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MEK5, a new target of the atypical protein kinase C isoforms in mitogenic signaling

M T Diaz-Meco1, J Moscat

  • 1Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Universidad Autónoma, 28049 Madrid, Spain.

Molecular and Cellular Biology
|February 7, 2001
PubMed

Insights

Atypical protein kinase Cs (aPKCs) interact with MEK5 in response to epidermal growth factor (EGF), activating the MEK5-ERK5 pathway. This interaction is crucial for cell proliferation signaling.

Area of Science:

  • Cellular signaling
  • Molecular biology
  • Biochemistry

Background:

  • The MEK5-ERK5 pathway is vital for mitogenic activation by epidermal growth factor (EGF).
  • Atypical protein kinase Cs (aPKCs) are essential for cell growth and proliferation and interact with p62 via an aPKC interaction domain.
  • MEK5 possesses a similar domain, suggesting a potential interaction with aPKCs.

Purpose of the Study:

  • To investigate the interaction between aPKCs and MEK5 in response to EGF.
  • To determine the role of this interaction in MEK5 activation and downstream signaling.
  • To elucidate the significance of MEK5 as a target in aPKC-mediated mitogenic signaling.

Main Methods:

  • Co-immunoprecipitation assays to detect protein interactions.
  • Western blotting to assess protein activation.
  • Reporter gene assays (e.g., Jun promoter activation) to evaluate pathway activity.

Main Results:

  • Demonstrated an EGF-inducible interaction between aPKCs and MEK5.
  • Showed this interaction is necessary and sufficient for MEK5 activation by EGF.
  • Confirmed that zetaPKC and lambda/iotaPKC activate the Jun promoter via the MEK5-ERK5 pathway's MEF2C element.

Conclusions:

  • MEK5 is a critical target of aPKCs in the context of EGF-induced mitogenic signaling.
  • The aPKC-MEK5 interaction is a key regulatory step in the MEK5-ERK5 pathway.
  • This finding provides new insights into the mechanisms controlling cell proliferation.

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