scholarly journals Control of the Embryonic Stem Cell State

Cell ◽  
2011 ◽  
Vol 144 (6) ◽  
pp. 940-954 ◽  
Author(s):  
Richard A. Young
Keyword(s):  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Embryonic Stem ◽  
Cell State ◽  
Stem Cell State

Research and Findings

2008 ◽  
Vol 12 (06) ◽  
pp. 72-75
Keyword(s):  
Stem Cell ◽  
Brain Injury ◽  
Embryonic Stem Cell ◽  
Chikungunya Virus ◽  
Embryonic Stem ◽  
Cell State ◽  
Infant Brain ◽  
Stem Cell State ◽  
Shed Light ◽  
Surprising Discovery

Surprising Discovery on Biodiversity and Biogeography May Lead to Discovery of Viruses Scientists in Singapore Shed Light on the Molecular Alliance between Key Proteins that Play a Role in Sustaining the Embryonic Stem Cell State Infant Brain Injury can be Caused by Chikungunya Virus if Mother Acquires Infection Near Time of Delivery

scholarly journals Global DNA Hypomethylation Prevents Consolidation of Differentiation Programs and Allows Reversion to the Embryonic Stem Cell State

PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e52629 ◽  
Author(s):  
Christine S. Schmidt ◽  
Sebastian Bultmann ◽  
Daniela Meilinger ◽  
Benedikt Zacher ◽  
Achim Tresch ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Embryonic Stem ◽  
Dna Hypomethylation ◽  
Cell State ◽  
Stem Cell State

scholarly journals BMP4-directed trophoblast differentiation of human embryonic stem cells is mediated through a ΔNp63 + cytotrophoblast stem cell state

Development ◽  
2013 ◽  
Vol 140 (19) ◽  
pp. 3965-3976 ◽  
Author(s):  
Yingchun Li ◽  
Matteo Moretto-Zita ◽  
Francesca Soncin ◽  
Anna Wakeland ◽  
Lynlee Wolfe ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Trophoblast Differentiation ◽  
Cell State ◽  
Stem Cell State

scholarly journals The contribution of lincRNAs at the interface between cell cycle regulation and cell state maintenance

2019 ◽  
Author(s):  
Adriano Biasini ◽  
Adam Alexander Thil Smith ◽  
Baroj Abdulkarim ◽  
Jennifer Yihong Tan ◽  
Maria Ferreira da Silva ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cell ◽  
Embryonic Stem Cell ◽  
Cell Cycle Progression ◽  
Embryonic Stem ◽  
Differentially Expressed ◽  
Cell Cycle Regulators ◽  
Cycle Progression ◽  
Cell State ◽  
The Impact

ABSTRACTCell cycle progression requires dynamic and tightly-regulated transitions between well-defined cell cycle stages. These transitions are controlled by the interplay of established cell cycle regulators. Changes in the activity of these regulators are thought to underpin differences in cell cycle kinetics between distinct cell types. Here, we investigate whether cell type-specific long intergenic noncoding RNAs (lincRNAs) contribute to embryonic stem cell adaptations, which have been shown to be essential for the maintenance of embryonic stem cell state.We used single cell RNA-sequencing data of mouse embryonic stem cells (mESC) staged as G1, S, or G2/M to identify genes differentially expressed between these phases. We found differentially expressed lincRNAs to be enriched amongst cell cycle regulated genes. These cell cycle associated lincRNAs (CC-lincRNAs) are co-expressed with protein-coding genes with established roles in cell cycle progression. Interestingly, 70% of CC-lincRNAs are differentially expressed between G1 and S, suggesting they may contribute to the maintenance of the short G1 phase that characterizes the embryonic stem cell cycle. Consistent with this hypothesis, the promoters of CC-lincRNAs are enriched in pluripotency transcription factor binding sites, and their transcripts are frequently co-regulated with genes involved in the maintenance of pluripotency. We tested the impact of 2 CC-lincRNA candidates and show that modulation of their expression is associated with impaired cell cycle progression, further underlining the contribution of mESC-specific lincRNAs to cell cycle modulation in these cells.

scholarly journals Mapping the stem cell state: eight novel human embryonic stem and embryonal carcinoma cell antibodies

2011 ◽  
Vol 34 (4pt2) ◽  
pp. e175-e188 ◽  
Author(s):  
A. Wright ◽  
N. Andrews ◽  
K. Bardsley ◽  
J. E. Nielsen ◽  
K. Avery ◽  
...  
Keyword(s):  
Stem Cell ◽  
Embryonal Carcinoma ◽  
Carcinoma Cell ◽  
Embryonic Stem ◽  
Embryonal Carcinoma Cell ◽  
Cell State ◽  
Stem Cell State

scholarly journals Oct-3/4 Maintains the Proliferative Embryonic Stem Cell State via Specific Binding to a Variant Octamer Sequence in the Regulatory Region of the UTF1 Locus

2005 ◽  
Vol 25 (12) ◽  
pp. 5084-5094 ◽  
Author(s):  
Masazumi Nishimoto ◽  
Satoru Miyagi ◽  
Toshiyuki Yamagishi ◽  
Takehisa Sakaguchi ◽  
Hitoshi Niwa ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Molecular Mechanisms ◽  
Specific Binding ◽  
Es Cells ◽  
Regulatory Region ◽  
Embryonic Stem ◽  
Cell State ◽  
Teratoma Formation ◽  
Stem Cell State

ABSTRACT The POU transcription factor Oct-3/4 has been shown to be critical for maintaining embryonic stem (ES) cell character. However, the molecular mechanisms underlying its function remain elusive. We have previously shown that among the POU transcription factor family of proteins, Oct-3/4 alone is able to bind to the regulatory region of the UTF1 gene bearing a variant octamer sequence together with Sox-2. Here, we demonstrate using Oct-3/4-Oct-6 chimeras that there is a precise correlation between the ability of proteins to form a complex on the UTF1 enhancer with Sox-2 and the ability to maintain the stem cell state in ES cells. Different chimeric proteins show differential abilities to form a Sox-2-containing complex on the UTF1 regulatory region, with a decrease in efficiency of the complex formation accompanied by a decrease in the level of UTF1 expression and the rate of cell proliferation. Overexpression of UTF1 in these slow-growing cells was able to restore their proliferation rate to wild-type levels. Moreover, UTF1 was also observed to have an effect on teratoma formation. These results suggest a molecular pathway by which Oct-3/4 induces rapid proliferation and tumorigenic properties of ES cells through activation of the UTF1 gene.

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