclusions:

  • Understanding RET activation provides insights into developmental disorders.
  • RET signaling pathways are critical targets for therapeutic strategies.
  • This review highlights the multifaceted role of RET in health and disease.