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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
27
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pubmed:dateCreated |
2006-7-3
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pubmed:abstractText |
Wnt/beta-catenin signaling is essential to early development. Activation of Frizzled-1 by Wnts induces nuclear accumulation of beta-catenin and activation of Lef/Tcf-dependent gene expression. Casein kinase 2 has been shown to affect Wnt/beta-catenin signaling. How casein kinase 2 exerts an influence in Wnt signaling is not clear; casein kinase 2 has been reported to be constitutively active (i.e. not regulated). Herein we show to the contrary that casein kinase 2 activity is rapidly and transiently increased in response to Wnt3a stimulation and is essential for Wnt/beta-catenin signaling. Chemical inhibition of casein kinase 2 or suppression of its expression blocks Frizzled-1 activation of Lef/Tcf-sensitive gene expression. Treatment with pertussis toxin or knock down of Galpha(q) or Galpha(o) blocks Wnt stimulation of casein kinase 2 activation, as does suppression of the phosphoprotein Dishevelled, demonstrating that casein kinase 2 is downstream of heterotrimeric G proteins and Dishevelled. Expression of a constitutively active mutant of either Galpha(q) or Galpha(o) stimulates casein kinase 2 activation and Lef/Tcf-sensitive gene expression. Thus, casein kinase 2 is shown to be regulated by Wnt3a and essential to stimulation of the Frizzled-1/beta-catenin/Lef-Tcf pathway.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Signal Transducing,
http://linkedlifedata.com/resource/pubmed/chemical/Casein Kinase II,
http://linkedlifedata.com/resource/pubmed/chemical/Frizzled Receptors,
http://linkedlifedata.com/resource/pubmed/chemical/Fzd1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Pertussis Toxin,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, G-Protein-Coupled,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Neurotransmitter,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt3 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt3A Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt3a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/beta Catenin,
http://linkedlifedata.com/resource/pubmed/chemical/dishevelled proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
281
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
18394-400
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16672224-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:16672224-Animals,
pubmed-meshheading:16672224-Casein Kinase II,
pubmed-meshheading:16672224-Cell Line, Tumor,
pubmed-meshheading:16672224-Enzyme Activation,
pubmed-meshheading:16672224-Frizzled Receptors,
pubmed-meshheading:16672224-GTP-Binding Proteins,
pubmed-meshheading:16672224-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:16672224-Mice,
pubmed-meshheading:16672224-Pertussis Toxin,
pubmed-meshheading:16672224-Phosphoproteins,
pubmed-meshheading:16672224-Rats,
pubmed-meshheading:16672224-Receptors, G-Protein-Coupled,
pubmed-meshheading:16672224-Receptors, Neurotransmitter,
pubmed-meshheading:16672224-Signal Transduction,
pubmed-meshheading:16672224-Wnt Proteins,
pubmed-meshheading:16672224-Wnt3 Protein,
pubmed-meshheading:16672224-Wnt3A Protein,
pubmed-meshheading:16672224-beta Catenin
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pubmed:year |
2006
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pubmed:articleTitle |
Casein kinase 2 Is activated and essential for Wnt/beta-catenin signaling.
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pubmed:affiliation |
Department of Physiology and Biophysics, Diabetes and Metabolic Disease Research Center, School of Medicine, State University of New York at Stony Brook, New York 11794-8661, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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