CRISPR mediated deletion of RP11-326A19.4/CARMAL
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE142098 | GEO | 2019/12/17
REPOSITORIES: GEO
Similar Datasets
Project description:CRISPR mediated deletion of RP11-326A19.4/CARMAL
| PRJNA595900 | ENA
Project description:Transfection experiments aimed at understanding the impact of upregulation a lncRNA (RP11-326A19.4) on genome-wide transcription
2019-06-11 | GSE132451 | GEO
Project description:Transfection experiments aimed at understanding the impact of upregulating lncRNA RP11-326A19.4 on the transcriptome; follow-up of GSE132451
2019-12-17 | GSE142097 | GEO
Project description:To investigate the global genes regulated by lncRNA-SLCC1(RP11-400N13.2), high-throughput mRNA sequencing (RNA-Seq) was performed to compare the expression profile between DLD-1 cells transfected with control siRNA or lncSLCC1 siRNA.
2023-05-01 | GSE149783 | GEO
Project description:Methods and Materials The high throughput RNA sequencing (RNA-seq) data from kidney biopsies of LN patients and controls was applied studied to screen for candidate lncRNAs. Quantitative real-time polymerase chain reaction(RT-qPCR) was used to detect the expression of lncRNAs and individual IFN-stimulated genes (ISGs). Western blotting and dual-luciferace luciferase reporter assay was adopted to explore the specific function of the candidate lncRNA. Results The expression of lncRNA RP11-2B6.2 was significantly increased in the kidney tissues from LN patients compared with those from healthy controls, and positive correlated with the degree of disease activity and renal injuryinjuries. Additionally, expression of LncRNA RP11-2B6.2 could be stimulated by type I IFN. Silencing it RP11-2B6.2 significantly reduced the expression of a group of interferon-stimulating genes(ISGs) including IFIT1, OAS1, etc., Furthermore, it lncRNA RP11-2B6.2 affected the expression of IFN alpha and beta receptor subunit 1 (IFNAR1), phosphorylation of Jak1 and Stat1, and the luciferase activity induced by interferon stimulated response element(ISRE). Conclusion Long noncoding RNA RP11-2B6.2 is a positive regulator of the type I IFN signaling pathway in LN. It LncRNA RP11-2B6.2 may contribute to the pathogenesis of LN and provide served as a potentially therapeutic target.
2019-05-01 | GSE98422 | GEO
Project description:Objective: The aim of this study was to reveal the function of the long non-coding RNA (lncRNA) RP11-556E13.1 (RP11) and its clinical significance in hepatocellular carcinoma. Methods: LncRNA and mRNA expression profiling was performed using lncRNA and mRNA microarrays in 5 pairs of HCC and adjacent tissues. 112 paired HCC and adjacent tissue samples were analyzed by semiquantitative real-time polymerase chain reaction (sqRT-PCR) to evaluate the expression of RP11 and its possible associated clinical significance. Smart silencer RNA (siRNA) was used to knockdown the expression of RP11 in HCC cells. After knockdown, the function of RP11 was determined in vitro using some kinds of cell functional experiments in HCC cells including cell proliferation assay, cell apoptosis assay and cell cycle assay. Western blotting (WB) was performed to detect proteins that were presumably associated with these functional changes. An Affymetrix Human HTA2.0 microarray was used to detect differentially expressed genes in HCC cells after RP11 knockdown. GO enrichment and KEGG pathway enrichment analysis were then performed to elucidate the biological roles of these differentially expressed mRNAs.
2022-04-18 | GSE200861 | GEO
Project description:To further explore t of the role lncRNAs in glaucoma patients, we have employed lncRNAs microarray expression profiling as a discovery platform to identify abnormal genes under oxidative stress in HTMCs. Our results revealed that lncRNA-RP11 was significantly up-regulated under oxidative stress in HTMCs. Further studies found that lncRNA-RP11-820 directly binds miR-3178, through which regulates the expression of MYOD1. Importantly, MYOD1 can transcriptionally activate ECM genes. Furthermore, MYOD1 binds STAT3 to form a transcription complex, and transcriptionally activates ECM genes expression in HTMCs. Taken together, our data established taht oxidative stress induced lncRNA-RP11-820 plays a key role in regulating miR-3178/MYOD1/ECM axis in HTMCs.
