Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Mitogenic response to colony-stimulating factor 1.

C J Sherr1

  • 1Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude Children's Research Hospital, Memphis, TN 38105.

Trends in Genetics : TIG
|November 1, 1991
PubMed
Summary

Colony-stimulating factor 1 (CSF-1) drives macrophage proliferation by activating the CSF-1 receptor tyrosine kinase. This process involves immediate- and delayed-early gene responses crucial for cell cycle progression into S phase.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The INK4-ARF (CDKN2A/B) locus in hematopoiesis and BCR-ABL-induced leukemias.

Cold Spring Harbor symposia on quantitative biology·2008
Same author

p53-Dependent and -independent functions of the Arf tumor suppressor.

Cold Spring Harbor symposia on quantitative biology·2006
Same author

Cell cycle control and cancer.

Harvey lectures·2002
Same author

Dmp1 is haplo-insufficient for tumor suppression and modifies the frequencies of Arf and p53 mutations in Myc-induced lymphomas.

Genes & development·2001
Same author

The INK4a/ARF network in tumour suppression.

Nature reviews. Molecular cell biology·2001
Same author

Parsing Ink4a/Arf: "pure" p16-null mice.

Cell·2001

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Colony-stimulating factor 1 (CSF-1) regulates mononuclear phagocyte proliferation.
  • The CSF-1 receptor tyrosine kinase is central to CSF-1 mediated signaling.
  • Macrophage cell cycle progression is tightly regulated.

Purpose of the Study:

  • To elucidate the role of CSF-1 signaling in macrophage cell cycle progression.
  • To investigate the immediate- and delayed-early gene responses induced by CSF-1.
  • To identify molecular targets of CSF-1 signaling that facilitate G1 to S phase transition.

Main Methods:

  • Analysis of CSF-1 receptor tyrosine kinase signaling pathways.
  • Gene expression profiling of macrophages stimulated with CSF-1.

Related Experiment Videos

  • Investigation of immediate- and delayed-early gene products.

    • Main Results:

    • CSF-1 receptor activation triggers multiple intracellular signal transduction pathways.
    • CSF-1 is essential throughout G1 phase for macrophage entry into S phase.
    • CSF-1 induces distinct sets of immediate- and delayed-early genes during G1.
    • Delayed-early response targets include novel cyclin genes implicated in S phase commitment.

    Conclusions:

    • CSF-1 signaling is critical for macrophage proliferation and cell cycle progression.
    • Immediate-early gene products may modulate subsequent receptor signaling for G1 progression.
    • Novel cyclin genes induced by CSF-1 are potential key regulators of S phase commitment.