ampicillin sodium The following is the supplementary

The following is the supplementary data related to this article.
Authors\' contributions O.F. contributed to prepare experimental design, performed Ca measurements, helped with data and statistical analysis, immunocytochemistry, confocal imaging, and contributed in manuscript writing.
Disclosure of potential conflicts of interest
Acknowledgments This work was supported by the grants GACR 14-34077S, GACR P304/11/2373, GACR P304/12/G069 and GACR 10504P from the Grant Agency of the Czech Republic. This publication is partly a result of the “Advanced Bioimaging of Living Tissues” project, registration number #CZ.2.16/3.1.00/21527, which was financed from the budget of the European Regional Development Fund and public budgets of the Czech Republic through the Operational Programme Prague — Competitiveness. AV was supported by the Wellcome Trust, by the Alzheimer\'s research foundation (UK) and by the grant (agreement from August 27, 2013 no. 02.В.49.21.0003) between The Ministry of Education and Science of the Russian Federation and Lobachevsky State University of Nizhny Novgorod, by the grant of the Russian Scientific Foundation no.14-15-00633 and by the Ministry of Education of the Russian Federation, unique identity number RFMEFI57814X0079. Govindan Dayanithi belongs to the “Centre National de la Recherche Scientifique—The French Ministry of Research and Higher Education-Paris”, France. We thank David Arboleda and Lenka Baranovicova for their participation in preliminary experiments. We are grateful to Kip Allan Bauersfeld, IEM ASCR, for critical reading and helpful comments on the manuscript.
Introduction Human embryonic stem cells (hESCs) are undifferentiated cells derived from the inner cell mass of human blastocysts in the pre-implantation stage (Thomson et al., 1998; Trounson, 2006; Pera and Tam, 2010). The hESCs are characterized by the capacity to generate any cell type of all three germ layers (pluripotency) and to grow indefinitely in an undifferentiated state (self-renewal) (Pera and Tam, 2010; Young, 2011). They also have a uniquely short ampicillin sodium with an abbreviated G1 phase (Becker et al., 2006). Thanks to these remarkable properties, hESCs hold great promise for the development of tissue replacement therapy and provide a model system for the study of early embryonic development and lineage specification (Trounson, 2006). The molecular control of pluripotency and self-renewal in hESCs is attributed to an interactive network of transcription factors. OCT4, NANOG and SOX2 are uniquely expressed in pluripotent cells to orchestrate the transcriptional regulation of pluripotency by collaboratively activating the transcription of one another, constituting an autoregulatory circuitry (Boyer et al., 2005; Young, 2011). These three factors are responsible for driving the expression of genes essential to pluripotency and self-renewal (Boyer et al., 2005; Young, 2011). Regulation of this complex transcriptional network in stem cells deserves further analysis to fully understand the molecular basis of the initiation and maintenance of pluripotency/self-renewal and its pliability. FOX transcription factors display a vast diversity of biological functions, including cell proliferation, metabolism, apoptosis and differentiation (Myatt and Lam, 2007). Recent studies revealed the involvement of FOX factors in the regulation of self-renewal and pluripotency in embryonic stem (ES) cells. In particular, downregulation of FOXD3 in hESCs was shown to disrupt self-renewal and lead to cell differentiation towards the endoderm and mesoderm lineages (Arduini and Brivanlou, 2012), whereas FOXO1 was found to be essential for the regulation of hESC pluripotency via the direct transcriptional activation of OCT4 and SOX2 (Zhang et al., 2011). The proliferation-associated FOX factor FOXM1 plays important roles in the regulation of cell proliferation, metastasis, apoptosis and DNA damage repair (Wierstra, 2013b). Studies using various cell models have shown that FOXM1 is essential for proper cell cycle progression by regulating the G1/S and G2/M transitions and the execution of the mitotic program (Laoukili et al., 2005; Wang et al., 2005; Wonsey and Follettie, 2005; Laoukili et al., 2007). FOXM1 activates the expression of the cell cycle genes CCNB1, CCNB2, CDC25B and PLK1, which in turn leads to the activation of cyclin-dependent kinases (CDKs), thereby propelling cells through different cell cycle phases (Leung et al., 2001; Wang et al., 2002, 2005; Wonsey and Follettie, 2005).