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

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

PROVIDER: PRJNA1047545 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27018383_1.fastq.gz	Fastqsanger.gz
	SRR27018383_2.fastq.gz	Fastqsanger.gz
	SRR27018384_1.fastq.gz	Fastqsanger.gz
	SRR27018384_2.fastq.gz	Fastqsanger.gz
	SRR27018385_1.fastq.gz	Fastqsanger.gz

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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

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Effect of inhibition of Setdb1 on gene expression in AML12 cells

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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

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Project description:Proteomes of Mycoplasma gallisepticum strains with overexpression and knockdown of WhiA transcription factor. The overexpression was introduced on a transposon vector carrying M. gallisepticum whiA gene with strong constitutive promoter and strong SD sequence. The knockdown was made by CRISPRi. dCas9 protein and sgRNA against whiA gene were introduced on a transposon vector.

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Project description:To investigate effect of WNT hyperactivation by CTNNB1 overexpression or APC knockdown on gene expression and probe possible mechanism of cell viability effect, we overexpressed GFP/CTNNB1, or induce knockdown of APC by shNT1 (non-targeting) and shAPC

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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).

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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.

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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

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