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Identification of in vivo roles of ErbB4-JMa and its direct nuclear signaling using a novel isoform-specific knock out mouse

ABSTRACT: Identification of in vivo roles of ErbB4-JMa and its direct nuclear signaling using a novel isoform-specific knock out mouse

PROVIDER: PRJNA834110 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19038743.fastq.gz	Fastqsanger.gz
	SRR19038744.fastq.gz	Fastqsanger.gz
	SRR19038745.fastq.gz	Fastqsanger.gz
	SRR19038746.fastq.gz	Fastqsanger.gz
	SRR19038747.fastq.gz	Fastqsanger.gz

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Similar Datasets

Identification of in vivo roles of ErbB4-JMa and its direct nuclear signaling using a novel isoform-specific knock out mouse

Project description:Like all receptor tyrosine kinases (RTKs), ErbB4 signals through a canonical signaling involving phosphorylation cascades. However, ErbB4 can also signal through a non-canonical mechanism whereby the intracellular domain is released into the cytoplasm by regulated intermembrane proteolysis (RIP) and translocates to the nucleus where it regulates transcription. These different signaling mechanisms depend on the generation of alternative spliced isoforms, a RIP cleavable ErbB4-JMa and an uncleavable ErbB4-JMb. Non-canonical signaling by ErbB4-JMa has been implicated in the regulation of brain, heart, mammary gland, lung, and immune cell development. However, most studies on non-canonical ErbB4 signaling have been performed in vitro due to the lack of an adequate mouse model. We created an ErbB4-JMa specific knock out mouse and demonstrate that RIP-dependent, non-canonical signaling by ErbB4-JMa is required for the regulation of GFAP expression during cortical development. We also show that ErbB4-JMa signaling is not required for the development of the heart, mammary glands, sensory ganglia. Furthermore, we identify genes whose expression during cortical development is regulated by ErbB4, and show that the expression of two of them, CRYM and DBi, depend on ErbB4-JMa. Thus, we provide the first animal model to study the roles of non-canonical RTK in vivo.

2022-08-02 | GSE202063 | GEO

Identification of in vivo roles of ErbB4-JMa and its direct nuclear signaling using a novel isoform-specific knock out mouse.

Project description:Like all receptor tyrosine kinases (RTKs), ErbB4 signals through a canonical signaling involving phosphorylation cascades. However, ErbB4 can also signal through a non-canonical mechanism whereby the intracellular domain is released into the cytoplasm by regulated intramembrane proteolysis (RIP) and translocates to the nucleus where it regulates transcription. These different signaling mechanisms depend on the generation of alternative spliced isoforms, a RIP cleavable ErbB4-JMa and an uncleavable ErbB4-JMb. Non-canonical signaling by ErbB4-JMa has been implicated in the regulation of brain, heart, mammary gland, lung, and immune cell development. However, most studies on non-canonical ErbB4 signaling have been performed in vitro due to the lack of an adequate mouse model. We created an ErbB4-JMa specific knock out mouse and demonstrate that RIP-dependent, non-canonical signaling by ErbB4-JMa is required for the regulation of GFAP expression during cortical development. We also show that ErbB4-JMa signaling is not required for the development of the heart, mammary glands, sensory ganglia. Furthermore, we identify genes whose expression during cortical development is regulated by ErbB4, and show that the expression of three of them, CRYM and DBi, depend on ErbB4-JMa whereas WDFY1 relies on ErbB4-JMb. Thus, we provide the first animal model to directly study the roles of ErbB4-JMa and non-canonical ErbB4 signaling in vivo.

| S-EPMC9568506 | biostudies-literature

Murine Liver Tissues: Control vs. ErbB4 knocked out

Project description:Transcriptional profiling of ErbB4-/- mouse liver tissues comparing controls. Two-condition experiment, ErbB4-/- vs. control mouse liver tissues. Biological replicates: 3 controls, 3 ErbB4-/- mice.

2014-09-04 | E-GEOD-61056 | biostudies-arrayexpress

Epigenetic changes in amygdala and cortex of fear-conditioned and ErbB4 Knock-out mice

Project description:Chromatin accessibility provides an important window into the regulation of gene expression. Recently, the Assay of Transposase Accessible Chromatin with sequencing (ATAC-seq) was developed to profile genome-wide chromatin accessibility. Here we applied a read-downsampling approach to call robust ATAC-seq peaks in order to profile the regions of differential chromatin accessibility of central amygdala and cortex between different experimental conditions; fear-conditioned vs. control mice and ErbB4 knock-out vs. wild-type mice.

2019-02-21 | GSE111021 | GEO

Murine Liver Tissues: Control vs. ErbB4 knocked out

Project description:Transcriptional profiling of ErbB4-/- mouse liver tissues comparing controls.

