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

Multiple signal transduction pathways mediate c-Jun protein phosphorylation

C C Franklin1, T Unlap, V Adler

  • 1Division of Hematology/Oncology, University of Alabama, Birmingham 35294.

Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|May 1, 1993
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

Measurement of [Formula: see text] production with additional jet activity, including [Formula: see text] quark jets, in the dilepton decay channel using pp collisions at [Formula: see text].

The European physical journal. C, Particles and fields·2017
Same author

Measurement of the [Formula: see text] production cross section in the all-jets final state in pp collisions at [Formula: see text][Formula: see text].

The European physical journal. C, Particles and fields·2016
Same author

Event generator tunes obtained from underlying event and multiparton scattering measurements.

The European physical journal. C, Particles and fields·2016
Same author

Measurement of differential cross sections for Higgs boson production in the diphoton decay channel in pp collisions at [Formula: see text].

The European physical journal. C, Particles and fields·2016
Same author

Measurement of the differential cross section for top quark pair production in pp collisions at [Formula: see text].

The European physical journal. C, Particles and fields·2015
Same author

Measurements of the [Formula: see text][Formula: see text] production cross sections in the [Formula: see text] channel in proton-proton collisions at [Formula: see text] and [Formula: see text] and combined constraints on triple gauge couplings.

The European physical journal. C, Particles and fields·2015

Mitogen-activated protein (MAP) kinase activation is not required for c-Jun phosphorylation in vivo. Pharmacological agents and dominant-negative RasAsn17 did not affect c-Jun phosphorylation, suggesting alternative signaling pathways are involved.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Biochemistry

Background:

  • c-Jun protein phosphorylation is crucial for its transcriptional activity.
  • Mitogen-activated protein (MAP) kinases, including pp42 MAP kinase, are known to phosphorylate c-Jun in vitro.
  • The in vivo role of pp42 MAP kinase in mediating c-Jun phosphorylation remains unclear.

Purpose of the Study:

  • To investigate the role of pp42 MAP kinase in c-Jun phosphorylation in U937 monocytic leukemia cells.
  • To determine if MAP kinase activation is necessary for in vivo c-Jun phosphorylation.
  • To explore the involvement of Ras signaling and isoprenylation in c-Jun phosphorylation.

Main Methods:

  • U937 cells were treated with phorbol 12-myristate 13-acetate (PMA), cycloheximide, AIF4, and okadaic acid.

Related Experiment Videos

  • Cotransfection with dominant-negative RasAsn17 and a truncated c-Jun construct (c-Jun234) was performed.
  • Inhibitors of isoprenylation, lovastatin and perillic acid, were used to assess Ha-Ras involvement.

    • Main Results:

    • PMA, cycloheximide, AIF4, and okadaic acid stimulated c-Jun phosphorylation.
    • Cycloheximide and okadaic acid did not affect pp42 MAP kinase phosphorylation.
    • Dominant-negative RasAsn17 did not inhibit PMA-induced c-Jun phosphorylation.
    • Isoprenylation inhibitors had no effect on PMA-induced c-Jun or pp42 MAP kinase phosphorylation.

    Conclusions:

    • MAP kinase activation is not essential for in vivo c-Jun phosphorylation in U937 cells.
    • The Ras signaling pathway and Ha-Ras isoprenylation do not appear to mediate PMA-induced c-Jun phosphorylation.
    • Alternative signaling pathways likely regulate c-Jun phosphorylation in response to PMA and other stimuli.