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Stimulation of p300-mediated transcription by the kinase MEKK1

R H See1, D Calvo, Y Shi

  • 1Department of Pathology, Harvard Medical School and Department of Radiation Biology, Harvard School of Public Health, Boston, Massachusetts 02115.

The Journal of Biological Chemistry
|March 30, 2001
PubMed

Insights

Mitogen-activated/extracellular response kinase kinase 1 (MEKK1) enhances p300-mediated transcription and apoptosis. MEKK1 may directly phosphorylate p300, regulating its activity and role in cell death.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • p300 and CREB-binding protein (CBP) are transcriptional coactivators with histone acetyltransferase activity.
  • p300/CBP are crucial for development, cell fate, and differentiation across various organisms.
  • Phosphorylation of p300/CBP suggests a regulatory role in their activity.

Purpose of the Study:

  • To investigate the role of mitogen-activated/extracellular response kinase kinase 1 (MEKK1) in regulating p300 activity.
  • To determine if MEKK1 affects p300-mediated transcription and apoptosis.

Main Methods:

  • Investigated MEKK1's effect on p300-mediated transcription.
  • Identified domains within p300 responsive to MEKK1.
  • Assessed the involvement of JNK and potential direct phosphorylation by MEKK1.
  • Examined p300's role in MEKK1-induced apoptosis.

Main Results:

  • MEKK1 enhances p300-mediated transcription.
  • Specific domains of p300 respond to MEKK1-induced activation.
  • MEKK1-induced transcriptional activation of p300 does not require JNK.
  • MEKK1 likely phosphorylates p300 directly or via non-JNK kinases.
  • p300 is essential for MEKK1 to induce apoptosis.

Conclusions:

  • MEKK1 is a regulator of p300's transactivation potential.
  • p300 plays a significant role in MEKK1-induced apoptosis.
  • Phosphorylation by MEKK1 is a key mechanism for p300 regulation.

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