Cell cycle and G1 cyclins
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA140799 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29800: Lack of G1 cyclin arrest cell cycle synchronization time-course microarray in Glucose GSE29892: Alpha Factor arrest cell cycle synchronization time-course microarray in Galactose GSE29893: Alpha Factor arrest cell cycle synchronization time-course microarray in Glucose Refer to individual Series
2011-06-11 | E-GEOD-29894 | biostudies-arrayexpress
Project description:A long-term goal in cancer research has been to inhibit the cell cycle in tumour cells without causing toxicity in proliferative healthy tissues. The best evidence that this is achievable is provided by CDK4/6 inhibitors, which arrest the cell cycle in G1, are well-tolerated in patients, and are effective in treating ER+/HER2- breast cancer. CDK4/6 inhibitors are effective because they arrest tumour cells more efficiently than some healthy cell types and, in addition, they affect the tumour microenvironment to enhance anti-tumour immunity. We demonstrate here another reason to explain their efficacy. Tumour cells are specifically vulnerable to CDK4/6 inhibition because during the G1 arrest, oncogenic signals drive toxic cell overgrowth. This overgrowth causes permanent cell cycle withdrawal by either preventing progression from G1 or by inducing replication stress and genotoxic damage during the subsequent S-phase and mitosis. Inhibiting or reverting oncogenic signals that converge onto mTOR can rescue this excessive growth, DNA damage and cell cycle exit in cancer cells. Conversely, inducing oncogenic signals in non-transformed cells can drive these toxic phenotypes and sensitize cells to CDK4/6 inhibition. Together, this demonstrates how oncogenic signals that have evolved to stimulate constitutive tumour growth and proliferation driven subverted to cause toxic cell growth and irreversible cell cycle exit when proliferation is halted in G1.
2023-11-17 | PXD043792 | Pride
Project description:Endothelial cells derived from hESCs were separated into 4 different cell cycle phases via FACS and sequenced (i.e., early G1, late G1, G1/S, S/G2/M)
2021-01-01 | GSE159694 | GEO
Project description:This experiment measured the mono-methylation of lysine 37 of histone H3 in yeast cells at various phases of the cell cycle (G1, G1/S and S).
2021-04-28 | E-MTAB-9058 | biostudies-arrayexpress
Project description:We report that ancestral zinc-finger-domain transcriptional regulators, previously reported to control virulence/symbiosis, implement a cell cycle (SM-bM-^FM-^RG1) transcriptional switch. To unravel how this G1-phase transcriptional program is reinstated during a primitive cell cycle, we first defined G1-specific promoters in the model bacterium Caulobacter crescentus by comparative ChIP-Seq analysis. We then exploited one such promoter as genetic proxy, to identify two conserved developmental regulator paralogs, MucR1/2, that constitute a quadripartite and homeostatic regulatory module directing the switch from SM-bM-^FM-^RG1-phase transcription. Surprisingly, MucR orthologs that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support the G1 transcriptional switch in Caulobacter. Pan-genomic ChIP-Seq analyses in Sinorhizobium and Caulobacter show that this module targets orthologous genes. Thus, this ancestral bacterial lineage from which eukaryotic organelles descended may coordinate virulence/symbiosis with other cell cycle functions using a primordial transcription factor fold that is now primarily found in the eukaryotic domain of life. Examination of 5 transcripton factor binding in two different species
2014-05-25 | E-GEOD-52849 | biostudies-arrayexpress
Project description:Two models have been put forward for cyclin-dependent kinase (Cdk) control of the cell cycle. In the qualitative model, cell cycle events are ordered by distinct substrate specificities associated with successive waves of G1, S and mitotic cyclins. Alternatively, the gradual quantitative rise of Cdk activity from G1 phase to mitosis could lead to ordered substrate phosphorylation at sequential thresholds. Here, we study the relative contributions of qualitative and quantitative Cdk control in the budding yeast S. cerevisiae. S-phase cyclins can be replaced by a single mitotic cyclin, albeit at the cost of reduced fitness. The single cyclin can in addition replace G1 cyclins to support ordered cell cycle progression, fulfilling key predictions of the quantitative model. However, single-cyclin cells fail to polarize or grow buds and thus cannot sustain proliferation. Our results suggest that budding yeast has become dependent on G1 cyclin specificity to couple cell cycle progression to essential morphogenetic events.
2021-08-23 | PXD022757 | Pride
Project description:Lack of G1 cyclin arrest cln1,2,3-delta MET3pr-CLN2 cells Cell cycle syncronization time-course microarray in Glucose.
2011-06-11 | GSE29800 | GEO
Project description:We report that ancestral zinc-finger-domain transcriptional regulators, previously reported to control virulence/symbiosis, implement a cell cycle (S→G1) transcriptional switch. To unravel how this G1-phase transcriptional program is reinstated during a primitive cell cycle, we first defined G1-specific promoters in the model bacterium Caulobacter crescentus by comparative ChIP-Seq analysis. We then exploited one such promoter as genetic proxy, to identify two conserved developmental regulator paralogs, MucR1/2, that constitute a quadripartite and homeostatic regulatory module directing the switch from S→G1-phase transcription. Surprisingly, MucR orthologs that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support the G1 transcriptional switch in Caulobacter. Pan-genomic ChIP-Seq analyses in Sinorhizobium and Caulobacter show that this module targets orthologous genes. Thus, this ancestral bacterial lineage from which eukaryotic organelles descended may coordinate virulence/symbiosis with other cell cycle functions using a primordial transcription factor fold that is now primarily found in the eukaryotic domain of life.
2014-05-25 | GSE52849 | GEO
Project description:Lack of G1 cyclin arrest cln1,2,3-delta MET3pr-CLN2 cells Cell cycle syncronization time-course microarray in Glucose. Time-course experiment. Samples are hybridized onto the first timepoint.
2011-06-11 | E-GEOD-29800 | biostudies-arrayexpress
Project description:We will be using G&T method to sequence single cell genome and transcriptome derived from FS13B iPSCs cell line. The cell cycle state of each of the single cells is known. Hence, we will be analysing the genome and transcriptome of single cells from each of the cell cycle state to generate a copy number profile and transcriptome profile per given cell cycle stage: G1, S, G2, S.
| EGAS00001003293 | EGA