Effect of ROS (H2O2) on undifferentiated NSC
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE232232 | GEO | 2023/05/11
REPOSITORIES: GEO
Similar Datasets
Project description:Realease of reactiv oxigen species, such as H2O2, has been observed during inflammatory processes but is also a physiological side product of metabolism. We have observed that differentiation of neural progenitor cells (NPC) is affected by H2O2 exposure. We here asses the transcriptional drivers of the phenotypical changes NPCs undergo during differentiation in response to H2O2.
2024-05-01 | GSE233181 | GEO
Project description:<p>Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer characterized by Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration. The scarcity of NPC genomic data hinders the understanding of NPC biology, disease progression, and rational therapy design. Here, we performed whole-exome sequencing (WES) on 111 micro-dissected EBV-positive NPCs, with 15 cases subjected to further whole-genome sequencing (WGS), to determine its mutational landscape. We identified enrichment for genomic aberrations of multiple negative regulators of the NF-kB pathway in a total of 41% of cases including CYLD, TRAF3, NFKBIA and NLRC5. Functional analysis confirmed novel inactivating CYLD mutations as drivers for NPC cell growth. The EBV oncoprotein latent member protein 1 (LMP1) functions to constitutively activate NF-kB signaling, and we observed mutual exclusivity among somatic NF-kB pathway aberrations and LMP1-overexpression, suggesting that NF-kB activation is selected for by both somatic and viral events during NPC pathogenesis.</p>
| phs001244 | dbGaP
Project description:While the core members of the Polycomb family of proteins (PRC2, PRC1, PR-DUB) are well-characterized, little is known about the specific composition of and protein-protein interactions within these complexes in different cell types. We performed quantitative interaction proteomics and cross-linking mass spectrometry on core Polycomb complex members to identify novel interactors, the relative abundance (stoichiometry) of subunits, and the architecture of these complexes in mouse embryonic stem cells (mESCs) and neural progenitor cells (NPCs). Differentiation to NPCs resulted in dramatic binding changes for several substoichiometric interactors of PRC2 and PRC1. ChIP-seq of core PRC2 and PRC1 subunits in mESCs and NPCs also identified dynamic changes in the genomic localization of these complexes. We observed a loss of PRC2 from most H3K27me3 sites during differentiation, whereas PRC1 is retained at these sites. Additionally, we found PRC1 at enhancers and promoters of active genes independent of PRC2 binding. Overexpression studies using NPC-specific PRC1 interactors demonstrated that the subunit switching observed during differentiation can change PRC1 target site binding. Altogether, these findings extend our understanding of Polycomb family composition, architecture, and genome-wide localization. ChIP-seq samples for Suz12, Ezh2, Ring1b, Pcgf2, and inputs from mouse embryonic stems cells (mES) and neural progenitor cells (NPC) as well as NPC histone H3K4me1 ChIP-seq.
2016-05-17 | E-GEOD-74330 | biostudies-arrayexpress
Project description:Nuclear pore complexes (NPCs) are established players in cell division and differentiation. However studies on the contribution of individual NPC subunits to these processes are still scarce. Here we have used mouse embryonic stem cells (mESCs) to characterize the role of structural components of the NPCs, focusing on the short arm of the Y-complex that comprises Nup85, Seh1 and Nup43. We show that Seh1 and Nup43, although dispensable at the pluripotent stage, are required for normal cell growth rates at that stage and for mESC viability upon differentiation. Lack of Seh1 or Nup43 in mESCs is associated with a mild reduction of NPC density that is also observed when Seh1 interaction with Nup85 is impaired. Nevertheless, mESC proliferation and differentiation are not altered in these ∆E2-GFP-Nup85 mutants, indicating that it is the integrity of the Y-complex, rather than the number of NPCs, that is critical to ensure these processes.
2021-05-20 | PXD022190 | Pride
Project description:Purpose: Determine the mechanism of H2O2-induced signaling in melanocytes. Method: Primary human epidermal melanocytes were treated with H2O2 (200 μM) and incubated for 24 h. Total RNA (500 ng) from melanocytes were extracted and subjected to library synthesis. Results: H2O2-treated melanocytes exhibited upregulation of cell death and type 1 interferon-related genes. Conclusion: H2O2-induced melanocyte signaling was well evaluated using RNA sequencing.
