Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA433712 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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: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.

2018-06-13 | GSE110427 | GEO

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

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

| PRJNA433711 | ENA

ERK3 is essential for establishment of epithelial architecture

Project description:ERK3 is essential for establishment of epithelial architecture

| PRJNA433693 | ENA

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

ERK3 is essential for establishment of epithelial architecture

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-06-13 | GSE110429 | GEO

The atypical mitogen-activated protein kinase ERK3 is essential for establishment of epithelial architecture.

Project description: Not available

| S-EPMC5986203 | biostudies-literature

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

Adrenergic-induced ERK3 pathway drives lipolysis and suppresses energy dissipation

Project description:Beta-adrenergic stimulation stabilizes ERK3, resulting in the formation of a complex with MK5 and thereby driving lipolysis. A downstream target of the complex is FOXO1, which controls expression of the lipolytic enzyme ATGL. Deletion of ERK3 in mouse adipocytes inhibits lipolysis, but elevates energy dissipation.

2021-01-01 | GSE142424 | GEO

Chromatin accessibility analysis uncovers TFAP2A as a regulator on pro-angiogenesis of acquired resistance to anlotinib

Project description:Anlotinib, a multitarget agent a multi-target agent that inhibits tumor proliferation and angiogenesis, has been demonstrated to be effective for non-small cell lung cancer (NSCLC) at third-line or over third-line. However, the underlying mechanisms of anlotinib acquired-resistance is still unclear. Here we performed chromatin accessibility profiling on anlotinib-resistant NCI-H1975 and wild-type NCI-H1975. By integrating with transcriptome analysis, we found that anlotinib resistance was due to increased angiogenic capacity, and revealed that TFAP2A was involved in anlotinib resistance. Next, TFAP2A was knock-down in anlotinib-resistant cells and RNAseq was performed to see down-regulated genes with TFAP2A KD.

2020-11-09 | GSE142031 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data