Conditional inactivation of the Men1 gene leads to pancreatic and pituitary tumorigenesis but does not affect normal development of these tissues

Biondi, C. A., Gartside, M. G., Waring, P., Loffler, K. A., Stark, M. S., Magnuson, M. A., Kay, G. F. and Hayward, N. K. (2004) Conditional inactivation of the Men1 gene leads to pancreatic and pituitary tumorigenesis but does not affect normal development of these tissues. Molecular And Cellular Biology, 24 8: 3125-3131. doi:10.1128/MCB.24.8.3125-3131.2004

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Author Biondi, C. A.
Gartside, M. G.
Waring, P.
Loffler, K. A.
Stark, M. S.
Magnuson, M. A.
Kay, G. F.
Hayward, N. K.
Title Conditional inactivation of the Men1 gene leads to pancreatic and pituitary tumorigenesis but does not affect normal development of these tissues
Journal name Molecular And Cellular Biology   Check publisher's open access policy
ISSN 0270-7306
1098-5549
Publication date 2004-01-01
Year available 2004
Sub-type Article (original research)
DOI 10.1128/MCB.24.8.3125-3131.2004
Open Access Status File (Publisher version)
Volume 24
Issue 8
Start page 3125
End page 3131
Total pages 7
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Abstract Mutations of the MEN1 gene, encoding the tumor suppressor menin, predispose individuals to the cancer syndrome multiple endocrine neoplasia type 1, characterized by the development of tumors of the endocrine pancreas and anterior pituitary and parathyroid glands. We have targeted the murine Men1 gene by using Cre recombinase-loxP technology to develop both total and tissue-specific knockouts of the gene. Conditional homozygous inactivation of the Men1 gene in the pituitary gland and endocrine pancreas bypasses the embryonic lethality associated with a constitutional Men1(-/-) genotype and leads to beta-cell hyperplasia in less than 4 months and insulinomas and prolactinomas starting at 9 months. The pituitary gland and pancreas develop normally in the conditional absence of menin, but loss of this transcriptional cofactor is sufficient to cause beta-cell hyperplasia in some islets; however, such loss is not sufficient to initiate pituitary gland tumorigenesis, suggesting that additional genetic events are necessary for the latter.
Keyword Biochemistry & Molecular Biology
Cell Biology
Multiple Endocrine Neoplasia
Tumor-suppressor Gene
Cre-mediated Recombination
Expression
Protein
Type-1
Q-Index Code C1
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: 2005 Higher Education Research Data Collection
School of Medicine Publications
 
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Created: Wed, 15 Aug 2007, 13:05:35 EST