Analysis of mRNA levels of GPCR and GPCR-related signaling proteins in 3 mouse cell lines: AtT20, BV2 and N18
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE25886 | GEO | 2011/02/01
SECONDARY ACCESSION(S): PRJNA142481
REPOSITORIES: GEO
Similar Datasets
Project description:Measurements of mRNA levels for non-chemosensory GPCRs, G proteins and selected G protein targets. Three mouse cell lines (AtT20, BV2 and N18), 4 replicates each. Overall data set includes mRNA levels for ~24,000 genes.
2011-02-01 | E-GEOD-25886 | biostudies-arrayexpress
Project description:Measurements of mRNA levels for non-chemosensory GPCRs, G proteins and selected G protein targets.
2011-02-01 | GSE25894 | GEO
Project description:Measurements of mRNA levels for non-chemosensory GPCRs, G proteins and selected G protein targets. HEK293 cell line, 4 replicates. Overall data set includes mRNA levels for ~24,000 genes.
2011-02-01 | E-GEOD-25894 | biostudies-arrayexpress
Project description:BackgroundG protein coupled receptors (GPCRs) are one of the most widely studied gene superfamilies. Thousands of GPCR research studies have utilized heterologous expression systems such as human embryonic kidney cells (HEK293). Though often treated as 'blank slates', these cell lines nevertheless endogenously express GPCRs and related signaling proteins. The outcome of a given GPCR study can be profoundly influenced by this largely unknown complement of receptors and/or signaling proteins. Little easily accessible information exists that describes the expression profiles of the GPCRs in cell lines. What is accessible is often limited in scope - of the hundreds of GPCRs and related proteins, one is unlikely to find information on expression of more than a dozen proteins in a given cell line. Microarray technology has allowed rapid analysis of mRNA levels of thousands of candidate genes, but though often publicly available, the results can be difficult to efficiently access or even to interpret.ResultsTo bridge this gap, we have used microarrays to measure the mRNA levels of a comprehensive profile of non-chemosensory GPCRs and over a hundred GPCR signaling related gene products in four cell lines frequently used for GPCR research: HEK293, AtT20, BV2, and N18.ConclusionsThis study provides researchers an easily accessible mRNA profile of the endogenous signaling repertoire that these four cell lines possess. This will assist in choosing the most appropriate cell line for studying GPCRs and related signaling proteins. It also provides a better understanding of the potential interactions between GPCRs and those signaling proteins.
| S-EPMC3024950 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-02-01 | GSE25901 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE25886: Analysis of mRNA levels of GPCR and GPCR-related signaling proteins in 3 mouse cell lines: AtT20, BV2 and N18 GSE25894: Analysis of mRNA levels of GPCR and GPCR-related signaling proteins in the HEK293 cell line Refer to individual Series
2011-02-01 | E-GEOD-25901 | biostudies-arrayexpress
Project description:Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the loss of dopaminergic (DA) neurons in the substantia nigra (SN) and subsequent DA depletion in the striatum. Microglia activation and nigral iron accumulation play important roles in the pathogenesis of PD. Activated microglia show increased iron deposits. However, the relationship between microglia activation and iron accumulation remains unclear. In the present study, we aimed to determine how iron levels affect interleukin-6 (IL-6) synthesis, and the effect of IL-6 on cellular iron metabolism in BV2 microglial cells.IL-6 mRNA was up-regulated after FAC treatment for 12 h in BV2 cells. Iron regulatory protein 1 (IRP1) and divalent metal transporter 1 (DMT1) were up-regulated and iron exporter ferroportin 1 (FPN1) was down-regulated in BV2 cells after 24 h of IL-6 treatment. Phosphorylated JNK increased significantly compared to the control after BV2 cells were treated with IL-6 for 1 h. Pretreatment with SP600125 attenuated the up-regulation of IRP1 and DMT1 and down-regulation of FPN1 (compared to IL-6-treated group). These results suggest that iron load could increase IL-6 mRNA expression in BV2 cells. Further, IL-6 likely up-regulates IRP1 and DMT1 expression and down-regulates FPN1 expression in BV2 microglial cells through JNK signaling pathways.
