RNAsequencing analysis of WT and RhoA-deficient mouse aveolar type 2 cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE175932 | GEO | 2021/06/02
REPOSITORIES: GEO
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Project description:RNAsequencing analysis of WT and RhoA-deficient mouse aveolar type 2 cells
| PRJNA734317 | ENA
Project description:The goal of this study is to identify transcriptomic effects of RhoA G17V expression in mouse CD4+ T lymphocytes. To this end, mice conditionally expressing RhoA G17V were generated by replacing exon 3 of RhoA with a minigene containing RhoA exons 3 to 6 flanked by loxP sites followed by a neomycin selection cassette and a mutant Rhoa exon 3 encoding the G17V substitution. These mice were then crossed with the CD4CreERT2 line (Tg(Cd4-cre/ERT2)11Gnri, Jackson Laboratories), which expresses a 4-hydroxi-tamoxifen-inducible form of the Cre recombinase under the control of the mouse Cd4 promoter to generate conditional inducible CD4 specific RhoA G17V mice (Rhoaco-G17V/+ CD4CreERT2). Mice were treated with vehicle only or Tamoxifen to induce expression of the RhoA G17V in CD4+ T cells. CD4CreERT2 mice were included as a negative control. CD4+ T cells were isolated from single cell suspensions of spleen by negative selection using the mouse naive CD4+ T Cell Isolation Kit (Milteny#130-104-453) according to the manufacturer’s protocol. Total RNA was extracted and standard Illumina poly-A RNA seq was performed. Naive mouse CD4+ T cells expressing RhoA G17V displayed an enrichment in a Tfh gene expression program.
2017-09-01 | GSE101340 | GEO
Project description:Rho family small GTPases serve as molecular switches in the regulation of diverse cellular functions including actin cytoskeleton remodeling, cell migration, gene transcription, and cell proliferation. Importantly, Rho overexpression is frequently seen in many carcinomas. However, published studies have almost invariably utilized immortal or tumorigenic cell lines to study Rho GTPase functions and there are no studies on the potential of Rho small GTPase to overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial cells (hMECs). We found that ectopic expression of wild-type RhoA as well as a constitutively-active RhoA mutant (G14V) in primary hMEC strains led to their immortalization and preneoplastic transformation. Significantly, RhoA-T37A mutant, known to be incapable of interacting with many well known Rho-effectors ,was also capable of immortalizing hMECs.Our results demonstrate that RhoA can induce the preneoplastic transformation of hMECs by altering multiple pathways linked cellular transformation and breast cancer. Through microarray analysis, we want to identify genes and pathways linked to RhoA induced hMECs immortalization. Experiment Overall Design: 4 samples, in triplicate analyses per sample.
2008-10-26 | E-GEOD-12917 | biostudies-arrayexpress
Project description:Using mice with a keratinocyte-restricted deletion of the RhoA gene, we explored its role in the regulation of gene expression in vivo and in vitro RNA was isolated from RhoA-null or wildtype keratinocytes, in two different conditions, freshly isolated (in vivo) or cultured (in vitro), using the RNeasy kit (Qiagen, Germany). Hybridization to GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA) was carried out at the Copenhagen University Hospital Microarray Center using standard protocols. 2 biological replicates were analyzed for each in vivo genotype (2 samples from RhoA-null, 2 from wildtype), while 3 replicates for each in vitro genotype.
