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Effect of L-Proline on mouse embryonic stem cells (ESCs)

ABSTRACT: We found that the non-essential amino acid L-Proline (L-Pro) acts as a signaling molecule that promotes the conversion of embryonic stem cells (ESCs) into mesenchymal-like, spindle-shaped, highly motile, invasive pluripotent stem cells. This embryonic stem cell-to-mesenchymal-like transition (esMT) is accompanied by a genome-wide remodeling of the transcriptome We used microarrays to elucidate whether a diverse transcriptional program is the basis of the morphological and motility differences between ESCs and L- Proline treated ESCs (PiCs) Total RNA was extracted from Control (ESCs) and L-Proline treated mouse embryonic stem cells (PiCs) and hybridized on Affimetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Gabriella Minchiotti

PROVIDER: E-GEOD-50603 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Effect of L-Proline on mouse embryonic stem cells (ESCs)

Project description:We found that the non-essential amino acid L-proline (L-Pro) acts as a signaling molecule that promotes the conversion of embryonic stem cells (ESCs) into mesenchymal-like, spindle-shaped, highly motile, invasive pluripotent stem cells.This embryonic stem cell-to-mesenchymal-like transition (esMT) is accompanied by a genome-wide remodeling of the H3K9me3 and H3K36me3 histone marks. Examination of 2 different histone modifications in untreated ESCs and L-Pro treated ESCs

2013-08-31 | E-GEOD-50477 | biostudies-arrayexpress

Effect of L-Proline on mouse embryonic stem cells (ESCs)

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REX1 is the critical target of RNF12 in imprinted X chromosome inactivation in mice.

Project description:In mice, imprinted X-chromosome inactivation (iXCI) of the paternal X in the pre-implantation embryo and extra-embryonic tissues is followed by X-reactivation in the epiblast precursors of the inner cell mass (ICM) of the blastocyst, to facilitate initiation of random XCI (rXCI) in all embryonic tissues. RNF12 is an E3 ubiquitin-ligase that plays a key role in XCI. RNF12 targets pluripotency protein REX1 for degradation to initiate rXCI in embryonic stem cells (ESCs) and loss of the maternal copy of Rnf12 leads to embryonic lethality due to iXCI failure. Here, we show that loss of Rex1 rescues the rXCI phenotype observed in Rnf12-/- ESCs, and that REX1 is the prime target of RNF12 in ESCs. Genetic ablation of Rex1 in Rnf12-/- mice rescues the Rnf12-/- iXCI phenotype, and results in viable and fertile Rnf12-/-:Rex1-/- female mice displaying normal iXCI and rXCI. Our results show that REX1 is the critical target of RNF12 in XCI.

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Effect of L-Proline on mouse embryonic stem cells (ESCs)

2013-08-31 | GSE50477 | GEO

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Expression data from control (F/F) and Snai1 knockout (KO) embryoid body (EB) and teratoma ™

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2013-12-10 | E-GEOD-53106 | biostudies-arrayexpress

A mass spectrometry survey of chromatin-associated proteins in pluripotency and early lineage commitment

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2019-07-04 | PXD011782 | Pride

Transcription profiling of mouse Pooh cell line (POU5F1/Oct-4/3 overexpressing human)

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