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Related Concept Videos

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MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Calmodulin-dependent Signaling

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Related Experiment Video

Updated: Jun 21, 2026

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
08:00

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

Published on: July 10, 2019

Reactive oxygen species decrease cAMP response element binding protein expression in cardiomyocytes via a protein

Nazira Ozgen1, Jianfen Guo, Zoya Gertsberg

  • 1Center for Molecular Therapeutics, Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Molecular Pharmacology
|July 22, 2009
PubMed
Summary

Oxidative stress from hydrogen peroxide (H2O2) activates signaling pathways that phosphorylate CREB but decrease its protein levels in cardiomyocytes. This PKD1-dependent decrease in CREB abundance may contribute to heart failure pathogenesis.

Related Experiment Videos

Last Updated: Jun 21, 2026

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
08:00

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

Published on: July 10, 2019

Area of Science:

  • Cardiovascular Biology
  • Cell Signaling
  • Oxidative Stress

Background:

  • Reactive oxygen species (ROS) significantly impact cellular processes, including growth and apoptosis.
  • Signaling pathways regulating cellular growth and apoptosis are influenced by ROS.

Purpose of the Study:

  • To investigate the effects of long-term, low-concentration hydrogen peroxide (H2O2) treatment on signaling pathways in cardiomyocytes.
  • To elucidate the mechanism by which H2O2 affects cAMP response element-binding protein (CREB) phosphorylation and abundance.

Main Methods:

  • Long-term H2O2 treatment of cardiomyocytes.
  • Analysis of signaling pathway activation (ERK, S6K, PKD).
  • Assessment of CREB phosphorylation and protein abundance.
  • Mutagenesis studies and proteasome inhibition.
  • Use of kinase inhibitors and siRNA for PKD1.

Main Results:

  • H2O2 activated ERK, S6K, and PKD pathways, increasing CREB phosphorylation at Ser(133).
  • Despite increased phosphorylation, CREB protein abundance decreased, with no change in reporter gene activity.
  • H2O2-induced CREB reduction was proteasome-dependent and mediated by PKD1, independent of CREB phosphorylation.

Conclusions:

  • Oxidative stress via H2O2 leads to a decrease in CREB protein levels through a PKD1-dependent, proteasome-mediated pathway.
  • This mechanism, independent of CREB phosphorylation, may influence cardiac growth and apoptosis.
  • The findings suggest a role for this pathway in the pathogenesis of heart failure.