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Simple differentiation method using FBS identifies DUSP6 as a marker for fine-tuning of FGF-ERK signaling activity in human pluripotent stem cells

ABSTRACT: Simple differentiation method using FBS identifies DUSP6 as a marker for fine-tuning of FGF-ERK signaling activity in human pluripotent stem cells

PROVIDER: PRJNA560087 | ENA |

REPOSITORIES: ENA

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Simple differentiation method using FBS identifies DUSP6 as a marker for fine-tuning of FGF-ERK signaling activity in human pluripotent stem cells

Project description:Assessment of differentiation potential is a basic requirement to obtain qualified human pluripotent stem cells (hPSCs). Here, we report a simple differentiation method using fetal bovine serum (FBS) to estimate differentiation potential and propensity of hPSCs. PluriTest using RNA-sequencing showed that cells differentiated after treatment with 5% FBS. Expression patterns of three germ layer markers revealed that cells cultured in Knockout Serum Replacement-containing medium (KSR) with mouse feeder cells had higher differentiation potential than cells cultured in a chemically defined medium (E8) with recombinant matrix proteins, especially into the mesoderm and endoderm lineages. Analysis of differentially expressed genes between KSR and E8 identified DUSP6 as a marker for where cells had been cultured. Expression of DUSP6 correlated with FGF-ERK signaling activity. Fine-tuning of FGF-ERK signaling activity to a range that can shut down DUSP6 transcription but sustain NANOG transcription partially increased the differentiation potential. Our data suggest that differentiation with 5% FBS is good to estimate differentiation potential and propensity at the early stage, and that DUSP6 is an excellent marker to monitor ERK signaling activity.

2020-02-18 | GSE135799 | GEO

Post-transcriptional tuning of FGF signaling mediates neural crest induction

Project description:Post-transcriptional tuning of FGF signaling mediates neural crest induction

| PRJNA630815 | ENA

Gene expression data of BCR-ABL1 transformed B cell precursors from Dusp6 wild-type and Dusp6 knockout mice

Project description:To elucidate the mechanism of Dusp6-mediated pre-B cell survival signaling, we investigated the gene expression pattern in BCR-ABL1-transformed Dusp6+/+ and Dusp6-/- B cell precursors. BCR-ABL1 transformed B cell precursors of Dusp6 wildtype and Dusp6 knockout mice were subjected to RNA isolation

2013-06-03 | E-GEOD-34832 | biostudies-arrayexpress

Phospho-proteomic analysis of DUSP6 deficient Caco-2 cells

Project description:Dual-specificity phosphatase 6 (Dusp6)-deficiency enhances baseline colon barrier integrity and confers amelioration of dextran sulfate sodium (DSS)-induced colonic injury. DUSP6 is a phosphatase, and therefore it is plausible that DUSP6 knockout alters the phosphorylation status of other proteins. To access the protein phosphorylation landscape and functional network in DUSP6 deficient Caco-2 cells, we applied phosphopeptide enrichment and isobaric labeling strategies with MS-based proteomics, and identified 1323 phosphorylation sites on 580 phosphoproteins.

2021-11-02 | PXD029014 | Pride

Gene expression data of BCR-ABL1 transformed B cell precursors from Dusp6 wild-type and Dusp6 knockout mice

2013-06-03 | GSE34832 | GEO

Effect of DUSP6 overexpression or knockdown on gene expression in AML12 cells

Project description:DUSP6 plays important roles in MAPK signaling pathway, but whether and how it is involved in liver funciton remains to be explored. Here, we performed RNA-seq analyses in AML12 cells where DUSP6 is disrupted. We overexpressed GFP-DUSP6 or GFP in AML12 cells, and tested the effects of DUSP6 increase on gene expression in AML12 cells. Meanwhile, we knocked down DUSP6 in AML12 cells and tested the effects of DUSP6 decrease on gene expression in AML12 cells. Taken together, we analyzed the changes of gene expression mediated by DUSP6, which provides new insights for the function of DUSP6 in liver