2014-09-04 | GSE61056 | GEO

Epigenetic changes in amygdala and cortex of fear-conditioned and ErbB4 Knock-out mice

Project description:Epigenetic changes in amygdala and cortex of fear-conditioned and ErbB4 Knock-out mice

| PRJNA435600 | ENA

VAV3 in ERBB4-mediated cancer cell migration

Project description:ERBB4 is a member of the epidermal growth factor receptor (EGFR)/ERBB subfamily of receptor tyrosine kinases that regulates cellular processes including proliferation, migration and survival. ERBB4 signaling is involved in embryogenesis and homeostasis of adult tissues, but also in human pathologies such as cancer, neurological disorders and cardiovascular diseases. A mass spectrometry screen revealed guanine nucleotide exchange factor (GEF) VAV3, an activator of Rho family GTPases, as a novel ERBB4-interacting protein in breast cancer cells. The ERBB4-VAV3-interaction was confirmed by targeted mass-spectrometry, coimmunoprecipitation experiments, and further defined by demonstrating that kinase activity and tyrosine residues 1022 and 1162 of ERBB4, as well as the intact phosphotyrosine-interacting SH2 domain of VAV3 were necessary for the interaction. ERBB4 was also shown to stimulate tyrosine phosphorylation of the VAV3 activation domain, which is required for GEF activity of VAV proteins. In addition to VAV3, also the other members of the VAV family, VAV1 and VAV2 were shown to coprecipitate with ERBB4. Analyses of the effects of overexpression of dominant-negative VAV3 constructs or downregulation of VAV3 expression by shRNAs in breast cancer cells demonstrated that active VAV3 was involved in ERBB4-stimulated migration. These findings define the VAV GTPases as novel effectors of ERBB4 activity in a signaling pathway relevant for cancer cell migration.

2020-06-24 | PXD019430 | Pride

Quantitative phosphoproteomics analysis of ERBB3/ERBB4 signaling

Project description:The four members of the epidermal growth factor receptor (EGFR/ERBB) family form homo- and heterodimers which mediate ligand-specific regulation of many key cellular processes in normal and cancer tissues. While signaling through the EGFR has been extensively studied on the molecular level, signal transduction through ERBB3/ERBB4 heterodimers is less well understood. Here, we generated isogenic mouse Ba/F3 cells that express full-length and functional membrane-integrated ERBB3 and ERBB4 or ERBB4 alone, to serve as a defined cellular model for biological and phosphoproteomics analysis of ERBB3/ERBB4 signaling. ERBB3 co-expression significantly enhanced Ba/F3 cell proliferation upon neuregulin-1 (NRG1) treatment. For comprehensive signaling studies we performed quantitative mass spectrometry (MS) experiments to compare the basal ERBB3/ERBB4 cell phosphoproteome to NRG1 treatment of ERBB3/ERBB4 and ERBB4 cells. We employed a workflow comprising differential isotope labeling with mTRAQ reagents followed by chromatographic peptide separation and final phosphopeptide enrichment prior to MS analysis. Overall, we identified 9686 phosphorylation sites which could be confidently localized to specific residues. Statistical analysis of three replicate experiments revealed 492 phosphorylation sites which were significantly changed in NRG1-treated ERBB3/ERBB4 cells. Bioinformatics data analysis recapitulated regulation of mitogen-activated protein kinase and Akt pathways, but also indicated signaling links to cytoskeletal functions and nuclear biology. Comparative assessment of NRG1-stimulated ERBB4 Ba/F3 cells indicated that ERBB3 did not trigger defined signaling pathways but more broadly enhanced phosphoproteome regulation in cells expressing both receptors. In conclusion, our data provide the first global picture of ERBB3/ERBB4 signaling and provide numerous potential starting points for further mechanistic studies

2016-01-15 | PXD002665 | Pride

Gene expression profile of mouse embryonic stem cells derived cardiomyocytes following the knockdown of ErbB4

Project description:To identify the potential target genes that were affected by the expression of ErbB4 in mouse embryonic stem cells-derived cardiomyocytes Embryonic Stem Cells-Derived Cardiomyocytes were transfected with si-ErbB4 for 48 hours

2015-09-11 | E-GEOD-69897 | biostudies-arrayexpress

Gene Expression Profiling on Stably Expressing Full Length (FL) JM-a CYT-1 or CYT-2 ERBB4 isoforms in MCF10A cells

Project description:Convergent and divergent effects of two FL ERBB4 isoforms on gene expression in normal-like MCF10A mammary epithelial cells lacking endogeneous ERBB4 expression. Control vector (VEC) and ERBB4 expression MCF10A cells(CYT1 or CYT2) were serum starved for 48 hours and incubated with or without ERBB4 ligand NRG1 for 2h. RNA samples were collected and analyzed.

2014-05-07 | E-GEOD-57346 | biostudies-arrayexpress

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