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Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

ABSTRACT: Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

PROVIDER: PRJNA577683 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10281000.fastq.gz	Fastqsanger.gz
	SRR10281001.fastq.gz	Fastqsanger.gz
	SRR10281002.fastq.gz	Fastqsanger.gz
	SRR10281003.fastq.gz	Fastqsanger.gz
	SRR10281004.fastq.gz	Fastqsanger.gz

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Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

Project description:Quiescent hematopoietic stem cells (HSCs) are typically dormant, and only a few quiescent HSCs are active. The relationship between “dormant” and “active” HSCs remains unresolved. Here we generated a G0 marker (G0M) mouse line that visualizes quiescent cells. G0M identifies a small population of active HSCs (G0Mlow), which are distinct from dormant HSCs (G0Mhigh), within the conventional quiescent HSC fraction. Single-cell RNA-Seq analyses showed that the gene expression profiles of these populations were nearly identical, yet differed in their Cdk4/6 activity. Furthermore high-throughput small molecule screening revealed that high concentrations of cytoplasmic calcium ([Ca2+]c) were linked to dormancy of HSCs. These findings indicate that G0M separates dormant and active adult HSCs, which are regulated by Cdk4/6 and [Ca2+]c. This G0M mouse line represents a useful resource for investigating physiologically important stem cell subpopulations.

2019-12-20 | GSE139013 | GEO

Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

Project description:Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

| PRJNA578092 | ENA

Discrimination of dormant and active hematopoietic stem cells by G0 markers reveals dormancy regulation by cytoplasmic calcium

Project description:High-throughput small molecule screening revealed that high concentrations of cytoplasmic calcium ([Ca2+]c) were linked to dormancy of HSCs.To clarify molecular difference between [Ca2+]chigh and [Ca2+]clow cells, we performed RNA-Seq analysis using [Ca2+]chigh and [Ca2+]clow cells.

2019-12-20 | GSE138884 | GEO

affy_sunflower_2010_13-ROS and hormones in sunflower seed dormancy.

Project description:affy_sunflower_2010_13 - affy_sunflower_2010_13 - It concerns the interaction between ROS and hormones in dormancy release in sunflower seeds. ABA is responsible for dormancy maintenance, while GA and ethylene promote seed germination. Based on our results, ROS could represent good candidate to shift from a hormone signalling to another determining the dormancy state in sunflower seeds.-We aim to understand the mechanisms controlling sunflower seed dormancy at the transcriptomic level, by the application of treatments which maintain dormancy as ABA, or alleviate dormancy as ROS and ethylene. Transcripts comparison will be performed between dormant and non-dormant sunflower embryo imbibed 24h on water, on ABA, on methylviologen, a pro-oxidant compound or on ethylene. 12 arrays - SUNFLOWER; treated vs untreated comparison

2013-08-01 | E-GEOD-44165 | biostudies-arrayexpress

RNA-Seq of seed dormancy in red rice

Project description:Red rice fully dormant seeds do not germinate even under favourable germination conditions. In several species, including rice, seed dormancy can be removed by dry-afterripening (warm storage); thus, dormant and nondormant seeds can be compared for the same genotype. A weedy (red) rice genotype with strong dormancy was used for mRNA expression profiling, by RNA-Seq, of dormant and nondormant dehulled caryopses (here addressed as seeds) at two temperatures (30 °C and 10 °C) and two durations of incubation in water (8 hours and 8 days). Aim of the study was to highlight the differences in the transcriptome of dormant and nondormant imbibed seeds.

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affy_sunflower_2010_13-ROS and hormones in sunflower seed dormancy.

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Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway [DMSO vs DORMANT]

Project description:Eradicating tumor dormancy that develops following oncogene-targeted therapy, including after epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer (NSCLC), is an attractive therapeutic strategy but the mechanisms governing the establishment of tumor dormancy are poorly understood. We observe that blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state, characterized by extensive epigenetic remodeling and high YAP/TEAD activity. YAP/TEAD trigger an epithelial-to-mesenchymal transition (EMT) program and engage the EMT transcription factor SLUG to directly repress pro-apoptotic BMF, limiting drug-induced apoptosis. Pharmacological co-inhibition of YAP or TEAD, or genetic deletion of YAP1, all deplete dormant cells by enhancing EGFR/MEK induced apoptosis. Thus, YAP activation can promote the survival of EGFR-mutant NSCLC cells in the chronic absence of EGFR signaling. Eradicating this population enhances the efficacy of targeted therapies which could ultimately lead to prolonged treatment responses in cancer patients.

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Modeling androgen deprivation therapy-induced prostate cancer dormancy and its clinical implications

Project description:Purpose: Treatment-induced tumor dormancy is a state in cancer progression where residual disease is present but remains asymptomatic. Dormant cancer cells are treatment-resistant and responsible for cancer recurrence and metastasis. Prostate cancer (PCa) treated with androgen-deprivation therapy (ADT) often enters a dormant state. ADT-induced PCa dormancy remains poorly understood due to the challenge in acquiring clinical dormant PCa cells and the lack of representative models. We, therefore, aimed to develop clinically relevant models that can be used for studying ADT-induced PCa dormancy. Experimental design: Dormant PCa models were established by castrating mice bearing PCa patient-derived xenografts (PDXs) of hormonal naïve or sensitive PCa. Dormancy status and tumor relapse were monitored and evaluated. Paired pre- and post-castration (dormant) PDX tissues were subjected to morphological and transcriptome profiling analyses. Results: We established eleven ADT-induced dormant PCa models that closely mimicked the clinical courses of ADT-treated PCa. We identified two ADT-induced dormancy subtypes that differed in morphology, gene expression, and relapse rates. We discovered transcriptomic differences in pre-castration PDXs that predisposed the dormancy response to ADT. We further developed a dormancy subtype-based, predisposed gene signature that was significantly associated with ADT response in hormonal naïve PCa and clinical outcome in castration-resistant PCa treated with ADT or androgen-receptor pathway inhibitors.

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Identifying dormant cells in colorectal cancer spheroids

Project description:Cellular dormancy and heterogeneous cell cycle lengths provide important explanations for treatment failure following adjuvant therapy with S-phase cytotoxics in colorectal cancer (CRC) yet the molecular control of the dormant versus cycling state remains unknown. In CRCs dormant cells are found to be highly clonogenic and resistant to chemotherapies. We sought to understand the molecular features of dormant CRC cells to facilitate rationale identification of compounds to target both dormant and cycling tumour cells.

2018-05-21 | GSE114012 | GEO

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