Emergency spatiotemporal shift

The response of protein kinase D to stress signals in the cardiovascular system

Brent M. Wood, Julie B C Bossuyt

Research output: Contribution to journalReview article

2 Citations (Scopus)

Abstract

Protein Kinase D isoforms (PKD 1-3) are key mediators of neurohormonal, oxidative, and metabolic stress signals. PKDs impact a wide variety of signaling pathways and cellular functions including actin dynamics, vesicle trafficking, cell motility, survival, contractility, energy substrate utilization, and gene transcription. PKD activity is also increasingly linked to cancer, immune regulation, pain modulation, memory, angiogenesis, and cardiovascular disease. This increasing complexity and diversity of PKD function, highlights the importance of tight spatiotemporal control of the kinase via protein-protein interactions, post-translational modifications or targeting via scaffolding proteins. In this review, we focus on the spatiotemporal regulation and effects of PKD signaling in response to neurohormonal, oxidant and metabolic signals that have implications for myocardial disease. Precise targeting of these mechanisms will be crucial in the design of PKD-based therapeutic strategies.

Original languageEnglish (US)
Article number9
JournalFrontiers in Pharmacology
Volume8
Issue numberJAN
DOIs
StatePublished - Jan 24 2017

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Physiological Stress
Post Translational Protein Processing
Cardiovascular System
Cardiomyopathies
Oxidants
Protein Kinases
Cell Movement
Actins
Cell Survival
Protein Isoforms
Oxidative Stress
Emergencies
Cardiovascular Diseases
Pain
Genes
Neoplasms
Proteins
Therapeutics
protein kinase D

Keywords

  • Cardiovascular disease
  • GPCR
  • Heart failure
  • Metabolism
  • Oxidative stress
  • Protein kinase D

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Emergency spatiotemporal shift : The response of protein kinase D to stress signals in the cardiovascular system. / Wood, Brent M.; Bossuyt, Julie B C.

In: Frontiers in Pharmacology, Vol. 8, No. JAN, 9, 24.01.2017.

Research output: Contribution to journalReview article

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