Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11-12
pubmed:dateCreated
2009-7-15
pubmed:abstractText
CK2 is a highly conserved tetrameric serine/ threonine kinase present in all eukaryotic organisms. It is constitutively active, and appears to be regulated by level of expression and activity, and subcellular localization. In turn, it has been postulated to control the function of many proteins through changes in phosphorylation that affect protein stability, protein-protein interactions, and subcellular localization. Through these mechanisms, CK2 regulates many fundamental cellular properties. An enzyme that carries out such a master regulatory function is likely to be important in organismic development and in cancer. We have shown that overexpression of CK2 catalytic subunits is capable of promoting tumorigenesis, and that loss of CK2 catalytic subunits in development can be lethal. Through studies in cells, mice, and frogs, we and others have identified the Wnt and NF-kappaB pathways as two key signal transduction pathways that are regulated by CK2 activity, in embryonic development and in cancer. These results suggest that inhibiting CK2 could be useful in treating cancer, but dangerous to developing organisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1420-9071
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
66
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1850-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Protein kinase CK2 in health and disease: CK2 and its role in Wnt and NF-kappaB signaling: linking development and cancer.
pubmed:affiliation
Section of Hematology-Oncology, Department of Medicine, Boston University School of Medicine and Boston Medical Center, 650 Albany Street, Boston, Massachusetts 02118, USA.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural