Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA277171 | ENA |
REPOSITORIES: ENA
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Project description:Expression profiling of latently infected cells using a custom tiling microarray HUVEC and TIME cells were infected BCBL-1-derived KSHV. Mock infected HUVEC and TIME cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. KSHV-infected cells are induced to enter lytic cycle with valproate or Adenovirus-RTA. Cells were harvested at indicated time points and analyzed.
2010-07-07 | GSE21972 | GEO
Project description:Hedgehog (Hh) signaling is critical for organogenesis, tissue homeostasis, and stem cell maintenance. Smoothened (SMO), the primary effector of Hh signaling, is expressed ectopically in human breast cancer, as well as in other cancers. Constitutive activation of SMO in mouse mammary glands leads to paracrine stimulation of proliferation, as well as hyperplasia. In canonical signaling, SMO functions via GLI transcription factor activation. However, recent data from Drosophila and mammalian cell lines indicate that SMO can function non-canonically as a G-protein coupled receptor (GPCR) by coupling to heterotrimeric G proteins, particularly those in the pertussis toxin (PTX)-sensitive G-alpha-i (Gai) class. Whether SMO functions as a GPCR in mammalian tissues in vivo is not known. Using genetically modified mouse models, we demonstrate here that SMO-induced stimulation of proliferation is PTX sensitive, and requires Gai2, but not Gai1 or Gai3. Our findings provide evidence for a non-canonical GPCR function of activated SMO in vivo, a finding that may have clinical significance given that most SMO-targeted agents were selected based largely on their ability to block canonical GLI-mediated transcription. Primary mammary epithelial cell RNA was deep-sequenced from mT-mG/SmoM2;MMTV-Cre (EGFP), mT-mG/SmoM2;MMTV-Cre (tdTomato), and mT-mG/SmoM2;+ cells to examine the effects of SmoM2 overexpression in the mammary gland.
2015-09-08 | E-GEOD-70210 | biostudies-arrayexpress
Project description:Differences in gene expression profiles regarding the expression of genes encoding for proteins with G protein-coupled receptor (GPCR) activity between SCLC and NSCLC and normal lung samples was successfully examined.
2012-08-25 | GSE40275 | GEO
Project description:Expression profiling of latently infected cells using a custom tiling microarray HUVEC and TIME cells were infected BCBL-1-derived KSHV. Mock infected HUVEC and TIME cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. KSHV-infected cells are induced to enter lytic cycle with valproate or Adenovirus-RTA. Cells were harvested at indicated time points and analyzed. Three condition experiment: mock infected, latently infected cells and lytically infected. Three cell types (BJAB cells served as uninfected controls for the BCBL-1 cells).
2010-07-07 | E-GEOD-21972 | biostudies-arrayexpress
Project description:G protein coupled receptor (GPCR) signalling covers three major mechanisms. GPCR agonist engagement allows for the G proteins to bind to the receptor leading to a classical downstream signalling cascade. The second mechanism is via the utilization of the β-arrestin signalling molecule and thirdly via transactivation dependent signalling. GPCRs can transactivate protein tyrosine kinase receptors (PTKR) to activate respective downstream signalling intermediates. In the past decade GPCR transactivation dependent signalling was expanded to show transactivation of serine/threonine kinase receptors (S/TKR). Kinase receptor transactivation enormously broadens the GPCR signalling paradigm. This work utilizes next generation RNA-sequencing to study the contribution of transactivation dependent signalling to total protease activated receptor (PAR)-1 signalling. Transactivation, assessed as gene expression, accounted for 50 percent of the total genes regulated by thrombin acting through PAR-1 in human coronary artery smooth muscle cells. GPCR transactivation of PTKRs is approximately equally important as the transactivation of the S/TKR with 209 and 177 genes regulated respectively, via either signalling pathway. This work shows that genome wide studies can provide powerful insights into GPCR mediated signalling pathways
2017-09-05 | GSE99770 | GEO
Project description:G protein-coupled receptor 37-like 1 (GPR37L1) is an orphan GPCR, and its function remains largely unknown. Here we report that Gpr37l1 and GPR37L1 are among the most highly expressed GPCR transcripts in mouse and human dorsal root ganglia (DRGs) and are selectively expressed in satellite glial cells (SGCs). Peripheral neuropathy following PTX-induced pain resulted in a downregulation of GPR37L1 plasma membrane expression in DRGs. Transgenic mice with Gpr37l1 deficiency exhibited impaired resolution of neuropathic pain symptoms following PTX-induced pain, whereas overexpression of Gpr37l1 in mouse DRGs reversed pain. GPR37L1 regulates the surface expression and function of these potassium channels. Thus, GPR37L1 in SGCs offers a new target for neuropathy protection and pain control.
2024-03-06 | GSE260669 | GEO
Project description:We used microarrays to compare the gene transcription level between HUVEC-kGPCR and HUVEC-vector stable cells. The goal is to identify the genes that are affected by KSHV kGPCR expression. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
2015-03-05 | GSE66503 | GEO
Project description:Receptor quaternary organization explains G protein-coupled receptor family structure.
| PRJNA397769 | ENA
Project description:Acidic tissue microenvironment is commonly found in a variety of pathophysiological conditions. GPR4 is a proton-sensing G protein-coupled receptor that is fully activated by acidic extracellular pH but has lesser activity at the physiological pH 7.4 and minimal activity at more alkaline pH. To determine the effects of GPR4 activation by acidosis on vascular endothelial cells, we examined the global gene expression of the acidosis response in primary human umbilical vein endothelial cells (HUVEC) with varying level of GPR4. HUVEC with endogenous or overexpressed GPR4 level (designated as HUVEC/Vector & HUVEC/GPR4 cells). Two treatment conditions: pH 6.4 vs. pH 8.4 for 5 h. Biological replicates: 4 HUVEC/Vector replicates (pH6.4 vs pH 8.4), and 4 HUVEC/GPR4 replicates (pH6.4 vs pH 8.4).
2013-04-25 | E-GEOD-40060 | biostudies-arrayexpress