2023-12-31 | GSE249146 | GEO

DUSP6 mediates resistance to JAK2 inhibition and drives leukemic progression (microarray)

Project description:Chronic myeloproliferative neoplasms (MPNs) exhibit a propensity for transformation to secondary acute myeloid leukemia (sAML), for which the underlying mechanisms remain poorly understood, resulting in limited treatment options and dismal clinical outcomes. Here, we performed bulk transcriptome profiling accompanied by single cell RNA-sequencing on CD34+ stem/progenitor cells from serial patient samples obtained at the chronic MPN and sAML phases, identifying aberrantly increased expression of dual-specificity phosphatase 6 (DUSP6) underlying disease transformation. Genetic and pharmacologic targeting of DUSP6 led to inhibition of S6 and JAK/STAT signaling, resulting in potent suppression of cell proliferation, while also reducing inflammatory cytokine production in primary samples. Furthermore, ectopic DUSP6 expression augmented proliferation and mediated JAK2 inhibitor resistance, while DUSP6 inhibition reduced colony-forming potential of JAK2 inhibitor-persistent patient cells. Mechanistically, DUSP6 perturbation dampened S6 signaling via inhibition of RSK1, which we identified as a second indispensable candidate associated with poor clinical outcome. Ectopic expression of DUSP6 in patient-derived xenograft (PDX) models exacerbated disease severity and led to early lethality, whereas DUSP6 knockdown suppressed leukemic engraftment. Finally, pharmacological inhibition of DUSP6 potently and specifically suppressed disease development across Jak2 V617F and MPL W515L MPN mouse models, as well as sAML PDXs, without inducing toxicity in healthy controls. These findings underscore DUSP6 in driving disease transformation and therapeutic resistance, and highlight the DUSP6-RSK1 axis as a novel, druggable pathway in myeloid malignancies.

2022-10-25 | GSE214360 | GEO

Post-transcriptional tuning of FGF signaling mediates neural crest induction

Project description:Ectodermal patterning is required for the establishment of multiple components of the vertebrate body plan. Previous studies have demonstrated that precise combinations of extracellular signals determine the induction of neural or neural crest progenitors. Yet, we still have a limited understanding of how the response to inductive signals is optimized to generate the proper transcriptional output in target cells. Here we show that post-transcriptional attenuation of signaling gradients is essential for the formation of the neural crest. We found that neural crest cells display enhanced expression of Dicer, which promotes the maturation of a set of cell-type-specific miRNAs. These miRNAs target multiple components of the FGF signaling pathway, a central player in the process of neural induction in avian embryos. Loss of neural crest miRNAs prevented the attenuation of this neuralizing signal, leading to the expansion of the neural plate at the expense of neural crest cells. Thus, the post-transcriptional attenuation of FGF signaling is pre-requisite for neural crest specification. These findings demonstrate how post-transcriptional repression may reshape signaling gradients to set the boundaries between distinct spatial domains of progenitor cells.

2020-12-07 | GSE150007 | GEO

Fine-tuning gene networks using simple sequence repeats.

Project description: Not available

| S-EPMC3479488 | biostudies-literature

RNA sequencing analysis of WT and Dusp6-/- rat cardiac infiltrated macrophages transcriptomes

Project description:Dual-specificity phosphatase 6 (DUSP6), a member of MAPK phosphatase, serves a specific and conserved function on the dephosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in multiple species. Utilizing a rat strain harboring nonsense mutation of Dusp6, we found that Dusp6 deficiency improves cardiac function by attenuating cardiomyocyte death and fibrosis in acute inflammatory phase after MI. To investigate the effect of DUSP6 on macrophages in acute inflammatory phase of MI, we performed RNA-seq analysis using CD45+HIS36+ macrophages isolated from Dusp6-deficient and WT infarcted LV tissues 72 h after MI by fluorescent activated cell sorting (FACS).

2022-07-13 | GSE195978 | GEO

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