pubmed-article:16672224 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16672224 | lifeskim:mentions | umls-concept:C0105770 | lld:lifeskim |
pubmed-article:16672224 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:16672224 | lifeskim:mentions | umls-concept:C0108555 | lld:lifeskim |
pubmed-article:16672224 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:16672224 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:16672224 | lifeskim:mentions | umls-concept:C0205224 | lld:lifeskim |
pubmed-article:16672224 | pubmed:issue | 27 | lld:pubmed |
pubmed-article:16672224 | pubmed:dateCreated | 2006-7-3 | lld:pubmed |
pubmed-article:16672224 | 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. | lld:pubmed |
pubmed-article:16672224 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:language | eng | lld:pubmed |
pubmed-article:16672224 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16672224 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16672224 | pubmed:month | Jul | lld:pubmed |
pubmed-article:16672224 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:16672224 | pubmed:author | pubmed-author:WangHsien-yuH... | lld:pubmed |
pubmed-article:16672224 | pubmed:author | pubmed-author:GaoYuanY | lld:pubmed |
pubmed-article:16672224 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16672224 | pubmed:day | 7 | lld:pubmed |
pubmed-article:16672224 | pubmed:volume | 281 | lld:pubmed |
pubmed-article:16672224 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16672224 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16672224 | pubmed:pagination | 18394-400 | lld:pubmed |
pubmed-article:16672224 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:16672224 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:16672224 | pubmed:articleTitle | Casein kinase 2 Is activated and essential for Wnt/beta-catenin signaling. | lld:pubmed |
pubmed-article:16672224 | 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. | lld:pubmed |
pubmed-article:16672224 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16672224 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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