We are analyzing https://link.springer.com/article/10.1007/s11010-005-3078-0.

Title:
CK2 as a positive regulator of Wnt signalling and tumourigenesis | Molecular and Cellular Biochemistry
Description:
CK2 is upregulated in rapidly dividing cells including most human tumours. Transgenic overexpression of CK2 in lymphoid or mammary lineages predisposes to transformation. Multiple signalling and oncogene pathways could be regulated by CK2 in this process. Our studies suggest that phosphorylation of critical oncogenes by CK2, as well as by other serine-threonine kinases, regulates their stability via susceptibility to the proteasomal degradation system. β-catenin is a transcriptional co-factor in the Wnt signalling pathway that is regulated in this fashion. Inactivating mutations in the adenomatosis polyposis coli (APC) gene, which encodes a carrier protein for β-catenin, or stabilizing mutations in β-catenin itself, frequently occur in human tumours. CK2 and the monomeric serine-threonine kinase GSK3 have opposing actions on β-catenin: GSK-3 phosphorylation of the N-terminus of β-catenin promotes degradation; while phosphorylation by CK2 in the armadillo repeat protein interaction domain protects it. β-catenin is overexpressed in mammary tumours occurring in mice transgenic for CK2 or a dominant negative form of GSK3, and also in mammary tumours arising following treatment with the environmental carcinogen DMBA. Experiments are underway to determine whether expression of both CK2 and kinase inactive GSK3 further accelerates tumorigenesis. Inhibitors of GSK3 under development for treatment of diabetes could promote tumours, while CK2 inhibitors should be useful agents for treatment of cancer.
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Keywords {🔍}

kinase, google, scholar, pubmed, seldin, article, protein, wnt, signalling, mammary, david, landesmanbollag, βcatenin, gsk, cancer, privacy, cookies, content, tumours, oncogene, gene, access, cell, publish, search, dominguez, phosphorylation, signaling, glycogen, synthase, nature, usa, analysis, data, information, log, journal, research, regulator, farago, cells, transgenic, pathway, mutations, mice, treatment, discover, varmus, activation, casein,

Topics {✒️}

glycogen synthase kinase-3 breast cancer cells serine-threonine kinases month download article/chapter wnt signalling pathway protein kinase ck2 voltage-gated potassium channel kinase inactive gsk3 beta-catenin-tcf signaling β-catenin promotes degradation wnt signalling nuclear factor-kappab armadillo repeat region privacy choices/manage cookies regulatory beta subunit sirna selection server cancer cell biology full article pdf putative mammary oncogene cellular biochemistry aims multiple signalling related subjects mammary epithelial cells check access instant access proteasomal degradation system wingless signaling acts targeting ck2-driven mammary lineages predisposes establish cell fate cell-autonomous defect european economic area adenomatosis polyposis coli environmental carcinogen dmba saint-jeannet jp small interfering rnas early embryonic lethality mammary gland tumorigenesis conditions privacy policy mammary tumours occurring mammary tumours arising esther landesman-bollag wnt signaling dominant negative form dorsoventral axis formation carrier protein accepting optional cookies song dh article molecular journal finder publish

Schema {🗺️}

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         headline:CK2 as a positive regulator of Wnt signalling and tumourigenesis
         description:CK2 is upregulated in rapidly dividing cells including most human tumours. Transgenic overexpression of CK2 in lymphoid or mammary lineages predisposes to transformation. Multiple signalling and oncogene pathways could be regulated by CK2 in this process. Our studies suggest that phosphorylation of critical oncogenes by CK2, as well as by other serine-threonine kinases, regulates their stability via susceptibility to the proteasomal degradation system. β-catenin is a transcriptional co-factor in the Wnt signalling pathway that is regulated in this fashion. Inactivating mutations in the adenomatosis polyposis coli (APC) gene, which encodes a carrier protein for β-catenin, or stabilizing mutations in β-catenin itself, frequently occur in human tumours. CK2 and the monomeric serine-threonine kinase GSK3 have opposing actions on β-catenin: GSK-3 phosphorylation of the N-terminus of β-catenin promotes degradation; while phosphorylation by CK2 in the armadillo repeat protein interaction domain protects it. β-catenin is overexpressed in mammary tumours occurring in mice transgenic for CK2 or a dominant negative form of GSK3, and also in mammary tumours arising following treatment with the environmental carcinogen DMBA. Experiments are underway to determine whether expression of both CK2 and kinase inactive GSK3 further accelerates tumorigenesis. Inhibitors of GSK3 under development for treatment of diabetes could promote tumours, while CK2 inhibitors should be useful agents for treatment of cancer.
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            casein kinase II
            glycogen synthase kinase 3
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            protein kinase CK2
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            Cancer Research
            Medical Biochemistry
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      headline:CK2 as a positive regulator of Wnt signalling and tumourigenesis
      description:CK2 is upregulated in rapidly dividing cells including most human tumours. Transgenic overexpression of CK2 in lymphoid or mammary lineages predisposes to transformation. Multiple signalling and oncogene pathways could be regulated by CK2 in this process. Our studies suggest that phosphorylation of critical oncogenes by CK2, as well as by other serine-threonine kinases, regulates their stability via susceptibility to the proteasomal degradation system. β-catenin is a transcriptional co-factor in the Wnt signalling pathway that is regulated in this fashion. Inactivating mutations in the adenomatosis polyposis coli (APC) gene, which encodes a carrier protein for β-catenin, or stabilizing mutations in β-catenin itself, frequently occur in human tumours. CK2 and the monomeric serine-threonine kinase GSK3 have opposing actions on β-catenin: GSK-3 phosphorylation of the N-terminus of β-catenin promotes degradation; while phosphorylation by CK2 in the armadillo repeat protein interaction domain protects it. β-catenin is overexpressed in mammary tumours occurring in mice transgenic for CK2 or a dominant negative form of GSK3, and also in mammary tumours arising following treatment with the environmental carcinogen DMBA. Experiments are underway to determine whether expression of both CK2 and kinase inactive GSK3 further accelerates tumorigenesis. Inhibitors of GSK3 under development for treatment of diabetes could promote tumours, while CK2 inhibitors should be useful agents for treatment of cancer.
      datePublished:
      dateModified:
      pageStart:63
      pageEnd:67
      sameAs:https://doi.org/10.1007/s11010-005-3078-0
      keywords:
         breast cancer
         casein kinase II
         glycogen synthase kinase 3
         GSK3
         protein kinase CK2
         Wnt signalling
         Biochemistry
         general
         Cardiology
         Cancer Research
         Medical Biochemistry
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