Kaiso-Deficient Mice Show Resistance to Intestinal Cancer. Prokhortchouk, A., Sansom, O., Selfridge, J., Caballero, I. M., Salozhin, S., Aithozhina, D., Cerchietti, L., Meng, F. G., Augenlicht, L. H., Mariadason, J. M., Hendrich, B., Melnick, A., Prokhortchouk, E., Clarke, A., & Bird, A. Molecular and Cellular Biology, 26(1):199–208, January, 2006.
Paper doi abstract bibtex Kaiso is a BTB domain protein that associates with the signaling molecule p120-catenin and binds to the methylated sequence mCGmCG or the nonmethylated sequence CTGCNA to modulate transcription. In Xenopus laevis, xKaiso deficiency leads to embryonic death accompanied by premature gene activation in blastulae and upregulation of the xWnt11 gene. Kaiso has also been proposed to play an essential role in mammalian synapse-specific transcription. We disrupted the Kaiso gene in mice to assess its role in mammalian development. Kaiso-null mice were viable and fertile, with no detectable abnormalities of development or gene expression. However, when crossed with tumor-susceptible ApcMin/+ mice, Kaiso-null mice showed a delayed onset of intestinal tumorigenesis. Kaiso was found to be upregulated in murine intestinal tumors and is expressed in human colon cancers. Our data suggest that Kaiso plays a role in intestinal cancer and may therefore represent a potential target for therapeutic intervention.
@article{prokhortchouk_kaiso-deficient_2006,
title = {Kaiso-{Deficient} {Mice} {Show} {Resistance} to {Intestinal} {Cancer}},
volume = {26},
issn = {0270-7306},
url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1317619/},
doi = {10.1128/MCB.26.1.199-208.2006},
abstract = {Kaiso is a BTB domain protein that associates with the signaling molecule p120-catenin and binds to the methylated sequence mCGmCG or the nonmethylated sequence CTGCNA to modulate transcription. In Xenopus laevis, xKaiso deficiency leads to embryonic death accompanied by premature gene activation in blastulae and upregulation of the xWnt11 gene. Kaiso has also been proposed to play an essential role in mammalian synapse-specific transcription. We disrupted the Kaiso gene in mice to assess its role in mammalian development. Kaiso-null mice were viable and fertile, with no detectable abnormalities of development or gene expression. However, when crossed with tumor-susceptible ApcMin/+ mice, Kaiso-null mice showed a delayed onset of intestinal tumorigenesis. Kaiso was found to be upregulated in murine intestinal tumors and is expressed in human colon cancers. Our data suggest that Kaiso plays a role in intestinal cancer and may therefore represent a potential target for therapeutic intervention.},
number = {1},
urldate = {2020-12-01},
journal = {Molecular and Cellular Biology},
author = {Prokhortchouk, Anna and Sansom, Owen and Selfridge, Jim and Caballero, Isabel M. and Salozhin, Sergey and Aithozhina, Dana and Cerchietti, Leandro and Meng, Fan Guo and Augenlicht, Leonard H. and Mariadason, John M. and Hendrich, Brian and Melnick, Ari and Prokhortchouk, Egor and Clarke, Alan and Bird, Adrian},
month = jan,
year = {2006},
pmid = {16354691},
pmcid = {PMC1317619},
pages = {199--208},
}
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In Xenopus laevis, xKaiso deficiency leads to embryonic death accompanied by premature gene activation in blastulae and upregulation of the xWnt11 gene. Kaiso has also been proposed to play an essential role in mammalian synapse-specific transcription. We disrupted the Kaiso gene in mice to assess its role in mammalian development. Kaiso-null mice were viable and fertile, with no detectable abnormalities of development or gene expression. However, when crossed with tumor-susceptible ApcMin/+ mice, Kaiso-null mice showed a delayed onset of intestinal tumorigenesis. Kaiso was found to be upregulated in murine intestinal tumors and is expressed in human colon cancers. 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In Xenopus laevis, xKaiso deficiency leads to embryonic death accompanied by premature gene activation in blastulae and upregulation of the xWnt11 gene. Kaiso has also been proposed to play an essential role in mammalian synapse-specific transcription. We disrupted the Kaiso gene in mice to assess its role in mammalian development. Kaiso-null mice were viable and fertile, with no detectable abnormalities of development or gene expression. However, when crossed with tumor-susceptible ApcMin/+ mice, Kaiso-null mice showed a delayed onset of intestinal tumorigenesis. Kaiso was found to be upregulated in murine intestinal tumors and is expressed in human colon cancers. 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