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  The ectopic expression of Pax4 in the mouse pancreas converts progenitor cells into α and subsequently β cells.

Collombat, P., Xu, X., Ravassard, P., Sosa-Pineda, B., Dussaud, S., Billestrup, N., et al. (2009). The ectopic expression of Pax4 in the mouse pancreas converts progenitor cells into α and subsequently β cells. Cell, 138(3), 449-462. doi:10.1016/j.cell.2009.05.035.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0012-D7BA-E Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0027-F26D-5
Genre: Journal Article

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 Creators:
Collombat, P.1, Author              
Xu, X., Author
Ravassard, P., Author
Sosa-Pineda, B.2, Author              
Dussaud, S., Author
Billestrup, N., Author
Madsen, O. D., Author
Serup, P., Author
Heimberg, H., Author
Mansouri, A.1, Author              
Affiliations:
1Research Group of Molecular Cell Differentiation, MPI for biophysical chemistry, Max Planck Society, ou_578588              
2Department of Molecular Cell Biology, MPI for biophysical chemistry, Max Planck Society, ou_578585              

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Free keywords: Cellbio; Devbio; Proteins
 Abstract: We have previously reported that the loss of Arx and/or Pax4 gene activity leads to a shift in the fate of the different endocrine cell subtypes in the mouse pancreas, without affecting the total endocrine cell numbers. Here, we conditionally and ectopically express Pax4 using different cell-specific promoters and demonstrate that Pax4 forces endocrine precursor cells, as well as mature α cells, to adopt a β cell destiny. This results in a glucagon deficiency that provokes a compensatory and continuous glucagon+ cell neogenesis requiring the re-expression of the proendocrine gene Ngn3. However, the newly formed α cells fail to correct the hypoglucagonemia since they subsequently acquire a β cell phenotype upon Pax4 ectopic expression. Notably, this cycle of neogenesis and redifferentiation caused by ectopic expression of Pax4 in α cells is capable of restoring a functional β cell mass and curing diabetes in animals that have been chemically depleted of β cells.

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Language(s): eng - English
 Dates: 2009-08-07
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Method: Peer
 Identifiers: eDoc: 434092
DOI: 10.1016/j.cell.2009.05.035
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Title: Cell
Source Genre: Journal
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Pages: - Volume / Issue: 138 (3) Sequence Number: - Start / End Page: 449 - 462 Identifier: -