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  Truncation of the catalytic domain of the cylindromatosis tumor suppressor impairs lung maturation

Trompouki, E., Tsagaratou, A., Kosmidis, S. K., Dollé, P., Qian, J., Kontoyiannis, D. L., et al. (2009). Truncation of the catalytic domain of the cylindromatosis tumor suppressor impairs lung maturation. Neoplasia, 11, 469-476. doi:10.1593/neo.81424.

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Trompouki et al. 2009.pdf (Verlagsversion), 2MB
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 Urheber:
Trompouki, Eirini1, Autor           
Tsagaratou, Ageliki2, Autor
Kosmidis, Stylianos K2, Autor
Dollé, Pascal2, Autor
Qian, Jun2, Autor
Kontoyiannis, Dimitris L2, Autor
Cardoso, Wellington V2, Autor
Mosialos, George2, Autor
Affiliations:
1Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243641              
2External Organizations, ou_persistent22              

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 Zusammenfassung: Cyld encodes a 956-amino acid deubiquitinating enzyme (CYLD), which is a negative regulator of nuclear factor κB and mitogen-activated protein kinase pathways. Mutations that truncate and inactivate the carboxyl-terminal deubiquitinating domain of CYLD underlie the development of skin appendage tumors in humans, whereas down-regulation of Cyld expression has been associated with the development of various types of human malignancies including lung cancer. To establish an animal model of human CYLD inactivation and characterize the biological role of CYLD in vivo, we generated mice carrying a homozygous deletion of Cyld exon 9 (CyldΔ9/Δ9 mice) using a conditional approach. Deletion of exon 9 would cause a carboxyl-terminal truncation of CYLD and inactivation of its deubiquitinating activity. In accordance with previous studies, fibroblasts from CyldΔ9/Δ9 embryos had hyperactive nuclear factor κB and c-Jun kinase pathways compared with control fibroblasts. CyldΔ9/Δ9 newborn mice were smaller than wild-type littermates with a short and kinky tail and nomajor developmental defects. However, CyldΔ9/Δ9 mice died shortly after birth from apparent respiratory dysfunction. Histological examination of E18.5 CyldΔ9/Δ9 lungs demonstrated an immature phenotype characterized by hyperplasic mesenchyme but apparently normal epithelial, smooth muscle. and endothelial structures. Our study identifies an important role of CYLD in lung maturation, which may underlie the development of many cases of lung cancer.

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Sprache(n): eng - English
 Datum: 2009-05
 Publikationsstatus: Erschienen
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 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1593/neo.81424
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Titel: Neoplasia
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: New York, NY : Stockton Press
Seiten: - Band / Heft: 11 Artikelnummer: - Start- / Endseite: 469 - 476 Identifikator: ISSN: 1522-8002
CoNE: https://pure.mpg.de/cone/journals/resource/963017852322