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Gene expression changes after depletion of Cyclin F and atypical E2Fs in HeLa cells.

ABSTRACT: Gene expression changes after depletion of Cyclin F and atypical E2Fs in HeLa cells.

PROVIDER: PRJNA551429 | ENA |

REPOSITORIES: ENA

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Gene expression changes after depletion of Cyclin F and atypical E2Fs in HeLa cells.

Project description:Using RNAi technology, Cyclin F, E2F7+8, or the combination of all proteins in were knocked down HeLa cells. The goal was to study which gene expression programmes are altered by cyclin F depletion in G2/M cells. Furthermore, we had performed experiments suggesting that cyclin F mediates degradation of the atypical E2F repressor proteins E2F7 and E2F8. Therefore we investigated using combinatorial knockdown if additional depletion of E2F7/8 rescues gene expression changes caused by cyclin F. Our resuilts show that cyclin F depletion downregulates expression hundreds of E2F target genes, which could be prevented by additional E2F7/8 depletion.

2019-08-29 | GSE133416 | GEO

Gene expression data following Cyclin T2 and Cyclin T1 depletion by shRNA in HeLa cells

Project description:We have characterized gene expression changes in HeLa cells following long term depletion of Cyclin T2 or Cyclin T1 using shRNA

2011-08-03 | GSE28339 | GEO

Gene expression data following Cyclin T2 and Cyclin T1 depletion by shRNA in HeLa cells

Project description:We have characterized gene expression changes in HeLa cells following long term depletion of Cyclin T2 or Cyclin T1 using shRNA HeLa cells were transduced with VSV-G pseudotyped lentiviral vectors expressing shRNA against either Cyclin T2 or Cyclin T1. As a control, cells were transduced with shRNA vector with four nucleotides mismatch in the Cyclin T1 mRNA that has been previously shown to have minimal effects on mRNA expression levels. The vectors have a GFP reporter that can be used to estimate transduction efficiency. Five days post-transduction, cells were harvested and total RNA extracted. Transcriptional profiling was carried out on these RNA samples. Two independent biological replicate experiments were carried out in this analysis and the xpression values normalized by GC-RMA and averaged. The following comparisons were made: MM to Cyclin T2 and MM to Cyclin T1.

2011-08-02 | E-GEOD-28339 | biostudies-arrayexpress

BRCA1 depletion effect on HeLa cells

2010-06-09 | GSE22259 | GEO

BRCA1 depletion effect on HeLa cells

Project description:Analysis of HeLa cells following depletion of BRCA1 tumor supressor using RNAi against BRCA1. Results provide insight into the molecular mechanisms underlying loss of the BRCA1 function. Six samples (three control samples and three BRCA1 depleted samples) have been analysed. For the control, the samples derived from the HeLa cells treated with RNAi against GFP were used.

2010-06-23 | E-GEOD-22259 | biostudies-arrayexpress

SMARCB1 loss induces druggable cyclin D1 deficiency via upregulation of MIR17HG in atypical teratoid rhabdoid tumors

Project description:Atypical teratoid rhabdoid tumor (ATRT) is a fatal pediatric malignancy of the central neural system lacking effective treatment options. It belongs to rhabdoid tumor family usually caused by biallelic inactivation of SMARCB1, encoding a key subunit of SWI/SNF chromatin remodelling complexes. Previous studies proposed that SMARCB1 loss drives rhabdoid tumor by promoting cell cycle through activating transcription of cyclin D1 while suppressing p16. However, low cyclin D1 protein expression is observed in most ATRT patient tumors. The underlying mechanism and therapeutic implication of this molecular trait remain unknown. Here, we show that SMARCB1 loss in ATRT leads to the reduction of cyclin D1 expression by upregulating MIR17HG, a microRNA (miRNA) cluster known to generate multiple miRNAs targeting CCND1. Furthermore, we find that this cyclin D1 deficiency in ATRT results in marked in vitro and in vivo sensitivity to the CDK4/6 inhibitor palbociclib as a single agent. Our study identifies a novel genetic interaction between SMARCB1 and MIR17HG in regulating cyclin D1 in ATRT and suggests a rationale to treat ATRT patients with FDA-approved CDK4/6 inhibitors.

2020-06-08 | GSE147851 | GEO

A unique and divergent cyclin/cyclin-dependent kinase complex controls DNA replication during atypical cell-cycles of Plasmodium berghei gametogonyA unique and divergent cyclin/cyclin-dependent kinase complex controls DNA replication during atypical cell-cycles of Plasmodium berghei gametogony

Project description:Cell-cycle transitions are generally triggered by variations in the activity of cyclin-dependent kinases (CDKs) bound to cyclins. Malaria parasites express ancestral CDKs and cyclins, whose functions and interdependency remain elusive. Here, we show that the unique Plasmodium berghei CDK-related kinase 5 (CRK5), is a critical cell-cycle regulator of gametogony required for transmission to the mosquito. It is essential for DNA replication and phosphorylates canonical S/TPxK CDK motifs on components of the pre-replicative complex otherwise regulated by distinct kinases in other eukaryotes. Over a replicative cycle, CRK5 stably interacts with a single Haemosporidia-specific cyclin (SOC2) with no evidence of SOC2 degradation. Regulation of CRK5 activity relies instead on dynamic phosphorylation of a C-terminus extension that mediates its interaction with SOC2. Our results present evidence that during the atypical cell cycles of Plasmodium gametogony, a unique and divergent cyclin/CDK pair fulfils the functional space of multiple eukaryotic cell-cycle kinases to initiate DNA replication.

2020-02-18 | PXD017283 | Pride

A divergent cyclin/cyclin-dependent kinase complex controls progression through the atypical replicative cycles during Plasmodium berghei gametogony

Project description:A divergent cyclin/cyclin-dependent kinase complex controls progression through the atypical replicative cycles during Plasmodium berghei gametogony

| PRJNA604771 | ENA

A divergent cyclin/cyclin-dependent kinase complex controls the atypical replication of Plasmodium berghei during gametogony and parasite transmission.

Project description:Cell cycle transitions are generally triggered by variation in the activity of cyclin-dependent kinases (CDKs) bound to cyclins. Malaria-causing parasites have a life cycle with unique cell-division cycles, and a repertoire of divergent CDKs and cyclins of poorly understood function and interdependency. We show that Plasmodium berghei CDK-related kinase 5 (CRK5), is a critical regulator of atypical mitosis in the gametogony and is required for mosquito transmission. It phosphorylates canonical CDK motifs of components in the pre-replicative complex and is essential for DNA replication. We also provide evidence for indirect regulation of the concomitant M-phase progression. During a replicative cycle, CRK5 stably interacts with a single Plasmodium-specific cyclin (SOC2), although we obtained no evidence of SOC2 cycling by transcription, translation or degradation. Our results provide evidence that during Plasmodium male gametogony, this unique cyclin/CDK pair fills the functional space of multiple eukaryotic cell-cycle kinases controlling DNA replication and M-phase progression.

2020-06-17 | PXD017622 | Pride

mRNA expression modification after XRN1 depletion in Hela Cells

Project description:mRNA expression modification after XRN1 depletion in Hela Cells

| PRJNA475123 | ENA