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Related Experiment Videos

The myb oncogene.

J S Lipsick1, M A Baluda

  • 1Jonsson Comprehensive Cancer Center, University of California, School of Medicine, Los Angeles 90024.

Gene Amplification and Analysis
|January 1, 1986
PubMed
Summary
This summary is machine-generated.

The c-myb gene, crucial in cell growth, can cause leukemia when altered by viruses. Research explores its nuclear functions, cell cycle regulation, and role in human cancers.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • The c-myb gene is a highly conserved, single-copy gene.
  • It is independently transduced by avian acute leukemia viruses (AMV and E26) and activated by insertional mutagenesis in hematopoietic tumors.
  • Truncation of the c-myb coding region is a common feature in retroviral activations.

Purpose of the Study:

  • To investigate the function of c-myb gene products, which are nuclear proteins.
  • To understand the regulation of c-myb expression, particularly its cell cycle dependence.
  • To explore the role of c-myb in leukemogenesis and human malignancies.

Main Methods:

  • Analysis of retroviral activations of c-myb.
  • Studying c-myb gene products' association with the nuclear matrix, half-lives, and DNA binding in vitro.

Related Experiment Videos

  • Investigating c-myb expression patterns in different cell types and tissues.
  • Utilizing new experimental systems, including a myb-related gene in Drosophila and murine myb studies.

    • Main Results:

    • c-myb gene products are nuclear proteins with short half-lives that bind DNA, suggesting roles in DNA replication or transcription.
    • c-myb expression is cell cycle dependent in many cell types but not in the thymus.
    • v-myb transformation's hematopoietic specificity is not fully understood, but hematopoietic growth factors are implicated.

    Conclusions:

    • The c-myb gene and its viral counterparts are implicated in leukemogenesis.
    • Further research is needed to define myb protein function, understand expression regulation, identify transforming alterations, and determine its role in human cancers.