2023-07-28 | GSE216447 | GEO
Project description:Transcriptome profiling (RNA-seq) of Col seedlings growing in liquid MS culture and exposed to 1 mM H2O2 treatment
2018-12-21 | GSE117297 | GEO
Project description:The plant hormone abscisic acid (ABA) modulates a number of plant developmental processes and responses to stress. In planta, ABA has been shown to induce reactive oxygen species (ROS) production through the action of plasma membrane-associated NADPH oxidases. Although quantitative proteomics studies have been performed to identify ABA- or hydrogen peroxide (H2O2)-dependent proteins, little is known about the ABA- and H2O2-dependent microsomal proteome changes. Here, we examined the effect of 50 µM of either H2O2 or ABA on the Arabidopsis microsomal proteome using tandem mass spectrometry and identified 86 specifically H2O2-dependent and 52 specifically ABA-dependent proteins that are differentially expressed. We observed differential accumulation of proteins involved in the TCA cycle notably in response to H2O2. Of these, aconitase 3 responded to both H2O2 and ABA. Additionally, over 30 proteins linked to RNA biology responded significantly to both treatments. Gene ontology categories such as ‘response to stress’ and ‘transport’ were enriched, suggesting that H2O2 or ABA directly and/or indirectly cause complex and partly overlapping cellular responses.
2017-08-22 | PXD006513 | Pride
Project description:Here we present the study on ChIP-chip mapping of the genomic binding sites for Sty1, Atf1, and the Atf1's binding partner Pcr1; the genome-wide transcriptional profiling of the atf1 and pcr1 strains in response to H2O2; and the phenotypic assessment of ~90 Atf1/Pcr1-bound or unbound genes for growth fitness under H2O2 conditions. ChIP-chip analysis shows that Atf1 and Pcr1 binding sites are overlapped in the genome and constitutively present before H2O2 stress. On the other hand, Sty1 recruitment primarily occurs at the Atf1/Pcr1 binding sites and is induced by H2O2. We found that Atf1/Pcr1 is clearly responsible for the high-level transcriptional response to H2O2. Furthermore, phenotypic assessment indicates that among the H2O2-induced genes, Atf1/Pcr1-bound genes exhibit a higher likelihood of functional requirement for growth fitness under the stress condition than the Atf1/Pcr1-unbound genes do. Notably, we found that the Atf1/Pcr1-bound genes regardless of their responsiveness to H2O2 show a high probability of requirement for growth fitness. .
2010-07-19 | GSE13053 | GEO
Project description:Nuclear pore complexes (NPCs) discriminate non-specific macromolecules from importin and exportin receptors, collectively termed karyopherins (Kaps), that mediate nucleocytoplasmic transport. This selective barrier function is attributed to the behavior of intrinsically disordered phenylalanine-glycine nucleoporins (FG Nups) that guard the NPC channel. However, NPCs in vivo are typically enriched with different Kaps, and how they impact on the NPC barrier remains unknown. Here, we show that two major Kaps, importinβ1/karyopherinβ1 (Kapβ1) and exportin 1/chromosomal maintenance 1 (CRM1) are required to fortify NPC barrier function in vivo. Their enrichment at the NPC is sustained by promiscuous binding interactions with the FG Nups resulting in a compensatory mechanism that is constrained by their respective cellular abundances and different binding kinetics as evidenced for another Kap, Importin-5. Hence, Kapβ1 and CRM1 engage in a balancing act to reinforce NPC barrier function. Consequently, NPC malfunction and nucleocytoplasmic leakage result from poor Kap enrichment.
2022-01-26 | PXD028074 | Pride
Project description:Nuclear pore complexes (NPCs) are giant cylindrical structures embedded into the nuclear envelope and mediate nucleocytoplasmic exchange. NPC longevity has been linked to aging but since they appear to rarely turn over, the underlying mechanisms remain understudied. Here, we show that upon nitrogen starvation and genetic interference with NPC architecture, Nups are rapidly degraded in budding yeast. We demonstrate that NPC turnover involves 25 vacuolar proteases and the core autophagic machinery. Autophagic degradation is mediated by the cytoplasmically exposed Nup159 that serves as intrinsic cargo receptor and directly binds to the autophagic marker protein Atg8. The inducible manner of this mechanism might explain why NPCs are long-lived under specific conditions
2019-11-13 | PXD011571 | Pride