Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1987 Aug;1(3):279-96.

Role of myc in the abrogation of IL3 dependence of myeloid FDC-P1 cells

Affiliations
  • PMID: 2453016

Role of myc in the abrogation of IL3 dependence of myeloid FDC-P1 cells

M Dean et al. Oncogene Res. 1987 Aug.

Abstract

We have constructed a recombinant retrovirus containing the murine c-myc and the neo gene and introduced the virus into the interleukin-3 (IL3) dependent myeloid cell line FDC-P1. Unregulated expression of the introduced c-myc gene is associated with both an increased viability and constitutive ornithine decarboxylase mRNA levels in FDC-P1 cells grown in the absence of IL3. FDC-P1 cells infected with the c-myc virus gave rise to IL3 independent lines. Three out of four independent lines have an activated endogenous c-myc or N-myc gene. We have also shown that c-myc mRNA levels are tightly regulated by IL3 in FDC-P1 cells. Taken together these results indicate that myc plays a critical role in the signal transduction pathway of IL3. Furthermore, activation of the N-myc gene may be one mechanism for myeloid cells to progress to complete IL3 independence.

PubMed Disclaimer

Publication types

Substances

LinkOut - more resources