Ontology highlight
ABSTRACT:
PROVIDER: PRJNA941433 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23728051_1.fastq.gz | Fastqsanger.gz | |||
| SRR23728051_2.fastq.gz | Fastqsanger.gz | |||
| SRR23728052_1.fastq.gz | Fastqsanger.gz | |||
| SRR23728052_2.fastq.gz | Fastqsanger.gz | |||
| SRR23728053_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:Transcriptome analysis of NesCre:Atg7 conditional knockout mice. Autophagy plays an important role in regulating protein metabolism and tissue homeostasis. Recent studies have reported that neural stem cell-specific Atg7 knockout mice (NesCre:Atg7f/f cKO mice) exhibit neonatal lethal due to severe neurodegeneration. However, the precise mechanisms of how neuronal fate is regulated by the autophagic pathway have not been elucidated. Here, we performed microarray experiments to analyze the changes in gene expression patterns in NesCre:Atg7 cKO mice. As a result, we could find a lot of candidate genes changed by Atg7 deficiency.
2022-10-07 | GSE214939 | GEO
Project description:Under defined differentiation conditions human embryonic stem cells (hESCs) can be directed toward a mesendodermal (ME) or neuroectoderm (NE) fate, the first decision during hESC differentiation. Coupled with G1 lengthening a divergent ciliation pattern emerged within the first 24 hours of induced lineage specification and these changes heralded a neuroectoderm decision before any neural precursor markers were expressed. By day 2, increased ciliation in NE precursors induced autophagy that resulted in the inactivation of Nrf2. Nrf2 binds directly to upstream regions of the OCT4 and NANOG genes to promote their expression and represses NE derivation. Nrf2 suppression was sufficient to rescue poorly neurogenic iPSC lines. Only after these events have been initiated do neural precursor markers get expressed at day 4. Thus we have identified a primary cilium-autophagy-Nrf2 (PAN) axis coupled to cell cycle progression that directs hESCs toward NE. Transcriptome analysis of hESC-derived neuroectoderm and mesendoderm cells
2016-03-24 | E-GEOD-69982 | biostudies-arrayexpress
Project description:To determine the role of autophagy in the maintenance of genome stability and nucleic acid metabolism, the chromatin-bound proteins in autophagy-deficient ATG7-/- HEK293 cells were compared with autophagy-proficient ATG7+/+ HEK293 cells by Data-independent acquisition mass spectrometry (DIA-MS).
2021-10-27 | PXD028956 | JPOST Repository
Project description:Cell competition regulates the fate decision of neural stem cells
| PRJNA925106 | ENA
Project description:Emergency myelopoiesis (EM) is critical for immune defense against pathogens, which requires rapid replenishing of mature myeloid cells. The EM process involves a rapid cell cycle switch from the quiescent hematopoietic stem cells (HSCs) to highly proliferative myeloid progenitors (MPs). How this cell cycle switch is regulated remains poorly understood. Here, we reveal that ATG7, a critical autophagy factor is essential for the rapid proliferation of MPs during human myelopoiesis. Peripheral blood (PB) mobilized HSPCs with ATG7 knock-down or HSPCs derived from ATG7-/- human embryonic stem cells (hESCs) exhibit severe defect in proliferation at MP stage during myeloid/granulocytes differentiation. ATG7 deficient MPs show substantially elevated P53 protein and up-regulation of P53 signaling pathway genes. Mechanistically, ATG7 dependent autophagy mediates P53 degradation in lysosome that allows normal proliferation of MPs. Together, we reveal an essential role of autophagy for P53 degradation in cell cycle switch during human myelopoiesis
2023-01-25 | GSE223219 | GEO
Project description:Autophagy genes play an important role in the T cell activation and proliferation. We examined the role of ATG7 during the process of CD8 T cell memory formation. In the absence of ATG7, antigen-specific CD8 T cells failed to survive past the contraction phase and failed to give rise to memory cells. We used microarrays to examine the global programme of gene expression underlying changes introduced in the absence of the ATG7 gene and identified distinct classes genes varied their expression during this time-point. Mouse LCMV-specific CD8 T cells were isolated at day 8 post LCMV infection for RNA extraction and hybridization on Affymetrix microarrays. We sought to compare the gene expression profiles in wild-type cells and cells lacking the ATG7 gene during the peak of their expansion.
