Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1028364 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To identify genes regulated by Cav1 Affymetrix Human Genome U133 Plus 2.0 GeneChip Hep3B cells with or without knockdown of Cav1
2016-03-01 | E-GEOD-75994 | biostudies-arrayexpress
Project description:In this experiment we demonstrate the use of an inhibitor of the KDM5 family of histone demethylases, KDM5-C70, on H3K4me3 marks in the multiple myeloma cell line MM1S. KDM5-C70 increases H3K4me3 in a global fashion across the genome. Examination of H3K4me3 mark across MM1S cells treated with either KDM5-C70 or vehicle control
2016-04-05 | E-GEOD-78206 | biostudies-arrayexpress
Project description:Microarray analysis of bladder RNA revealed down-regulation of CAV1, CAV2 and CAV3 gene transcription in both mice with obstruction-induced BSM hypertrophy, and in men with benign prostatic hyperplasia Knockout of NF-κB subunits or shRNA-mediated knockdown of GATA-6 in BSM increased CAV1, CAV2 and CAV3 transcription and promoter activity.
2018-12-17 | GSE107427 | GEO
Project description:To determine the role of Ago2/Cav1 interaction in Ago2 function, we used miRNA arrays to examine the levels of miRNA in cancer cells whose Ago2/Cav1 interaction was inhibited by P2 or P2S peptides. Disruption of Ago2/Cav1 interaction by P2 peptides resulted in fluctuations in different miRNAs in cancer cells
2024-04-18 | GSE239499 | GEO
Project description:ARP1, MM1S, and RPMI8226 myeloma cells lines were analyzed by ChIP-seq using antibodies against BRD4, MED1, IKZF1, ETV4
2019-03-13 | GSE128024 | GEO
Project description:Expression data comparing Hep3B Caveolin-1 (Cav1) knockdown cells with Hep3B non-target control cells
| PRJNA305915 | ENA
Project description:Immunoprecipitation was performed on Cav1 WT and KO cell line using Cav1 antibody. Proteins that interact with Cav1 were detected. Interleukin receptor (IR) antibody was also used on Cav1 WT and KO cells for immunoprecipitation. Proteins that interact with IR were detected.
2022-06-30 | MSV000089780 | MassIVE
Project description:Forkhead box protein 3 (FOXP3) is implicated in tumor progression and prognosis in various types of tumor cells. We have recently reported that FOXP3 inhibited proliferation of gastric cancer (GC) cells through activating the apoptotic signaling pathway. In this study, we found that over-expression of FOXP3 inhibited GC cell migration, invasion and proliferation. Then, the label-free quantitative proteomic approach was employed to further investigating the down-stream proteins regulated by FOXP3, resulting in a total of 3,978 proteins quantified, including 186 significantly changed proteins. Caveolin-1 (CAV1), as a main constituent protein of caveolae, was one of those changed proteins up-regulated in FOXP3-overexpressed GC cells, moreover, it was assigned as one of the node proteins in the protein-protein interaction network and the key protein involved in focal adhesion pathway by bioinformatics analysis. Further biological experiments confirmed that FOXP3 directly bound to the promoter regions of CAV1 to positively regulate CAV1 transcription in GC cells. In summary, our study suggested that FOXP3 can be considered as a tumor suppressor in GC via positively regulating CAV1 through transcriptional activation, and this FOXP3-CAV1 transcriptional regulation axis may play an important role in inhibiting invasion and metastasis of GC cells.
2017-11-03 | PXD007725 | Pride
Project description:Chronic ocular inflammation is associated with many retinal degenerative diseases that result in vision loss. The immune-privileged environment and complex organization of retinal tissue allow for the retina’s essential role in visual function processes, yet confound inquiries into cell-specific inflammatory effects that lead to retinal dysfunction and degeneration. Caveolin-1 (Cav1) is an integral membrane protein expressed in many retinal cell populations and has been implicated in retinal immune regulation. However, the direction (i.e., promotion or inhibition) in which Cav1 regulates inflammatory processes in the retina (as well as in other tissues) remains unclear. Previously, we showed that global-Cav1 depletion in the retina paradoxically resulted in reduced retinal inflammatory cytokine production with concurrent elevated retinal immune cell infiltration. We hypothesized that our previous results could be explained by cell-specific Cav1 functions in the retina. Here, we utilized our Chx10 (visual system homeobox 2)-Cre knockout model to deplete Cav1 specifically in the neural retinal (NR) compartment in order to clarify the role of neural retinal-specific Cav1 (NR-Cav1) in the retinal immune response to intravitreal LPS (lipopolysaccharide) challenge. Our data support that neural retinal-derived Cav1 promotes retinal tissue inflammation as Chx10-mediated Cav1 depletion was sufficient to suppress both retinal cytokine production and immune cell infiltration following inflammatory stimulation. Additionally, we identify Traf3 (tumor necrosis factor (TNF) receptor-associated factor 3) as a highly expressed potential immune modulator in retinal tissue that is upregulated with NR-Cav1 depletion. Furthermore, this study highlights the importance for understanding the role of Cav1 (and other proteins) in cell-specific contexts.
2021-09-08 | PXD016872 | Pride