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

Ionic signal transduction in growth factor action.

S W De Laat, W H Moolenaar, L H Defize

    Biochemical Society Symposium
    |January 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    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

    Recombinant Newcastle disease viruses with targets for PCR diagnostics for rinderpest and peste des petits ruminants.

    Journal of virological methods·2018
    Same author

    Erratum to: Identification of a restriction point at the M/G1 transition in CHO cells.

    Cellular and molecular life sciences : CMLS·2017
    Same author

    Competition for inorganic substrates among chemoorganotrophic and chemolithotrophic bacteria.

    Microbial ecology·2013
    Same author

    B-50/GAP-43 in neuronal development and repair.

    Restorative neurology and neuroscience·2011
    Same author

    Stable transmission of reversible modifications: maintenance of epigenetic information through the cell cycle.

    Cellular and molecular life sciences : CMLS·2010
    Same author

    Cell fate determination during G1 phase progression.

    Cellular and molecular life sciences : CMLS·2007

    Growth factors trigger cell responses via receptor binding, leading to ionic signals and lipid breakdown. However, stimulating receptor tyrosine kinase activity alone does not cause cell division, indicating complex signaling pathways are required for growth factor action.

    Area of Science:

    • Cellular Biology
    • Molecular Signaling
    • Biochemistry

    Background:

    • Growth factors are polypeptides that bind to cell surface receptors, initiating signal transduction pathways.
    • These pathways involve receptor tyrosine kinase activation, inositol lipid breakdown, and ionic signal production.
    • Understanding the interplay of these early responses is crucial for elucidating growth factor-mediated mitogenesis.

    Purpose of the Study:

    • To analyze the nature and origin of ionic signals induced by growth factors.
    • To differentiate early cellular responses to growth factors using monoclonal antibodies against the epidermal growth factor (EGF) receptor and phorbol esters.
    • To determine if stimulating receptor tyrosine kinase activity is sufficient for initiating downstream signaling and cell proliferation.

    Main Methods:

    Related Experiment Videos

    • Application of monoclonal antibodies targeting the EGF receptor (EGF-binding domain and sugar moieties).
    • Use of tumor-promoting phorbol esters (TPA) to mimic diacylglycerol effects.
    • Measurement of ionic signals (pH changes, calcium mobilization), protein kinase C activation, and DNA synthesis in human fibroblasts.

    Main Results:

    • Ionic signals are coupled to inositol lipid hydrolysis, producing diacylglycerol and inositol triphosphate.
    • Diacylglycerol activates protein kinase C, leading to increased cytoplasmic pH via Na+/H+ exchange, a response mimicked by TPA.
    • Monoclonal antibodies, including one against the EGF-binding domain, stimulated receptor tyrosine kinase activity but failed to induce ionic signals or DNA synthesis, even upon cross-linking.

    Conclusions:

    • Stimulation of intrinsic receptor tyrosine kinase activity can be dissociated from other early cellular responses like inositol lipid breakdown and ionic signaling.
    • Antibody binding to the EGF receptor, even at the EGF-binding site, is insufficient to trigger the breakdown of inositol lipids or subsequent mitogenic responses.
    • None of the early responses investigated, including receptor tyrosine kinase activation, are sufficient triggers for the mitogenic action of growth factors, suggesting a requirement for multiple coordinated signals.