Similar Datasets
Project description:Chromatin organization must be maintained during cell proliferation to preserve cellular identity and genome integrity. However, DNA replication results in transient displacement of DNA bound proteins, and it is unclear how they regain access to newly replicated DNA. Using quantitative MS-based proteomics coupled to Nascent Chromatin Capture, we provide time resolved binding kinetics for thousands of proteins behind replisomes within euchromatin and heterochromatin in human cells. This shows that most proteins regain access within the first 15 minutes after the passage of the fork. In contrast, 30% of the identified proteins do not, and this delay cannot be inferred from their known function, physicochemical properties, or nuclear abundance. Instead, differential chromatin organization affect their reassociation. We provide evidence that DNA replication not only disrupts but also promotes recruitment of transcription factors and chromatin remodellers, providing a significant advance in understanding how DNA replication could contribute to programmed changes of cell memory.We include here a reference to link the data with our manuscript:Tables SUPP1 and SUPP2:NCC data: PT7988 (Bio-rep1), PT8242 (Bio-rep2), PT8243 (Bio-rep3). 1-24 (24 high-pH RPLC fractions from TMT labeled peptides)Nuclear fraction data: PT7988 (Bio-rep1), PT8242 (Bio-rep2), PT8243 (Bio-rep3). 25-48 (24 high-pH RPLC fractions from TMT labeled peptides)Tables SUPP3-5:NCC data: PT9825 (Bio-rep1), PT9825 (Bio-rep2), PT9825 (Bio-rep3). (11-34, 35-58, 59-82) (24 high-pH RPLC fractions from TMT labeled peptides)Nuclear fraction data: PT9825 (Bio-rep1), PT9825 (Bio-rep2), PT9825 (Bio-rep3). (83-106, 107-130, 131-154). (24 high-pH RPLC fractions from TMT labeled peptides)
2023-02-02 | PXD035489 | Pride
Project description:Expression data from BIO-treated human epidermal keratinocytes
| PRJNA138575 | ENA
Project description:Many small molecular compounds reported were involved in improving reprogramming efficiency during inducing pluripotent stem cells (iPSC) or maintain a blastocyst-like state in embryonic stem cells (ESC), including BIO, CHIR99021 (CHIR), and vitamin C et al. However, the knowledge about these small molecules regulating miRNAs in ESC was limited. To understand the role of miRNAs during small molecules induced ESC maintenance and gain an insight how these small molecules regulates miRNAs expression; we performed small RNA sequencing using Illumina HiSeq 2000 under the compounds treatment. Retinoic acid (RA), a stimulus molecule for cellular differentiation, is set as negative control. The data show the miRNAs regulated by BIO, CHIR, vitamin C and RA.
2016-12-01 | GSE54145 | GEO
Project description:Development of radiation medical countermeasures under the U.S. Food and Drug Administration Animal Rule requires the capability to translate an effective animal to human drug dose. One method of human dose translation is using a biomarker and determining drug doses that modulate the biomarker to the desired level. BIO 300 Oral Powder (BIO 300) is a prophylactic radiation medical countermeasure that is currently being developed following the Animal Rule. The present study aimed to identify biomarkers that can be used for human dose conversion by conducting transcriptomics of whole blood collected from BIO 300-treated CD2F1 mice in the presence and absence of total-body irradiation (TBI). Mice were treated with vehicle or 50, 100 or 200 mg/kg BIO 300, twice daily, for 6 days. Whole blood samples were collected 24 and 48 h after the last dose of the drug. Animals were also treated with vehicle or 200 mg/kg BIO 300 for 6 days prior to 9.2 Gy TBI 24 h after the last dose, with blood collection 24 h after irradiation. RNA sequencing demonstrated 100 – 200 mg/kg doses caused significantly more differential gene expression at 48 h post-drug dose compared to 50 mg/kg. Pathway analysis of the transcriptome profile from vehicle-treated/radiation-exposed mice revealed that many inflammatory signaling pathways were activated in these animals. Signaling pathways enriched in BIO 300-treated/TBI mice were involved in cellular stress and immune response and were predicted to be inhibited. We also identified pathways that were in inverse states (activation/inhibition) in vehicle and BIO 300-treated mice with TBI. There were two pathways specifically activated in vehicle-treated animals with TBI and inhibited in BIO 300-treated animals (with or without TBI), pathogen-induced cytokine storm signaling and S100 family signaling. In comparison to previously published human data, pulmonary fibrosis idiopathic signaling and wound healing signaling were enriched in healthy volunteers treated with BIO 300 and BIO 300-treated mice with TBI. In all, four signaling pathways were identified that were activated in vehicle-treated animals exposed to total body radiation but inhibited in irradiated animals or healthy humans treated with BIO 300. These pathways should be explored to identify potential biomarkers of BIO 300 that can be used for human dose translation.
2024-08-14 | GSE268247 | GEO
Project description:The data contains 135 raw data produced from mass spectrometry (QExactive HF, Thermo Scientific), the bio-samples were sperm cells collected at nine sub-stages of mouse spermatogenesis. Proteins from each bio-samples were extracted and digested to peptides, then separated to five fractions and triplicated analyzed by mass spectrometry.
2020-12-01 | PXD017284 | Pride