2019-02-07 | GSE126170 | GEO
Project description:Downregulations of TCAM1P-004 and RP11-598D14.1 were frequently observed in HCC tumors as compared to adjacent non-tumor tissues. To further study the molecular functions of TCAM1P-004 and RP11-598D14.1, we attempted to identify the gene targets regulated by either lncRNAs. Knockdown of TCAM1P-004 or RP11-598D14.1 were achieved by transduction of lentivirus carrying respective shRNAs in non-tumor hepatocyte MIHA cells. Diffferentially expressed genes after knockdown of the lncRNAs were compared to cells tranduced with lentivirus carrying scramble shRNAs.
2018-10-24 | E-MTAB-7280 | biostudies-arrayexpress
Project description:RP11-115N4.1 was identified as the most differentially expressed lncRNA which was highly upregulated in peripheral blood of non-pregnant URSA patients (P = 3.63E-07, Fold change = 2.96),andthis dysregulation was further validated in approximately 26.7% additional patients (4/15). RP11-115N4.1 expression was detected in both lymphocytes and monocytes of human peripheral blood, andin vitro overexpression of RP11-115N4.1 decreased cell proliferation in K562 cellssignificantly. Furthermore, heat-shock HSP70 genes (HSPA1A and HSPA1B) were found to be significantly upregulated upon RP11-115N4.1 overexpression by transcriptome analysis (HSPA1A (P = 4.39E-08, Fold change = 4.17), HSPA1B (P = 2.26E-06, Fold change = 2.99)).RNApull down and RNA immunoprecipitation assay (RIP) analysis demonstrated that RP11-115N4.1 bound to HNRNPH3 protein directly, which in turn activateheat-shock proteins (HSP70) analyzed by protein-protein interaction and HNRNP` knockdown assays. Most importantly,the high expression of HSP70 was also verified in the serum of URSA patients and the supernatant of K562 cells with RP11-115N4.1 activation, andHSP70 in supernatant can exacerbate inflammatory responses in monocytes by inducing IL-6, IL-1β and TNF-α and inhibit the migration of trophoblast cells, which might associate with URSA.
2021-08-11 | GSE179996 | GEO
Project description:Through deep RNA-seq of human monocyte-derived macrophages, we identified RP11-184M15.1, a human macrophage-specific lincRNA, to be highly induced in the cytoplasm of IL-4-stimulated macrophage. Preliminary data showed that treatment of IL-4-stimulated THP1 human macrophages with RP11-184M15.1 small interfering RNA (siRNA) repressed apoptosis of resolving macrophages, as shown by decreased Annexin V+ macrophages, and reduced protein expression of cleaved PARP. Biotinylated RP11-184M15.1 pulldown coupled with mass spectrometry indicated an interaction between RP11-184M15.1 and zinc finger RNA-binding protein (ZFR). RIP corroborated the proposed interaction between RP11-184M15.1 and ZFR. RNAInter revealed mRNAs predicted to interact with ZFR, and some of those genes (e.g., ALYREF, CCNYL1) were also differentially expressed in RNA-seq data of control versus RP11-184M15.1 knockdown in IL-4-stimulated THP1 macrophages. qPCR validated that ALYREF and CCNYL1 expression are reduced with RP11-184M15.1 knockdown. In contrast, with ZFR siRNA, ALYREF and CCNYL1 mRNA expressions were elevated. Thus, a hypothesis to be further tested is that RP11-184M15.1 interacts with ZFR to regulate mRNA stability in IL-4-stimulated macrophages. Nuclear RNA export factor 1 (NXF1) was also validated by RIP to interact with RP11-184M15.1. NXF1 is a known interacting partner of ALYREF in the transcription-export (TREX) complex. With RP11-184M15.1 knockdown, the protein level of ALYREF decreased, and Ingenuity Pathway Analysis (IPA) of RNA-seq data of control versus RP11-184M15.1 knockdown revealed that THO complex subunit 5 homolog (THOC5), another component of the TREX complex, may be an upstream regulator. In addition, past studies have revealed that ALYREF and NXF1 are involved in nuclear export of inflammatory mRNAs and proinflammatory macrophage phenotype, respectively. With RP11-184M15.1 knockdown, there was decreased expression of inflammatory macrophage-associated genes. It may be possible that RP11-184M15.1 functions in mRNA export, along with NXF1 and ALYREF.
2022-11-23 | GSE218308 | GEO