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Identification of Novel CK2 Kinase Substrates Using a Versatile Biochemical Approach
11:11

Identification of Novel CK2 Kinase Substrates Using a Versatile Biochemical Approach

Published on: February 21, 2019

7.8K

Knockdown of protein kinase CK2 blocked gene expression mediated by brain-derived neurotrophic factor-induced serum

Shu-Ping Yang1, Chi-Yi Lo1, Hui-Min Tseng1

  • 1Institute of Neurosciences, National Chengchi University, Taipei, Taiwan.

The Chinese Journal of Physiology
|June 28, 2019
PubMed

Insights

Brain-derived neurotrophic factor (BDNF) activates protein kinase CK2, which mediates its neuroprotective effects by enhancing SRE-mediated transcription and Mcl-1 gene expression, thereby inhibiting apoptosis.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Brain-derived neurotrophic factor (BDNF) is crucial for neuronal survival, activating antiapoptotic pathways.
  • While BDNF signaling involves kinases like ERK1/2 and PI3K, its activation of protein kinase CK2 and subsequent effects on serum response element (SRE)-mediated transcription are not fully understood.
  • CK2 inhibition induces apoptosis, highlighting its role in cell survival.

Purpose of the Study:

  • To elucidate the role of protein kinase CK2 in BDNF-mediated neuroprotection.
  • To investigate the functional relevance of CK2-dependent phosphorylation of serum response factor (SRF) in BDNF signaling.
  • To determine the impact of CK2 activity on SRE-mediated transcription and antiapoptotic gene expression under neurotoxic conditions.

Main Methods:

  • Utilized PC12 cells treated with BDNF.
  • Employed CK2α small interfering RNA (siRNA) to inhibit CK2 activity.
  • Assessed SRE-mediated transcription, SRF phosphorylation, Mcl-1 gene expression, and cell viability under rotenone-induced cytotoxicity.

Main Results:

  • BDNF treatment increased SRE-mediated transcription, CK2 activity, and SRF phosphorylation in PC12 cells.
  • CK2α siRNA transfection abrogated BDNF's effects on SRE transcription, SRF phosphorylation, and Mcl-1 expression.
  • CK2 inhibition reduced BDNF's antiapoptotic effects, including protection against rotenone-induced cell death.

Conclusions:

  • Protein kinase CK2 is essential for BDNF-mediated neuroprotection.
  • CK2 mediates BDNF's effects on SRE-driven transcription, SRF phosphorylation, and Mcl-1 gene expression.
  • Targeting CK2 may offer therapeutic strategies for neurodegenerative diseases characterized by apoptosis.
Keywords:
AntiapoptosisMcl-1brain-derived neurotrophic factorprotein kinase CK2serum response element-mediated transcription

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