2015-01-07 | E-GEOD-64714 | biostudies-arrayexpress
Project description:The small GTPase RhoA regulates a variety of cellular processes, including cell motility, proliferation, survival and permeability. In addition, there are reports suggesting that the RhoA-ROCK axis plays a role in VEGF-mediated angiogenesis, whereas other work has shown opposite effects. To elucidate this conflicting data, we examined HUVEC and HCAEC after stable overexpression (lentiviral transduction) of constitutively active (G14V/Q63L), dominant-negative (T19N), or wild-type RhoA using a variety of in vitro angiogenesis assays (proliferation, migration, tube formation, angiogenic sprouting, endothelial cell viability) and a HUVEC xenograft assay in immune incompetent NSGTM mice in vivo. We observed that expression of active as well as wild-type RhoA but not expression of dominant-negative RhoA significantly increased endothelial cell death as well as inhibited endothelial cell proliferation, migration, tube formation and angiogenic sprouting of endothelial cells in vitro and reduced HUVEC-related angiogenesis in vivo. Inhibition of RhoA by C3 transferase antagonized inhibitory RhoA effects and strongly enhanced VEGF-induced angiogenic sprouting in control-treated cells. In contrast, inhibition of RhoA effectors ROCK1/2 and LIMK1/2 had no significant effect on RhoA-related effects, but again increased angiogenic sprouting and migration of control-treated cells. In line with these data, VEGF did not activate RhoA in HUVEC as measured by a FRET-based biosensor. Furthermore, global transcriptome and subsequent bioinformatic gene ontology (GO) enrichment analyses revealed that constitutively active RhoA induces a differentially expressed gene pattern that is enriched for GO biological process terms such as mitotic nuclear division, cell proliferation, cell motility and cell adhesion and includes a significant decrease in VEGFR-2 and NOS3 expression. Thus, our data demonstrate that increased RhoA activity has the potential to trigger endothelial dysfunction and anti-angiogenic effects independently of its well-characterized downstream effectors ROCK and LIMK.
2022-07-06 | GSE182806 | GEO
Project description:Rho family small GTPases serve as molecular switches in the regulation of diverse cellular functions including actin cytoskeleton remodeling, cell migration, gene transcription, and cell proliferation. Importantly, Rho overexpression is frequently seen in many carcinomas. However, published studies have almost invariably utilized immortal or tumorigenic cell lines to study Rho GTPase functions and there are no studies on the potential of Rho small GTPase to overcome senescence checkpoints and induce preneoplastic transformation of human mammary epithelial cells (hMECs). We found that ectopic expression of wild-type RhoA as well as a constitutively-active RhoA mutant (G14V) in primary hMEC strains led to their immortalization and preneoplastic transformation. Significantly, RhoA-T37A mutant, known to be incapable of interacting with many well known Rho-effectors ,was also capable of immortalizing hMECs.Our results demonstrate that RhoA can induce the preneoplastic transformation of hMECs by altering multiple pathways linked cellular transformation and breast cancer. Through microarray analysis, we want to identify genes and pathways linked to RhoA induced hMECs immortalization.
2008-09-26 | GSE12917 | GEO
Project description:RHOA is a recurrently mutated gene in diffuse-type gastric cancer, whose molecular influence in gastric cancer has not been well uncovered. We aimed to clarify the contribution of RHOA to pro-oncogenesis to improve the understanding of the role of RHOA as a therapeutic target. We performed microarray analysis after RHOA knockdown for HGC-27, AGS, CCK-81, and SW948.
2021-02-01 | GSE110237 | GEO
Project description:RHO subfamily of small GTPases comprise highly conserved family members RHOA, RHOB, and RHOC which cycle between GTP-bound 'active' and GDP-bound 'inactive' states. In the active form, RHO proteins interact with a variety of downstream effector proteins, controlling their activity and function. Many of the RHO subfamily effector proteins such as ROCK, PKN, and mDIA, are key regulators of actin cytoskeleton and cell motility. To identify novel effector proteins for RHOA,we carried out a GST-pulldown from heavy or light SILAC labelled HeLa cells using GST tagged GTP-bound RHOA, or GST alone control, as bait. Pulldowns were performed in duplicates with switched labellings. Specific interactors were destinguished from the background on the basis of SILAC Heavy to Light ratios between GST-RHOA and GST alone pulldowns.
2016-11-01 | PXD004934 | Pride
Project description:Asthma influences brain health both functionally (emotions) and structurally (neurodegeneration). Although airway inflammation is proposed to initiate afferent communications with the brain, the associated patterns of airway inflammation and gene-expression profiles are not established. Here, we investigate associations of gene expression in response to allergen challenge in the lung with functional magnetic resonance imaging (fMRI) in the brain.
2023-08-01 | GSE182733 | GEO
Project description:Microarray transcriptomic analysis of formalin-fixed, paraffin-embedded small intestinal tumors from control (Apcmin/+;Vil-Cre-/-;RhoADN/-) and DN-RhoA (Apcmin/+;Vil-CreTG/-;RhoADN/-) mice.
2014-11-21 | E-MTAB-2981 | biostudies-arrayexpress