文献求助 FEBS Lett

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http://www.ncbi.nlm.nih.gov/pubmed/222656913 P  q4 |9 Z% Z( R+ h( Y4 M
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FEBS Lett. 2012 Feb 17;586(4):422-7. doi: 10.1016/j.febslet.2012.01.015. Epub 2012 Jan 17.: i  [# \& g$ H' k
MiR-18a regulates expression of the pancreatic transcription factor Ptf1a in pancreatic progenitor and acinar cells.
  k4 C, R" l- J$ DYang Y, Ding L, An Y, Zhang ZW, Lang Y, Tai S, Guo F, Teng CB.5 ]: t4 |8 A/ |! ?7 R& m, ^( J
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Laboratory of Animal Development Biology, College of Life Science, Northeast Forestry University, Harbin, China.
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$ R/ s' K3 D& W+ C, s! ]The basic helix-loop-helix (bHLH) transcription factor Ptf1a plays stage-specific roles in the developing pancreas. During early pancreatic development, low levels of Ptf1a preferentially promote the differentiation of pancreatic progenitor cells into endocrine cells, whereas high levels of Ptf1a shift pancreatic progenitors towards an exocrine cell fate. In adults, Ptf1a is essential for the production of exocrine enzymes by pancreatic acinar cells. In this paper, we show that Ptf1a expression is repressed by miR-18a in pancreatic progenitors and acinar cells via its binding to the 3'UTR of Ptf1a mRNA. Furthermore, overexpression of miR-18a exerts little effect on pancreatic progenitors and acinar cells. These results indicate that miR-18a plays a fine-tuning role in regulating pancreatic progenitors and exocrine cells through the repression of Ptf1a expression.

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