CK2: A global regulator of cell death

Janeen H. Trembley, Fatima Qaiser, Betsy T. Kren, Khalil Ahmed

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations

Abstract

Protein kinase CK2 has emerged as a major signal involved in diverse cellular functions of health and disease. The nature of its broad of range of functions is underscored by the large number of potential substrates of CK2 present in various locales in the cell. CK2 has gained much attention for its role in cancer biology, which is attributed to its functions both in cell growth and proliferation as well as in the regulation of cell death. Indeed, it appears that CK2 impact on cell death may be one of its most important functions, especially in the context of cancer biology where both cell proliferation and cell death are dysregulated and elevated CK2 in cancer would have an effect on both of these activities. Just as CK2 has been proposed to have a global role in cell growth-related activities, it appears that it may have an analogous global role in the suppression of apoptosis when it is elevated and induce cell death when it is downregulated. In this review, we have highlighted the current status of CK2 involvement in the processes related to cell death with a focus on apoptosis. It is proposed that a newly identified mechanism of CK2 regulation of cell death relates to its impact on early intracellular dynamics of Ca2+ signaling which profoundly alter mitochondrial function and lead to cell death.

Original languageEnglish (US)
Title of host publicationProtein Kinase CK2 Cellular Function in Normal and Disease States
PublisherSpringer International Publishing
Pages159-181
Number of pages23
ISBN (Electronic)9783319145440
ISBN (Print)9783319145433
DOIs
StatePublished - Jan 1 2015

Keywords

  • Apoptosis
  • Bcl-2
  • Bcl-xL
  • Ca
  • Cell death
  • Endoplasmic reticulum
  • IAPs
  • Mitochondria
  • Mitochondrial membrane potential
  • Mitochondrial permeability transition
  • Protein kinase Ck2
  • Ros
  • Stress
  • Suppression of apoptosis
  • Survivin

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