@article {3132731,
	title = {The Genetic Program of Pancreatic \&beta;-Cell Replication In Vivo},
	journal = {Diabetes},
	volume = {65},
	number = {7},
	year = {2016},
	note = {1939-327xKlochendler, AgnesCaspi, InbalCorem, NoaMoran, MayaFriedlich, OrielElgavish, SharonaNevo, YuvalHelman, AharonGlaser, BenjaminEden, AmirItzkovitz, ShalevDor, YuvalJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov{\textquoteright}tDiabetes. 2016 Jul;65(7):2081-93. doi: 10.2337/db16-0003. Epub 2016 Mar 18.},
	month = {Jul},
	pages = {2081-93},
	edition = {2016/03/20},
	abstract = {The molecular program underlying infrequent replication of pancreatic β-cells remains largely inaccessible. Using transgenic mice expressing green fluorescent protein in cycling cells, we sorted live, replicating β-cells and determined their transcriptome. Replicating β-cells upregulate hundreds of proliferation-related genes, along with many novel putative cell cycle components. Strikingly, genes involved in β-cell functions, namely, glucose sensing and insulin secretion, were repressed. Further studies using single-molecule RNA in situ hybridization revealed that in fact, replicating β-cells double the amount of RNA for most genes, but this upregulation excludes genes involved in β-cell function. These data suggest that the quiescence-proliferation transition involves global amplification of gene expression, except for a subset of tissue-specific genes, which are "left behind" and whose relative mRNA amount decreases. Our work provides a unique resource for the study of replicating β-cells in vivo.},
	keywords = {*Transcriptome, Animals, Cell Division/*genetics, Cell Proliferation/*genetics, Flow Cytometry, Gene Expression Regulation, Insulin-Secreting Cells/cytology/*metabolism, Membrane Potential, Mitochondrial/physiology, Mice, Mice, Transgenic},
	isbn = {0012-1797 (Print)0012-1797},
	author = {Klochendler, A. and Caspi, I. and Corem, N. and Moran, M. and Friedlich, O. and Elgavish, S. and Nevo, Y. and Helman, A. and Glaser, B. and Eden, A. and Itzkovitz, S. and Dor, Y.}
}
