Differential targeting of protein kinase CK2 to the nuclear matrix upon transient overexpression of its subunits

Shihui Yu, Alan T. Davis, Chuanhai Guo, Jeffrey E. Green, Khalil Ahmed

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19 Scopus citations


Modest dysregulation of CK2 has been shown to enhance the oncogenic potential in transgenic models of cancer. Since nuclear matrix serves as an anchor for CK2 and plays a key role in growth-related activities, we examined the effects of CK2 overexpression on its signaling to the nuclear matrix. Expression plasmids pCl-CK2α, pCl-CK2β, and the bicistronic pCl-CK2αβ containing full length CDNAs encoding the various subunits were employed to transiently transfect two cell lines, BPH-1 and COS-1. Cytosol from transfected BPH-1 cells containing α or β or α + β or αβ showed a modest increase in CK2 activity by 26%, 1%, 20%, and 17%, respectively, over that in the controls transfected with pCl vector. However, the corresponding increase in CK2 activity in the NM fraction was 156%, 8%, 147%, and 152%, respectively. Immunoblot analysis of the CK2 in the NM accorded with these data. Similar results were obtained with COS-1 cells or other expression vectors. The results suggest that moderate overexpression of CK2 in the cells evokes a differential several-fold enhancement in NM associated CK2 relative to that in the cytosol. This process may have a bearing on the functional signaling of this kinase in relation to its possible role in oncogenesis.

Original languageEnglish (US)
Pages (from-to)127-134
Number of pages8
JournalJournal of Cellular Biochemistry
Issue number1
StatePublished - Jul 1 1999


  • Nuclear matrix
  • Overexpression
  • Prostate
  • Protein kinase CK2
  • Translocation


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