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Expression analysis of proline rich 15 (Prr15) in mouse and human gastrointestinal tumors

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons50413

Luttges,  A.
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50203

Himmelbauer,  H.
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50161

Fundele,  R. H.
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Zitation

Meunier, D., Patra, K., Smits, R., Hagebarth, A., Luttges, A., Jaussi, R., et al. (2011). Expression analysis of proline rich 15 (Prr15) in mouse and human gastrointestinal tumors. Molecular Carcinogenesis, 50(1), 8-15. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21061267 http://onlinelibrary.wiley.com/store/10.1002/mc.20692/asset/20692_ftp.pdf?v=1&t=gyyj619y&s=b79e3aed8bbbed13a558b0d47296bd8295c6a8e7 http://onlinelibrary.wiley.com/store/10.1002/mc.20692/asset/20692_ftp.pdf?v=1&t=gzpagztu&s=921ecca16209c188fbd1a9f1203a8eb56293fb8d.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-78A0-8
Zusammenfassung
Proline rich 15 (Prr15), which encodes a protein of unknown function, is expressed almost exclusively in postmitotic cells both during fetal development and in adult tissues, such as the intestinal epithelium and the testis. To determine if this specific expression is lost in intestinal neoplasias, we examined Prr15 expression by in situ hybridization (ISH) on mouse intestinal tumors caused by different gene mutations, and on human colorectal cancer (CRC) samples. Prr15/PRR15 expression was consistently observed in mouse gastrointestinal (GI) tumors caused by mutations in the Apc gene, as well as in several advanced stage human CRCs. In contrast, no Prr15 expression was detected in intestinal tumors derived from mice carrying mutations in the Smad3, Smad4, or Cdkn1b genes. These findings, combined with the fact that a majority of sporadic human CRCs carry APC mutations, strongly suggest that the expression of Prr15/PRR15 in mouse and human GI tumors is linked, directly or indirectly, to the absence of the APC protein or, more generally, to the disruption of the Wnt signaling pathway.