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The myb genes.

K M Weston1

  • 1Institute of Cancer Research, Chester Beatty Laboratories, London, UK.

Seminars in Cancer Biology
|December 1, 1990
PubMed
Summary
This summary is machine-generated.

The v-myb oncogene and its cellular progenitor c-myb are DNA-binding proteins regulating hematopoietic cell growth and differentiation. Truncation mutations enhance myb protein DNA binding, suggesting a role in oncogenesis.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • The v-myb oncogene and its cellular counterpart, c-myb, are DNA-binding proteins.
  • These proteins are crucial in regulating the transition between growth and differentiation in hematopoietic cells.

Purpose of the Study:

  • To investigate the oncogenic determinants of v-myb and activated c-myb.
  • To understand the role of N- and/or C-terminal truncation in myb protein function.

Main Methods:

  • Analysis of v-myb and c-myb gene mutations.
  • Assessment of DNA binding affinity of truncated myb proteins.

Main Results:

  • N- and/or C-terminal truncation of myb proteins increases their affinity for DNA.

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  • Myb-like genes are conserved across diverse organisms, with the DNA-binding domain being the most conserved feature.

    • Conclusions:

    • Truncation appears to be a key factor in the oncogenic potential of myb proteins.
    • The conserved DNA-binding domain highlights the fundamental role of myb proteins in cellular processes across species.