Investigating genes regulated by Nrg1 nuclear back signaling.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE268856 | GEO | 2024/10/17
REPOSITORIES: GEO
Similar Datasets
Project description:Hyperglycemia is a risk factor for breast cancer-related morbidity and mortality. Hyperglycemia induces Neuregulin 1 (Nrg1) overexpression in breast cancer, which subsequently promotes tumor progression. However, molecular mechanisms underlying hyperglycemia-induced Nrg1 overexpression remain poorly understood. Here, We used DNA-protein pull-down using Nrg1 enhancer sequence as bait followed by LC/MS and identified RBPJ as a key component of the Nrg1 enhanceosome. We show that hyperglycemia causes active histone modifications at the Nrg1 enhancer, forming enhanceosome complexes where RBPJ, P300, and SETD1A are recruited to upregulate Nrg1 expression.
2023-01-29 | PXD038668 | Pride
Project description:The Cryptococcus neoformans NRG1 gene was identified using gene microarrays to define putative transcription factor genes regulated by the cyclic AMP (cAMP) signal transduction pathway. Disruption of NRG1 results in delayed capsule formation and mating, two phenotypes that are directly controlled by cAMP signaling. Putative targets of the Nrg1 transcription factor were identified using a second genome microarray to define differences in the transcriptomes of the wild-type and nrg1 mutant strains. These experiments implicate Nrg1 in the transcriptional control of multiple genes involved in carbohydrate metabolism and substrate oxidation, as well as the UGD1 gene encoding a UDP-glucose dehydrogenase required for polysaccharide capsule production and cell wall integrity. In addition to being under transcriptional control of the cAMP pathway, Nrg1 contains a putative protein kinase A phosphorylation site; mutation of this motif results in reduced Nrg1 activity. Consistent with prior studies in hypocapsular mutants, the nrg1 mutant strain is attenuated in an animal model of disseminated cryptococcal disease.
2009-09-04 | GSE17887 | GEO
Project description:Transcriptome prolifing analysis was performed in 22Pc-EP cells to identify differentially regulated genes by enzalutamide and NRG1
2020-06-01 | GSE147976 | GEO
Project description:CX3CL1 was discovered as a chemokine, and is best known to function via interaction with its receptor CX3CR1. However, in this study, we report a unique role of CX3CL1 that is independent from this pathway. We show that CX3CL1 is naturally shedded by both α- and β-secretase. The membrane-anchored C-terminal fragment is further cleaved by γ-secretase to release the CX3CL1 intracellular domain (CX3CL1-ICD), which is translocated into the cell nucleus to control gene expression. Among the regulated genes, we noted prominent induction of TGFβ2/TGFβ3 signaling in cultured cells by CX3CL1-ICD. Mice overexpressing only the C-terminal fragment (Tg-CX3CL1-ct) strongly induced TGFβ3 expression, as evidenced by Western and RNAseq analyses. Phenotypically, Tg-CX3CL1-ct mice exhibited enhanced neurogenesis both during development and in adulthood. Enhanced adult neurogenesis was seen in both the subgranular zone and the subventricular zone. Together, we demonstrate that CX3CL1-ct has a back-signaling function by enhancing neurogenesis through TGFβ3 and other genes important for neurogenesis. Induction CX3CL1 back signaling may be a promising novel mechanism to replenish neuronal loss.
2019-06-08 | GSE129722 | GEO
Project description:Neuregulin (NRG) signaling through the receptor tyrosine kinase, ERBB3, is required for embryonic development, and dysregulated signaling has been associated with cancer progression. Here, we show that NRG1/ERBB3 signaling inhibits melanocyte (MC) maturation and promotes undifferentiated, migratory and proliferative cellular characteristics. Embryonic analyses demonstrated that initial MC specification and distribution were not dependent on ERBB3 signaling. However NRG1/ERBB3 signaling was both necessary and sufficient to inhibit differentiation of later stages of MC development in culture. Analysis of tissue arrays of human melanoma samples suggests that ERBB3 signaling may also contribute to metastatic progression of melanoma as ERBB3 was phosphorylated in primary tumors compared with nevi or metastatic lesions. Neuregulin 1-treated MCs demonstrated increased proliferation and invasion and altered morphology concomitant with decreased levels of differentiation genes, increased levels of proliferation genes and altered levels of melanoma progression and metastases genes. ERBB3 activation in primary melanomas suggests that NRG1/ERBB3 signaling may contribute to the progression of melanoma from benign nevi to malignancies. We propose that targeting ERBB3 activation and downstream genes identified in this study may provide novel therapeutic interventions for malignant melanoma. Gene expression changes are compared between Melan-Ink4a cells stimulated with NRG1-b1 (NRG1) for 21 days and NRG1 untreated Melan-INK4a cells in triplicate using Affymetrix Mouse GeneChip 1.0 ST chip .
