Related Experiment Videos

Cloning and expression of the ret proto-oncogene encoding a tyrosine kinase with two potential transmembrane domains

M Takahashi1, Y Buma, T Iwamoto

  • 1Laboratory of Experimental Pathology, Aichi Cancer Center Research Institute, Japan.

Oncogene
|November 1, 1988
PubMed

Insights

The ret proto-oncogene, a receptor tyrosine kinase, was sequenced. Its carboxy-terminal alterations significantly enhance its transforming potential, suggesting a role in oncogenesis.

Area of Science:

  • Molecular Biology
  • Oncogenesis
  • Signal Transduction

Background:

  • The ret proto-oncogene encodes a receptor tyrosine kinase involved in cell growth and differentiation.
  • Alterations in proto-oncogenes can lead to the formation of oncogenes, driving cancer development.
  • Understanding the structural and functional changes in ret is crucial for comprehending its role in oncogenesis.

Purpose of the Study:

  • To determine the nucleotide sequence of the ret proto-oncogene.
  • To analyze the structural relationship of the ret protein to other transmembrane receptors.
  • To investigate the impact of carboxy-terminal modifications on the transforming activity of the ret gene.

Main Methods:

  • Isolation of cDNA clones from a THP-1 human monocytic leukemia cell line library.
  • Nucleotide sequencing of the ret proto-oncogene.
  • Comparative sequence analysis between ret proto-oncogene and ret transforming gene.
  • Functional analysis of ret cDNA constructs with varying truncations.

Main Results:

  • The ret proto-oncogene sequence encodes a transmembrane receptor with a cytoplasmic tyrosine kinase domain and two potential transmembrane regions.
  • The ret transforming gene differs from the proto-oncogene by N-terminal truncation and replacement of the C-terminal 51 amino acids with 9 unrelated residues.
  • Ret cDNA with both N- and C-terminal truncations exhibited a 13-fold higher focus-forming activity compared to N-terminal truncation alone.
  • Transcription of the ret proto-oncogene was detected in normal mouse spinal cord and in specific mouse models of lymphadenopathy.

Conclusions:

  • The carboxy-terminal sequence of the ret proto-oncogene may play a role in its activation and transforming potential.
  • Structural alterations, particularly C-terminal modifications, are critical for the oncogenic activity of the ret gene.
  • The ret proto-oncogene is transcribed in the spinal cord, suggesting potential roles in neural development or function.

Related Concept Videos