Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA133203 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE23968: Large intergenic non-coding RNAs as novel modulators of reprogramming: ESCs, fibroblast, and fibroblast-derived iPSC (gene expression) GSE23970: Large intergenic non-coding RNAs as novel modulators of reprogramming: human embryonic stem cells, CD34+ cells, and CD34+ derived induced pluripotent stem cells (LincRNA expression) GSE23973: Large intergenic non-coding RNAs as novel modulators of reprogramming: siRNA (gene expression) GSE24181: Large intergenic non-coding RNAs as novel modulators of reprogramming: human embryonic stem cells, fibroblasts, and fibroblast-derived induced pluripotent stem cells (LincRNA expression) Refer to individual Series
2010-11-10 | E-GEOD-24182 | biostudies-arrayexpress
Project description:Large intergenic non-coding RNAs as novel modulators of reprogramming: human embryonic stem cells, fibroblasts, and fibroblast-derived induced pluripotent stem cells (LincRNA expression)
| PRJNA133715 | ENA
Project description:We recently showed that some human induced pluripotent stem cell (iPSC) clones were defective in neural differentiation and were marked with the activation of long term repeats (LTRs) of human endogenous retroviruses (HERVs). We herein demonstrated that these LTRs were transiently overexpressed during the generation of iPSCs and contributed to reprogramming. When the generation of iPSCs was completed, LTRs were re-suppressed to levels similar to those in human ES cells. However, differentiation-defective iPSC clones maintained high LTR expression levels, which indicated that these clones failed to complete reprogramming. lincRNA-RoR, a long intergenic non-coding RNA (lincRNA) that was previously shown to support the induction and maintenance of pluripotency, was detected among the LTR-driven transcripts. Short hairpin RNAs against the conserved sequence in LTRs or lincRNA-RoR markedly reduced the efficiency of iPSC generation. Reprogramming factors including OCT3/4, SOX2, and KLF4 bound to most LTRs. The expression of KLF4 was low in normal iPSC clones, but remained high in differentiation-defective clones. The forced expression of KLF4 in human embryonic stem cells led to the activation of LTRs and defects in neural differentiation. These results demonstrated that the transient overexpression of KLF4/LTR/lincRNA-RoR played crucial roles in reprogramming toward pluripotency in humans, whereas a failure in its re-silence resulted in differentiation defects. Four human induced pluripotent stem cell lines were subcloned into 55 separate lines. Bisulfite converted genomic DNA lysates from fibroblast, induced pluripotent stem cell, intermediate reprogrammed cell and embryonic stem cell lines were hybridized to Illumina HumanMethylation450 BeadChip.
2014-08-04 | E-GEOD-54848 | biostudies-arrayexpress
Project description:LincRNA expression profiles of human embryonic stem cells, CD34+ cells, and CD34+ derived induced pluripotent stem cells
2010-11-10 | GSE23970 | GEO
Project description:LincRNA expression profiles of human embryonic stem cells, CD34+ cells, and CD34+ derived induced pluripotent stem cells Total RNA was extracted from human ESCs, CD34+ cells, and CD34+ derived iPSC lines, then hybridized to Nimblegen tiling array GPL8792; Human lincRNA 391k Tiling Array V2
2010-11-10 | E-GEOD-23970 | biostudies-arrayexpress
Project description:We recently showed that some human induced pluripotent stem cell (iPSC) clones were defective in neural differentiation and were marked with the activation of long term repeats (LTRs) of human endogenous retroviruses (HERVs). We herein demonstrated that these LTRs were transiently overexpressed during the generation of iPSCs and contributed to reprogramming. When the generation of iPSCs was completed, LTRs were re-suppressed to levels similar to those in human ES cells. However, differentiation-defective iPSC clones maintained high LTR expression levels, which indicated that these clones failed to complete reprogramming. lincRNA-RoR, a long intergenic non-coding RNA (lincRNA) that was previously shown to support the induction and maintenance of pluripotency, was detected among the LTR-driven transcripts. Short hairpin RNAs against the conserved sequence in LTRs or lincRNA-RoR markedly reduced the efficiency of iPSC generation. Reprogramming factors including OCT3/4, SOX2, and KLF4 bound to most LTRs. The expression of KLF4 was low in normal iPSC clones, but remained high in differentiation-defective clones. The forced expression of KLF4 in human embryonic stem cells led to the activation of LTRs and defects in neural differentiation. These results demonstrated that the transient overexpression of KLF4/LTR/lincRNA-RoR played crucial roles in reprogramming toward pluripotency in humans, whereas a failure in its re-silence resulted in differentiation defects. OCT3/4, SOX2 and KLF4 bindings in human dermal fibroblast and iPSC
2014-08-04 | E-GEOD-56567 | biostudies-arrayexpress
Project description:Through expression profiling and functional screening we have identified the large intergenic non-coding RNA p21 (lincRNA-p21) as a barrier for reprogramming. LincRNA-p21 is induced by p53 but contrary to its role in the DNA damage response it does not promote apoptosis or cell senescence in reprogramming. Instead, lincRNA-p21 associates with the H3K9 methyltransferase Setdb1 and the maintenance DNA methyltransferase Dnmt1 in separate complexes that are facilitated by the RNA binding protein hnRNP-K.
2014-12-29 | GSE57967 | GEO
Project description:We recently showed that some human induced pluripotent stem cell (iPSC) clones were defective in neural differentiation and were marked with the activation of long term repeats (LTRs) of human endogenous retroviruses (HERVs). We herein demonstrated that these LTRs were transiently overexpressed during the generation of iPSCs and contributed to reprogramming. When the generation of iPSCs was completed, LTRs were re-suppressed to levels similar to those in human ES cells. However, differentiation-defective iPSC clones maintained high LTR expression levels, which indicated that these clones failed to complete reprogramming. lincRNA-RoR, a long intergenic non-coding RNA (lincRNA) that was previously shown to support the induction and maintenance of pluripotency, was detected among the LTR-driven transcripts. Short hairpin RNAs against the conserved sequence in LTRs or lincRNA-RoR markedly reduced the efficiency of iPSC generation. Reprogramming factors including OCT3/4, SOX2, and KLF4 bound to most LTRs. The expression of KLF4 was low in normal iPSC clones, but remained high in differentiation-defective clones. The forced expression of KLF4 in human embryonic stem cells led to the activation of LTRs and defects in neural differentiation. These results demonstrated that the transient overexpression of KLF4/LTR/lincRNA-RoR played crucial roles in reprogramming toward pluripotency in humans, whereas a failure in its re-silence resulted in differentiation defects. Nine samples were prepared as intermediate state of cells between human dermal fibroblast and iPSC. One iPSC clone and 4 subclones derived from defective iPSC exhibit normal differentiation ability.
2014-08-04 | E-GEOD-56568 | biostudies-arrayexpress
Project description:Large intergenic non-coding RNAs as novel modulators of reprogramming: siRNA (gene expression)
| PRJNA133191 | ENA