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Expression data from differentiating Flk1- and Flk1+ ES cells expressing Snail during Wnt inhibition

ABSTRACT: ES cells differentiated in the presence of the Wnt inhibitor DKK1 fail to express the transcription factor Snail and undergo EMT or mesoderm differentiation. We generated an ES cell line, A2.snail, that induced Snail expression upon addition of doxycycline addition. Microarrays were used to gain a global picture of Flk1- and Flk1+ cells generated one day after Snail was expressed during Wnt inhibition.

ORGANISM(S): Mus musculus

PROVIDER: GSE26524 | GEO | 2013/10/23

SECONDARY ACCESSION(S): PRJNA136637

REPOSITORIES: GEO

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Expression data from differentiating Flk1- and Flk1+ ES cells expressing Snail during Wnt inhibition

Project description:ES cells differentiated in the presence of the Wnt inhibitor DKK1 fail to express the transcription factor Snail and undergo EMT or mesoderm differentiation. We generated an ES cell line, A2.snail, that induced Snail expression upon addition of doxycycline addition. Microarrays were used to gain a global picture of Flk1- and Flk1+ cells generated one day after Snail was expressed during Wnt inhibition. A2.snail ES cells, which express Snail upon addition of doxycycline, were differentiated as embryoid bodies in differentiation media and DKK1. Snail-induced cultures uniquely develop a select population of Flk1+ cells. Total RNA was harvested from sorted control (no doxycycline) Flk1- cells and sorted Snail-induced (doxycycline at day 2) Flk1- and Flk1+ cells at day 3 of differentiation.

2013-10-23 | E-GEOD-26524 | biostudies-arrayexpress

Expression data from differentiating ES cells expressing Snail during Wnt inhibition

2011-09-22 | GSE24291 | GEO

Expression data from differentiating ES cells expressing Snail during Wnt inhibition

Project description:ES cells differentiated in the presence of the Wnt inhibitor DKK1 fail to express the transcription factor Snail and undergo EMT. We generated an ES cell line, A2.snail, that induced Snail expression upon addition of doxycycline addition. Microarrays were used to gain a global picture of ES cell differentiation at early timepoints after Snail was expressed during Wnt inhibition. A2.snail ES cells, which express Snail upon addition of doxycycline, were differentiated as embryoid bodies in differentiation media and DKK1. Total RNA was harvested from control (no doxycycline) and Snail-induced (doxycycline at day 2) cultures at 6, 12, and 24 hours after doxycycline addition (corresponding to days 2.25, 2.5, and 3 of differentiation).

2011-09-21 | E-GEOD-24291 | biostudies-arrayexpress

Mus musculus

Project description:Expression data from differentiating Flk1- and Flk1+ ES cells expressing Snail during Wnt inhibition

| PRJNA136637 | ENA

Separation of mouse ES cell-derived mesodermal cells based on the expression of Flk1, PDGFRa and CAR.

Project description:We found that mouse ES cell-derived Flk1+ cells could be subdivided into three population by the expression of PDGFRa and CAR (Flk1+PDGFRa-CAR-, Flk1+PDGFRa-CAR+, and Flk1+PDGFRa+CAR+). Therefore, global gene expression analysis was perfomed by microarray to characterize these mesodermal subsets.

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Role of Flk1 in pulmonary arterial hypertension [Flox]

Project description:To investigate the role of Flk1 in pulmonary arterial hypertension, we generated mice lacking Flk1 specifically in vascular endothelial cells. We exposed these mice to hypoxia and collected Flk1-KO endothelial cells by FACS for RNA-seq.

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Separation of mouse ES cell-derived mesodermal cells based on the expression of Flk1, PDGFRa and CAR.

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Changes in Flk1-positive endothelial cells in hypoxia [GFP]

Project description:To investigate the role of Flk1 in pulmonary arterial hypertension, we observed the behavior of Flk1 in a disease model using Flk1-GFP mice. Gene expression profiling analysis was performed using data obtained from RNA-seq of Flk1-positive cells on days 1 and 8 of hypoxia exposure, when Flk1 changes were greatest.

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Title: Non-canonical functions of SNAIL drive context-specific progression

Project description:SNAIL is a key transcriptional regulator in embryonic development and cancer. Its effects in physiology and disease are believed to be linked to its role as a master regulator of epithelial-to-mesenchymal transition (EMT). Here, we report EMT-independent oncogenic SNAIL functions in cancer. Using genetic models, we systematically interrogated SNAIL effects in various oncogenic backgrounds and tissue types. SNAIL related phenotypes displayed remarkable tissue- and genetic context-dependencies, ranging from protective effects as observed in KRAS- or WNT-driven intestinal cancers, to dramatic acceleration of tumorigenesis, as shown in KRAS-induced pancreatic cancer. Unexpectedly, SNAIL-driven oncogenesis was not associated with E-cadherin downregulation or induction of an overt EMT program. Instead, we show that SNAIL induces bypass of senescence and cell cycle progression through p16INK4A-independent inactivation of the Retinoblastoma (RB)-restriction checkpoint. Collectively, our work identifies novel non-canonical EMT-independent functions of SNAIL and unravel its complex context-dependent role in cancer.

2022-12-13 | PXD038726 | Pride

Open Chomatin Analysis of human pluripotent stem cell cell-derived FLK1+ vascular mesoderm cells in AATS versus AATSI basal medium

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