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

Citation
Sh. Yu et al., Differential targeting of protein kinase CK2 to the nuclear matrix upon transient overexpression of its subunits, J CELL BIOC, 74(1), 1999, pp. 127-134
Citations number
29
Categorie Soggetti
Cell & Developmental Biology
Journal title
JOURNAL OF CELLULAR BIOCHEMISTRY
ISSN journal
07302312 → ACNP
Volume
74
Issue
1
Year of publication
1999
Pages
127 - 134
Database
ISI
SICI code
0730-2312(19990701)74:1<127:DTOPKC>2.0.ZU;2-E
Abstract
Modest dysregulation of CK2 has been shown to enhance the oncogenic potenti al 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. Expr ession plasmids pCI-CK2 alpha, pCI-CK2 beta, and the bicistronic pCI-CK2 al pha beta containing full length cDNAs encoding the various subunits were em ployed to transiently transfect two cell lines, BPH-1 and COS-1. Cytosol fr om transfected BPH-1 cells containing alpha or beta or alpha + beta or alph a beta showed a modest increase in CK2 activity by 26%, 1%, 20%, and 17%, r espectively, 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 a ccorded 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 as sociated CK2 relative to that in the cytosol. This process may have a beari ng on the functional signaling of this kinase in relation to its possible r ole in oncogenesis. J. Cell. Biochem. 74:12 7-134, 1999. (C) 1999 Wiley-Lis s, Inc.