2014-10-26 | E-GEOD-57047 | biostudies-arrayexpress
Project description:Formation of the complex vertebrate nervous system begins when pluripotent cells of the early embryo are directed to acquire a neural fate. Although cell intrinsic controls play an important role in this process, the molecular nature of this regulation is not well defined. Here we assessed the role for Geminin, a nuclear protein expressed in embryonic cells, in neural fate acquisition from mouse embryonic stem (ES) cells. While Geminin knockdown does not affect the ability of ES cells to maintain or exit pluripotency, we found that it significantly impairs their ability to acquire a neural fate. Conversely, Geminin overexpression promotes neural gene expression, even in the presence of growth factor signaling that antagonizes neural transcriptional responses. These data demonstrate that Geminin’s activity contributes to mammalian neural cell fate acquisition. We investigated the mechanistic basis of this phenomenon and found that Geminin maintains a hyperacetylated and open chromatin conformation at neural genes. Interestingly, recombinant Geminin protein also rapidly alters chromatin acetylation and accessibility even when Geminin is combined with nuclear extract and chromatin in vitro. These findings define a novel activity for Geminin in regulation of chromatin structure. Together, these data support a role for Geminin as a cell intrinsic regulator of neural fate acquisition that promotes expression of neural genes by regulating chromatin accessibility and histone acetylation. Mouse embryonic stem cells were differentiated for two days in N2B27 medium, with or without Doxycycline-inducible shRNAmir knockdown of Geminin and compared by microarray. Three independent experiments were conducted, using two different mouse embryonic stem cell lines for Doxycycline-inducible knockdown of Geminin. The two ES lines express unique shRNAmir sequences targeting Geminin (shRNAmir #9 and #11) to control for off-target effects.
2011-03-18 | E-GEOD-25737 | biostudies-arrayexpress
Project description:Under defined differentiation conditions human embryonic stem cells (hESCs) can be directed toward a mesendodermal (ME) or neuroectoderm (NE) fate, the first decision during hESC differentiation. Coupled with G1 lengthening a divergent ciliation pattern emerged within the first 24 hours of induced lineage specification and these changes heralded a neuroectoderm decision before any neural precursor markers were expressed. By day 2, increased ciliation in NE precursors induced autophagy that resulted in the inactivation of Nrf2. Nrf2 binds directly to upstream regions of the OCT4 and NANOG genes to promote their expression and represses NE derivation. Nrf2 suppression was sufficient to rescue poorly neurogenic iPSC lines. Only after these events have been initiated do neural precursor markers get expressed at day 4. Thus we have identified a primary cilium-autophagy-Nrf2 (PAN) axis coupled to cell cycle progression that directs hESCs toward NE.
2016-03-24 | GSE69982 | GEO
Project description:Hypoxia augments human embryonic stem cell self-renewal via hypoxia-inducible factor 2M-NM-1 (HIF2M-NM-1) activated OCT4 (POU5F1) transcription. Hypoxia also increases the efficiency of reprogramming differentiated cells to a pluripotent-like state. Combined, these findings suggest that low oxygen (O2) tension would impair the purposeful differentiation of pluripotent stem cells. Here, we show that low O2 tension and HIF activity instead promotes appropriate hESC differentiation. Through gain and loss of function studies, we implicate O2 tension as a modifier of a key cell fate decision, namely whether neural progenitors differentiate towards neurons or glia. Furthermore, our data show that even transient changes in O2 concentration can affect cell fate through HIF by regulating the activity of MYC, a regulator of LIN28/let-7 that is critical for fate decisions in the neural lineage. We also identify key small molecules that can take advantage of this pathway to quickly and efficiently promote the development of mature cell types. We used microarrays to detail the global gene expression of human neural progenitor cells (NPC) cultured in physiological (2%) oxygen tension. By comparing NPCs with activated Hypoxia inducible factor (HIF) activity (DFX treatment) and NPCs with diminished HIF activity (HIF1M-NM-2 knockdown), we identified genes that are important for NPC fate decision under physiological oxygen concentration. We also used microarrays to obtain a global gene expression profiling during embryoid bodies formation using ES cells with diminished HIF activity. In HIF activation experiments, two ES lines and one iPS line-derived NPC were used, with or without DFX treatment for 5 days. In HIF1M-NM-2 knockdown experiments, NPCs were derived from either shHIF1M-NM-2 or control ES lines. In embryoid body formation experiments, day0 (ES stage) and day6 EBs were generated from either shHIF1M-NM-2 or control ES lines in 2% oxygen.
2014-09-30 | E-GEOD-61842 | biostudies-arrayexpress