| S-EPMC5495437 | biostudies-literature
Project description:G protein-coupled receptors (GPCRs) are the largest class of cell surface signaling proteins; they participate in all physiological processes and are the targets of 30% of marketed drugs. Typically, nanomolar-micromolar concentrations of ligand are used to activate GPCRs in experimental systems. However, by measuring cAMP with increased spatial and temporal resolution, we can now detect GPCR responses to an extraordinarily wide range of ligand concentrations: from attomolar to millimolar. Mathematical modeling shows that the addition of femtomolar concentrations of ligand can activate a significant proportion of cells provided that a cell can be activated by 1-2 binding events. In addition to cAMP, activation of the endogenous b2-adrenoceptor (b2AR) and muscarinic M3R by femtomolar concentrations of ligand in cell lines and human cardiac fibroblasts causes sustained increases in nuclear ERK or cytosolic PKC, respectively. These responses are spatially and temporally distinct from those that occur at higher concentrations of ligand, and result in a unique proteomic profile. This highly sensitive signaling is dependent on the GPCRs forming pre-assembled higher-order signaling complexes at the plasma membrane. Recognizing that GPCRs respond to ultra-low concentrations of neurotransmitters and hormones challenges established paradigms of drug action and provides a new dimension of GPCR activation that is quite distinct from that typically observed.
2018-10-11 | PXD011033 | Pride
Project description:Osmosensors play essential roles in maintaining body fluidic balance in the animal kingdom. However, the molecular identities of osmosensors in mammals are still elusive. TRP channels have been proposed to be candidate osmosensors, but their roles in regulating body fluid homeostasis are still controversial. The major difficulty in identifying osmosensors in animals, is in part because of the lack of efficient screening methods. Here, we designed and conducted a neuronal activity-based genetic screen to identify the first osmosensors in animal kingdom using C. elegans. Previous studies show G proteins are required for C. elegans sensing osmotic stimuli. Thus, we proposed that the osmosensors are GPCRs. To identify the GPCRs enriched in ASH neurons, which are the major osmosensing neurons, we did RNA-seq after FACS sorting for ASH. After screening the enriched GPCRs in ASH, we successfully found one GPCR, OSGR-1, functions as an osmosensor in C. elegans. We also found, its closest paralog, OSGR-2, is also an osmosensor. This is also the first shown that GPCRs are capable of sensing osmolarity, which will facilitate the identification of osmosensors in other animals.
2024-03-01 | GSE248324 | GEO
Project description:Acute myeloid leukemia (AML) is an aggressive and heterogenous hematological malignancy. In elderly patients, AML incidence is high and has a poor prognosis due to a lack of effective therapies. G-protein coupled receptors (GPCRs) play integral roles in physiological processes and human diseases. Particularly, one-third of adhesion GPCRs, the second largest group of GPCRs, are highly expressed in hematopoietic stem and progenitor cells or lineage cells. Therefore, we investigated the role of adhesion GPCRs in AML and whether they could be harnessed as anti-leukemia targets. Systematic screening of the impact of adhesion GPCRs on AML functionality by combined bioinformatic and functional analyses revealed high expression of ADGRE2 in AML, particularly in leukemic stem cells (LSCs), which was associated with poor patient outcomes. Silencing ADGRE2 not only exerted anti-leukemia effects in AML cell lines and AML patient-derived cells in vitro but also delayed AML progression in xenograft models in vivo. Mechanistically, ADGRE2 activated PLC-β/PKC/MEK/ERK signaling to enhance expression of AP-1 and transcriptionally drive expression of DUSP1, a protein phosphatase. DUSP1 de-phosphorylated Ser16 in the J-domain of the co-chaperone DNAJB1, which facilitated DNAJB1-HSP70 interaction and maintenance of proteostasis in AML. Finally, combined inhibition of MEK, AP-1, and DUSP1 exhibited robust therapeutic efficacy in AML xenograft mouse models. Collectively, this study deciphers the roles and mechanisms of ADGRE2 in AML and provides a promising therapeutic strategy for treating AML.
2024-03-19 | GSE261574 | GEO