Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA130187 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:mouse embryonic fibroblasts, embryonic stem cells, and induced pluripotent stem cells were compared via metabolomic analysis
2018-08-02 | MSV000082680 | GNPS
Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.
2020-11-16 | GSE134301 | GEO
Project description:Lipid metabolism is recognized as a key process for stem cell maintenance and differentiation but genetic factors that instruct stem cell function by influencing lipid metabolism remain to be delineated. Here we identify Tnfaip2 as an inhibitor of reprogramming of mouse fibroblasts into induced pluripotent stem cells. Tnfaip2 knockout embryonic stem cells (ESCs) exhibit differentiation failure and knockdown of the planarian orthologue, Smed-exoc3, abrogates in vivo differentiation of somatic stem cells, tissue homeostasis, and regeneration. Tnfaip2 deficient ESCs fail to induce synthesis of cellular triacylglycerol (TAG) and lipid droplets (LD) coinciding with reduced expression of Vimentin (Vim) – a known inducer of LD formation. Knockdown of Vim and Tnfaip2 act epistatically in enhancing cellular reprogramming of mouse fibroblasts. Similarly, planarians devoid of Smed-exoc3 displayed acute loss of TAGs. Supplementation of palmitic acid (PA) and palmitoyl-L-carnitine (a mitochondrial carrier of PA) restores the differentiation capacity of Tnfaip2 deficient ESCs as well as stem cell differentiation and organ maintenance in Smed-exoc3-depleted planarians. Together, these results identify a novel pathway, which is essential for stem cell differentiation and organ maintenance by instructing lipid metabolism.
2020-11-16 | GSE148758 | GEO
Project description:Somatic cells can be reprogrammed to generate induced pluripotent stem cells (iPSCs) by overexpression of four transcription factors, Oct4, Klf4, Sox2, and c-Myc. Bmi1 is responsible for conversion of adult mouse astrocytes and fibroblasts into neural stem cell-like cells and conversion of fibroblasts into iPSCs under enforced expression of Oct4. Here, in the first step of generating iPSCs, stable intermediate cells were generated from mouse astrocytes by Bmi1 in the absence of other transcription factors. These cells [called induced epiblast stem cell (EpiSC)-like cells (iEpiSCLCs)] are similar to EpiSCs in terms of expression of specific markers, epigenetic state, and ability to differentiate into three germ layers. Treatment with MEK/ERK and GSK3 pathway inhibitors in the presence of leukemia inhibitory factor resulted in conversion of iEpiSCLCs into iPSCs that were similar to mouse embryonic stem cells (mESCs), suggesting that Bmi1 is sufficient to reprogram astrocytes to pluripotency. Next, Bmi1 function was replaced with Shh activators (oxysterol and purmorphamine), which demonstrated that specific combinations of small molecules alone can reprogram mouse fibroblasts into iPSCs. These iPSCs resembled mESCs in terms of global gene expression profile, epigenetic status, and developmental potential, demonstrating that combinations of small molecules can compensate for reprogramming factors and are sufficient to directly reprogram mouse somatic cells into iPSCs. 4 Affymetrix and 4 Agilent samples
2013-06-29 | E-GEOD-48411 | biostudies-arrayexpress
Project description:Somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by Oct4, Sox2, Klf4, plus c-Myc. Recently, Sox2 plus Oct4 were shown to reprogram fibroblasts and Oct4 alone to reprogram mouse and human neural stem cells (NSCs) into iPS cells. Here we report that Bmi1 leads to dedifferentiation of mouse fibroblasts into NSC-like cells and, in combination with Oct4, replaces Sox2, Klf4 and c-Myc during reprogramming fibroblasts to iPS cells. Furthermore, activation of sonic hedgehog signalling (by Shh, purmorphamine, or oxysterol) replaces the effects of Bmi1, and, in combination with Oct4, reprograms mouse embryonic and adult fibroblasts into iPS cells. One-and two-factor iPS cells are similar to mouse embryonic and adult fibroblasts into iPS cells in global gene expression profile, epigenetic status, in vitro and in bibo differentiation into all three ferm layers, as well as teratoma formation and germline transmission in vivo. These data support that fibroblasts can be reprogrammed into iPS cells by Oct4 alone. Total RNAs were isolated from indicated cells and labeled with Cy3. Hybridization was performed once for each sample.
2010-09-18 | E-GEOD-24208 | biostudies-arrayexpress
Project description:Pluripotent stem cells induced from adult neural stem cells by reprogramming with two factors
| PRJNA107393 | ENA
Project description:Transcriptional characterisation of the nuclear reprogramming process of fibroblasts, neutrophils and keratinocytes into induced pluripotent stem cells.
| PRJNA414347 | ENA
Project description:Somatic cells can be reprogrammed to generate induced pluripotent stem cells (iPSCs) by overexpression of four transcription factors, Oct4, Klf4, Sox2, and c-Myc. Bmi1 is responsible for conversion of adult mouse astrocytes and fibroblasts into neural stem cell-like cells and conversion of fibroblasts into iPSCs under enforced expression of Oct4. Here, in the first step of generating iPSCs, stable intermediate cells were generated from mouse astrocytes by Bmi1 in the absence of other transcription factors. These cells [called induced epiblast stem cell (EpiSC)-like cells (iEpiSCLCs)] are similar to EpiSCs in terms of expression of specific markers, epigenetic state, and ability to differentiate into three germ layers. Treatment with MEK/ERK and GSK3 pathway inhibitors in the presence of leukemia inhibitory factor resulted in conversion of iEpiSCLCs into iPSCs that were similar to mouse embryonic stem cells (mESCs), suggesting that Bmi1 is sufficient to reprogram astrocytes to pluripotency. Next, Bmi1 function was replaced with Shh activators (oxysterol and purmorphamine), which demonstrated that specific combinations of small molecules alone can reprogram mouse fibroblasts into iPSCs. These iPSCs resembled mESCs in terms of global gene expression profile, epigenetic status, and developmental potential, demonstrating that combinations of small molecules can compensate for reprogramming factors and are sufficient to directly reprogram mouse somatic cells into iPSCs.
2013-06-29 | GSE48411 | GEO
Project description:<p>The purpose of this study is to compare mutation load in induced pluripotent stem cells derived from skin fibroblasts.</p>
| phs001277 | dbGaP
Project description:Somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by Oct4, Sox2, Klf4, plus c-Myc. Recently, Sox2 plus Oct4 were shown to reprogram fibroblasts and Oct4 alone to reprogram mouse and human neural stem cells (NSCs) into iPS cells. Here we report that Bmi1 leads to dedifferentiation of mouse fibroblasts into NSC-like cells and, in combination with Oct4, replaces Sox2, Klf4 and c-Myc during reprogramming fibroblasts to iPS cells. Furthermore, activation of sonic hedgehog signalling (by Shh, purmorphamine, or oxysterol) replaces the effects of Bmi1, and, in combination with Oct4, reprograms mouse embryonic and adult fibroblasts into iPS cells. One-and two-factor iPS cells are similar to mouse embryonic and adult fibroblasts into iPS cells in global gene expression profile, epigenetic status, in vitro and in bibo differentiation into all three ferm layers, as well as teratoma formation and germline transmission in vivo. These data support that fibroblasts can be reprogrammed into iPS cells by Oct4 alone.
2010-09-18 | GSE24208 | GEO