2010-05-07 | E-GEOD-21463 | biostudies-arrayexpress
Project description:In DRG neurons NRG1 type III intacellular domain (ICD) moves to the nucleus upon contact with Schwann cells. We aimed to investigate genes up/down regulated by ICD.
2014-09-26 | GSE61784 | GEO
Project description:Hyperglycemia is a risk factor for breast cancer-related morbidity and mortality. Hyperglycemia induces Neuregulin 1 (Nrg1) overexpression in breast cancer, which subsequently promotes tumor progression. However, molecular mechanisms underlying hyperglycemia-induced Nrg1 overexpression remain poorly understood. Here, We used DNA-protein pull-down using Nrg1 enhancer sequence as bait followed by LC/MS and identified RBPJ as a key component of the Nrg1 enhanceosome. We show that hyperglycemia causes active histone modifications at the Nrg1 enhancer, forming enhanceosome complexes where RBPJ, P300, and SETD1A are recruited to upregulate Nrg1 expression.
2022-12-21 | MSV000090951 | MassIVE
Project description:A homologue of the transcriptional repressor ScNrg1 described previously in the budding yeast and Candida albicans NRG1 wich plays an essential role in repressing hyphal development in both Saccharomyces cerevisiae and C. albicans, was found in Ustilago maydis. In S. cerevisiae it regulates a set of stress-responsive genes, also in Cryptococcus neoformans is involved in pathogenesis. In this work, we describe the effect of the absence of the U. maydis NRG1 gene in cell response to acid pH, mannosylerithritol lipids production, and cellular response to several stressful conditions. In U. maydis, NRG1 is required for filamentous growth and appears to be essential to respond to pH changes, and oxidative stress accurately. By comparing gene expression in a wild type strain versus nrg1 mutant strain of the fungus trough RNA_Seq analyses, it turned out to act as transcriptional factor altering the expression of 368 genes (205 up-regulated, 163 downregulated). Most relevant cellular processes affected by NRG1 are osmotic stress pathway, pH response, internal environmental sensor mechanism, represented by the genes Hog1, Rim101, and WCO1 respectively, also, all the genes present in the mannosylerithritol lipids production pathway, even under conditions not favorable for the production of glycolipids. Among previous specific functions described before for this transcriptional regulator as a glucose repressor, it seems to have an important role in metabolic adaptation, cellular transport, cell rescue defense and interaction with the environment.
2021-03-03 | GSE133840 | GEO
Project description:In a transgenic mouse model of Alzheimer disease (AD), cleavage of the amyloid precursor protein (APP) by the α-secretase ADAM10 prevented amyloid plaque formation and alleviated cognitive deficits. Furthermore, there was a positive influence of ADAM10 over-expression on neurotransmitter-specific formation of synapses and on synaptic plasticity. To assess the influence of ADAM10 on the gene expression profile in the brain we performed microarray analysis using RNA isolated from brains of five month old mice over-expressing either the α-secretase ADAM10 or a dominant-negative mutant (dn) of this enzyme. As compared to non-transgenic wild-type mice, 355 genes were found to be differentially expressed in ADAM10 transgenic mice and 143 genes in dnADAM10 mice. A higher number of genes was found to be differentially regulated in double-transgenic mouse strains additionally expressing the human APP V717I mutant (APP[V717I]). Thus, α-secretase cleavage of over-expressed APP[V717I] alters CNS gene expression additionally. Keywords: genetic modification
2009-01-22 | GSE10908 | GEO
Project description:The purpose of this study was to interrogate the role of EGF-family ligands, in particular Epidermal Growth Factor (EGF) and Neuregulin 1 (NRG1), as human intestinal stem cell niche factors. An established duodenal enteroid line derived from a 20.2 week post conception biological specimen was exposed to either EGF or NRG1 for five days, after which scRNA-seq was performed to assess changes in gene expression and cellular composition. In an independent experiment, scRNA-seq was performed on freshly isolated duodenal epithelium from a 15 week specimen cultured in the presence of EGF, NRG1, or both EGF and NRG1 after 2 passages.
2020-12-10 | E-MTAB-9720 | biostudies-arrayexpress