Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cdk1 activity levels drive periodic transcription independently of cell cycle progression

ABSTRACT: Cdk1 activity levels drive periodic transcription independently of cell cycle progression

PROVIDER: PRJNA289441 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Cdk1 activity levels drive periodic transcription independently of cell cycle progression

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-04-01 | E-GEOD-70717 | biostudies-arrayexpress

Cdk1 activity levels drive periodic transcription independently of cell cycle progression

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-04-01 | GSE70717 | GEO

Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

Project description:We addressed the role of cell cycle regulator CDK1 during differentiation by either inhibiting its activity with the specific inhibitor RO3306 (10µM) or by knocking its expression down using specific shRNAs, during mesendoderm differentiation. Human pluripotent stem cells (H9 cells) were synchronized in their cell cycle and then induced to differentiate into mesendoderm for 24h. shRNAs against CDK1 were induced 4 days before starting the differentiation. The CDK1 inhibitor was added to the medium 8h after the induction of differentiation. At the end of the experiment, the cells were harvested and processed for total RNA extraction. RNA-IP was carried out using RiboCluster Profiler RIP-Assay Kit (MBL) following the manufacture’s recommendations.

2021-05-31 | GSE130827 | GEO

Small RNA-seq analysis shows reduced tRNA levels in cdk1-as1 mutants

Project description:Purpose: Determine whether Cdk1 only regulates a specific subset of tDNAs, or whether Cdk1 has a more global impact on tDNA expression; Method: We study the expression of tRNA genes in WT cells and cdk1-as1 mutants during S phase by small-RNAseq; Result: We found that expression of at least 77% of all tDNAs is significantly downregulated in S-phase in the cdk1-as1 mutant compared with the WT strain; Conclussions: Cdk1 promotes transcription of the majority of tRNA genes during the cell cycle.

2018-09-10 | GSE116224 | GEO

Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

Project description:Effect of Cell cycle regulator CDK1 on Cell Differentiation (RNA-IP CDK1 inh KD)

| PRJNA541529 | ENA

An extensive program of periodic alternative splicing linked to cell cycle progression

Project description:Progression through the mitotic cell cycle requires periodic regulation of gene function at the levels of transcription, translation, protein-protein interactions, post-translational modification and degradation. However, the role of alternative splicing (AS) in the temporal control of cell cycle is not well understood. By sequencing the human transcriptome through two continuous cell cycles, we identify ~1,300 genes with cell cycle-dependent AS changes. These genes are significantly enriched in functions linked to cell cycle control, yet they do not significantly overlap genes subject to periodic changes in steady-state transcript levels. Many of the periodically spliced genes are controlled by the SR protein kinase CLK1, whose level undergoes cell cycle-dependent fluctuations via an auto-inhibitory circuit. Disruption of CLK1 causes pleiotropic cell cycle defects and loss of proliferation, whereas CLK1 over-expression is associated with various cancers. These results thus reveal a large program of CLK1-regulated periodic AS intimately associated with cell cycle control.

2016-05-19 | GSE81485 | GEO

Dihydroartemisinin suppresses the tumorigenesis and cycle progression of colorectal cancer by targeting CDK1/CCNB1/PLK1 signaling

Project description:Dihydroartemisinin (DHA), a well-known antimalarial drug, has been widely investigated as its anti-tumor effects in multiple malignancies. However, its effects and regulatory mechanisms in colorectal cancer (CRC) are still unproved. In this study, the in vitro experiments including CCK8, EdU, Transwell, flow cytometry analyses and in vivo tumorigenesis model were conducted to assess the effects of DHA on the bio-behaviors of CRC cells. Additionally, RNA-seq combined with gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses was used to obtain the targets of DHA and these were verified by molecular docking, qRT-PCR and Western blot. As a result, we found that DHA significantly suppressed the proliferation, DNA synthesis and invasive capabilities, and induced cell apoptosis and cell cycle arrest in HCT116, DLD1 and RKO cells in vitro and in vivo. Further analyses indicated that the targets of DHA were predominantly enriched in cell cycle-associated pathways, including CDK1, CCNB1 and PLK1, and DHA could bind with CDK1/CCNB1 complex and inhibit the activation of CDK1/CCNB1/PLK1 signaling. Moreover, cucurbitacin E, a specific inhibitor of CDK1/CCNB1 axis enhanced the inhibitory effects of DHA on DNA synthesis and colony formation in HCT116 and DLD1 cells. In short, DHA could suppress the tumorigenesis and cycle progression of CRC cells by targeting CDK1/CCNB1/PLK1 signaling.

2021-10-04 | GSE185141 | GEO

Cdk1 controls global epigenetic landscape in embryonic stem cells

Project description:In this study, we found that in ES cells the majority of Cdk1 substrates are localized on chromatin. Cdk1 phosphorylates a large number of proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. High levels of Cdk1 in ES cells phosphorylate and partially inactivate Dot1l, the histone H3 lysine 79 methyltransferase responsible for placing activating H3K79 marks on gene bodies. Decrease of Cdk1 activity during ES cell differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ES cells.

2020-04-04 | GSE134645 | GEO

Arid1a regulates cell cycle exit of transit-amplifying cells through inhibiting the Aurka-Cdk1 axis in mouse incisor

Project description:We show that Arid1a maintains tissue homeostasis through promoting cell cycle exit and differentiation of TACs by inhibiting the Aurka-Cdk1 axis.

2021-04-04 | GSE166800 | GEO

RNA-seq of cardiac-specific Cdk1 knockout mice at 4 days after experimental myocardial infarction

Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte (CM) proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.

2024-10-31 | E-MTAB-14505 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data