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Transcriptome analysis of control and ERK3-depleted Human Colonic Primary Epithelial cells (HCPECs)

ABSTRACT: Transcriptome analysis of control and ERK3-depleted Human Colonic Primary Epithelial cells (HCPECs)

PROVIDER: PRJNA560922 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10004176.fastq.gz	Fastqsanger.gz
	SRR10004177.fastq.gz	Fastqsanger.gz
	SRR10004178.fastq.gz	Fastqsanger.gz
	SRR10004179.fastq.gz	Fastqsanger.gz
	SRR10004180.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of control and ERK3-depleted Human Colonic Primary Epithelial cells (HCPECs)

Project description:RNA sequencing analysis of control and ERK3 knockdown HCPECs was performed to understand the physiological relevance of ERK3 in maintaining basal as well as LPS-mediated innate immune responses in HCPECs. Results revealed that ERK3 is required for the regulation of several key cytokines and chemokines even at the steady state. In particular, we discovered that ERK3 is indespansable for the transcriptional regulation of CXCL8/IL-8, CXCL10, MCP-1/CCL2 and GCP-2/CXCL6. Concomitantly, a functional interpretation of the differentially expressed (DE) genes with topGO indicated an important role of ERK3 in regulation of genes involved in, among others, immune responses and leukocyte chemotaxis.

2020-04-27 | GSE136002 | GEO

ERK3 is essential for establishment of epithelial architecture [ERK3 KD]

Project description:Establishment and maintenance of epithelial architecture are essential for embryonic development and adult physiology. Here, we show that ERK3, a poorly characterized atypical MAPK, regulates epithelial architecture in vertebrates. In Xenopus embryonic epidermal epithelia, ERK3 knockdown impairs adherens and tight junction protein distribution, as well as tight junction barrier function, resulting in epidermal breakdown. Moreover, in human breast epithelial cancer cells, inhibition of ERK3 expression induces thickened epithelia with aberrant adherens and tight junctions. Microarray results suggest an involvement of TFAP2A, a transcription factor important for epithelial gene expression, in ERK3-dependent gene expression changes. TFAP2A knockdown phenocopies ERK3 knockdown in both Xenopus embryos and human cells, and ERK3 is required for full activation of TFAP2A-dependent transcription. Our findings thus reveal that ERK3 regulates epithelial architecture, possibly in cooperation with TFAP2A. We used microarrays to study the changes in ERK3-dependent gene expression profiles during pronephros and epidermal development in Xenopus laevis embryos.

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ERK3 is essential for establishment of epithelial architecture [ERK3 KD vs. TFAP2A KD]

Project description:Establishment and maintenance of epithelial architecture are essential for embryonic development and adult physiology. Here, we show that ERK3, a poorly characterized atypical MAPK, regulates epithelial architecture in vertebrates. In Xenopus embryonic epidermal epithelia, ERK3 knockdown impairs adherens and tight junction protein distribution, as well as tight junction barrier function, resulting in epidermal breakdown. Moreover, in human breast epithelial cancer cells, inhibition of ERK3 expression induces thickened epithelia with aberrant adherens and tight junctions. Microarray results suggest an involvement of TFAP2A, a transcription factor important for epithelial gene expression, in ERK3-dependent gene expression changes. TFAP2A knockdown phenocopies ERK3 knockdown in both Xenopus embryos and human cells, and ERK3 is required for full activation of TFAP2A-dependent transcription. Our findings thus reveal that ERK3 regulates epithelial architecture, possibly in cooperation with TFAP2A. We used microarrays to compare the changes in ERK3-dependent gene expression profiles with those in TFAP2A-dependent gene expression profiles in Xenopus laevis embryos.

2018-06-13 | GSE110428 | GEO

ERK3 is essential for establishment of epithelial architecture [ERK3 KD]

Project description:ERK3 is essential for establishment of epithelial architecture [ERK3 KD]

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ERK3 is essential for establishment of epithelial architecture [ERK3 KD vs. TFAP2A KD]

Project description:ERK3 is essential for establishment of epithelial architecture [ERK3 KD vs. TFAP2A KD]

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ERK3 is essential for establishment of epithelial architecture

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MSP-induced Transcriptional Signature in Mouse Primary Colonic Epithelial Cells

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IL-17A treatment of mouse primary colonic epithelial spheroids in 3 differentiation states

Project description:The objective was to determine the transcriptional effect of IL-17A on primary colonic epithelial cells in various differentiation states in vitro. The three states included 1) stem/progenitor cell spheroids grown in 50% L-WRN media as described in our previous publication (PMID: 24232249), 2) differentiating colonic epithelial spheroids (DM) placed in differentiation media without L-WRN for 24 hours, 3) terminally differentiated colonocyte spheroids placed in differentiation media without L-WRN for 48 hours as described in our previous publication (PMID: 27264604). Each condition was cultured with or without 20ng/ml recombinant mouse IL-17A for the final 24 hours.

2018-04-10 | E-MTAB-6365 | biostudies-arrayexpress

MSP-induced Transcriptional Signature in Mouse Primary Colonic Epithelial Cells

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ERK3-MK5 signaling regulates myogenic differentiation and muscle regeneration by promoting FoxO3 degradation

Project description:The physiological functions and downstream effectors of the atypical mitogen-activated protein kinase ERK3 remain to be characterized. We recently reported that mice expressing catalytically-inactive ERK3 (Mapk6KD/KD) exhibit a reduced post-natal growth rate as compared to control mice. Here, we show that genetic inactivation of ERK3 impairs post-natal skeletal muscle growth and adult muscle regeneration after injury. Loss of MK5 phenocopies the muscle phenotypes of Mapk6KD/KD mice. At the cellular level, genetic or pharmacological inactivation of ERK3 or MK5 induces precocious differentiation of C2C12 or primary myoblasts, concomitant with MyoD activation. Reciprocally, ectopic expression of activated MK5 inhibits myogenic differentiation. Mechanistically, we show that MK5 directly phosphorylates FoxO3, promoting its degradation and reducing its association with MyoD. Depletion of FoxO3 rescues in part the premature differentiation of C2C12 myoblasts observed upon inactivation of ERK3 or MK5. Our findings reveal that ERK3 and its substrate MK5 act in a linear signaling pathway to control post-natal myogenic differentiation.

2021-12-04 | GSE190021 | GEO

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