Osteogenic Differentiation of Mouse Embryonic Stem Cells and Mouse Embryonic Fibroblasts in a Three-Dimensional Self-Assembling Peptide Scaffold

2006 ◽  
Vol 0 (0) ◽  
pp. 060913044658040 ◽  
Author(s):  
Elena Garreta ◽  
Elsa Genové ◽  
Salvador Borrós ◽  
Carlos E. Semino
2015 ◽  
Vol 29 (1) ◽  
pp. 34-43 ◽  
Author(s):  
Annette M. Krais ◽  
Karl-Rudolf Mühlbauer ◽  
Jill E. Kucab ◽  
Helena Chinbuah ◽  
Michael G. Cornelius ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0130332 ◽  
Author(s):  
Boxian Huang ◽  
Song Ning ◽  
Lili Zhuang ◽  
Chunyan Jiang ◽  
Yugui Cui ◽  
...  

2009 ◽  
Vol 30 (5) ◽  
pp. 1171-1181 ◽  
Author(s):  
Gordin Zupkovitz ◽  
Reinhard Grausenburger ◽  
Reinhard Brunmeir ◽  
Silvia Senese ◽  
Julia Tischler ◽  
...  

ABSTRACT Histone deacetylases (HDACs) are chromatin-modifying enzymes that are involved in the regulation of proliferation, differentiation and development. HDAC inhibitors induce cell cycle arrest, differentiation, or apoptosis in tumor cells and are therefore promising antitumor agents. Numerous genes were found to be deregulated upon HDAC inhibitor treatment; however, the relevant target enzymes are still unidentified. HDAC1 is required for mouse development and unrestricted proliferation of embryonic stem cells. We show here that HDAC1 reversibly regulates cellular proliferation and represses the cyclin-dependent kinase inhibitor p21 in embryonic stem cells. Disruption of the p21 gene rescues the proliferation phenotype of HDAC1−/− embryonic stem cells but not the embryonic lethality of HDAC1−/− mice. In the absence of HDAC1, mouse embryonic fibroblasts scarcely undergo spontaneous immortalization and display increased p21 expression. Chromatin immunoprecipitation assays demonstrate a direct regulation of the p21 gene by HDAC1 in mouse embryonic fibroblasts. Transformation with simian virus 40 large T antigen or ablation of p21 restores normal immortalization of primary HDAC1−/− fibroblasts. Our data demonstrate that repression of the p21 gene is crucial for HDAC1-mediated control of proliferation and immortalization. HDAC1 might therefore be one of the relevant targets for HDAC inhibitors as anticancer drugs.


2019 ◽  
Author(s):  
Botao Zhao ◽  
Chunsun Fan

AbstractMicroRNAs (miRNAs) are a class of non-coding small RNAs that function in almost every known cellular activity. MiRNAs play an important role in gene regulation that controls embryonic stem cell (ESC) pluripotency and differentiation, as well as induced pluripotent stem cell (iPSC) reprogramming. In this study, we identified nine novel miRNAs by mining the deep sequencing dataset from mouse embryonic stem cells, mouse embryonic fibroblasts (MEF) and three kinds of reprogrammed pluripotent cells. Most of them are non-conserved but species-specific and cell-specific miRNAs. Eight miRNAs are derived from gene introns, including a “mirtron” miRNA, miR-novel-41. We also showed that miR-novel-27 is a mouse-specific miRNA and the 5′ arm of its precursor hairpin, embedding the mature miR-novel-27, uniquely exists in mouse species but not in any other Placentalia animals. Notably, the 5′ arm of the pre-miR-novel-27 hairpin shows nearly perfect palindrome to the 3′ arm suggesting that it was generated by inverted duplication of the 3′ arm. By this mechanism, the pre-miR-novel-27 hairpin was de novo gained in the mouse genome. This is a new type of de novo miRNA emergence mechanism in animals, which we called “inverted local half hairpin duplication” here. In addition, very limited nucleotide mutants accumulated on the newly emerged 5′ arm since its birth suggesting an especially young evolutionary history of the miR-novel-27 gene.


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