RNA sequencing analysis of IECs from WT and PIM1+/- mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA980152 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24834388_1.fastq.gz | Fastqsanger.gz | |||
| SRR24834388_2.fastq.gz | Fastqsanger.gz | |||
| SRR24834389_1.fastq.gz | Fastqsanger.gz | |||
| SRR24834389_2.fastq.gz | Fastqsanger.gz | |||
| SRR24834390_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:PIM1 is constitutively active and involved in various cellular processes, including cell survival, proliferation, and differentiation by phosphorylating a wide range of substrates. We investigated whether PIM1 is involved in the pathogenesis of ulcerative colitis (UC).We performed RNA sequencing analysis in intestinal epithelial cells (IECs) from PIM1-deficient mice and WT mice to study the molecular mechanisms through which PIM1 regulates goblet cell numbers.
2024-07-30 | GSE234120 | GEO
Project description:Purpose: RhoB regulates cell functions, such as vesicular transport, apoptosis, autophagy, DNA repair, angiogenesis, proliferation, migration and invasion. We investigated whether RhoB is involved in the pathogenesis of ulcerative colitis (UC).We performed RNA sequencing analysis in intestinal epithelial cells (IECs) from RhoB-deficient mice and WT mice to study the molecular mechanisms through which RhoB regulates goblet cell numbers and epithelial regeneration and confirmed findings in colonic organoids from RhoB-deficient mice and WT mice and siRhoB transfected SW480 cells.
2022-09-27 | GSE170994 | GEO
Project description:RNA sequencing analysis of IECs from WT and RhoB-/- mice
| PRJNA718050 | ENA
Project description:The Pim (proviral integration site for Moloney murine leukemia virus) proteins form a serine threonine kinase family that regulates cell proliferation, migration and cell survival. Here we demonstrate for the first time that a Pim1 kinase plays an essential role in antiviral innate immune responses. Specifically, our in vivo, in vitro and RNA-sequencing analyses showed that Pim1 was quickly upregulated after Toll-like receptor (TLR) stimulation in a NF-kB-dependent manner and then promoted IFN-b production by forming a cell-surface complex composed of TRIF-signaling molecules and IRF3 that promoted IRF3 phosphorylation, nuclear translocation, and IFN-b production. As shown by Pim1 knockdown and knockout, Pim1 was essential for this role but its kinase activity was not involved. Pim1-deficiency increased the susceptibility of mice to poly I:C-induced sepsis. Our study uncovers a previously unrecognized role for Pim1 in antiviral innate immune responses, thus providing a new target for controlling viral infection.
2022-12-14 | GSE195582 | GEO
Project description:RNA-seq analysis of WT and Pim1-/- BMDMs
| PRJNA801277 | ENA
Project description:Purpose: To explore the molecular mechanisms of MST4 regulating intestinal stem cell homeostasis, RNA sequencing was performed to analyze the geome-wide change of MST4 KO IECs compared to those of WT mice. Methods: Total mRNA was extracted from IECs which were isolated from small intestines of Mst4 KO mice and WT mice (8 weeks) in triplicate respectively. Then RNA quality was assessed using an Agilent Bioanalyzer 2100 and the sample reads were sequenced using Illumina Hiseq 4000 platform. As a reasult, we got the transcript data using Hisat2 followed by Stringtie. qRT–PCR validation was performed using TaqMan and SYBR Green assays. Results: We mapped about 60 million sequence reads per sample to the mouse genome and identified about 50,000 transcripts in IECs of mice. Apprioximately 2,000 transcripts showed different expression between Mst4 KO and WT IECs, with a fold change ≥2 and p value <0.05. Gene set enrichment analysis (GSEA) showed a significantly negative enrichment of Wnt/b-catenin target genes and altered expression of 15 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Conclusion: Our study present the datiled transcripts analysis of IECs isolated from small intestines, with biologic replicates. Based on RNA-seq transcriptome characterization , we conclude a molecular mechanism of MST4 regulating intestinal stem cell homeostasis and provide a framework to understand the crosstalk of MST4 and Wnt/b-catenin signaling.
2021-09-15 | GSE132565 | GEO
Project description:PIM1 is constitutively active and involved in various cellular processes, including cell survival, proliferation, and differentiation by phosphorylating a wide range of substrates. We investigated whether PIM1 is involved in the pathogenesis of ulcerative colitis (UC).We performed RNA sequencing analysis in Caco2 cells infected with vector or PIM1 to study the molecular mechanisms through which PIM1 regulates goblet cell numbers.
2024-07-30 | GSE234122 | GEO
Project description:It has been estimated that about 11% of cellular genes present a functional E box to which MYC can associate on the genome. MYC silencing demonstrated that MYC recruits PIM1 at specific MYC binding sites and confocal microscopy following growth factor treatment, showed an elevated degree of nuclear co-localization of PIM1 with nascent transcripts and with MYC suggesting that PIM1 is recruited by MYC to a large number of sites. To understand the actual extension of PIM1 and MYC co-operation in gene transcription we performed expression profile analysis of 293 cells silenced either for MYC or PIM1 at 120 minutes after serum treatment. MYC silencing affected the expression of 1026 genes of which 818 were up-regulated and 208 were down-regulated. Comparison of genes regulated by MYC with those regulated by PIM1, by RNAi silencing, showed that PIM1 contributes to the regulation of 207 genes out of the 1026 MYC-regulated genes. Thus, a subset of 20% of MYC-regulated genes, are also regulated by PIM1. The co-regulated includes genes involved in cell metabolism, protein synthesis, cycle progression, and oncogenesis. Interestingly, a large number of genes are transcriptional factors, which suggests that PIM1 participates in MYC-dependent regulatory networks. Keywords: expression profiles
2007-07-31 | GSE7960 | GEO
Project description:Age-related decline in brain endothelial cell (BEC) function critically contributes to cerebrovascular and neurodegenerative disease. Comprehensive atlases of the BEC transcriptome have become available but results from proteomic profiling are lacking. To gain insights into endothelial pathways affected by aging, we developed a magnetic-activated cell sorting (MACS)-based mouse BEC enrichment protocol compatible with high-resolution mass-spectrometry and analysed the profiles of protein abundance changes across multiple time points between 3 and 18 months of age and identified Arf6 as one of the most prominently downregulated vesicle-mediated transport protein during BEC aging. To understand the role of ARF6 in human ECs, first we compared GFP-AAV treated human iECs differentiated from ARF6-KO vs WT iPSCs, next we compared ARF6-GFP-AAV vs GFP-AAV treated iECs differentiated from WT iPSCs. During the ARF6-KO vs WT iEC comparison we found 983 vs 741 proteins significantly down- and upregulated, respectively. Enrichment analyses of significantly downregulated proteins revealed mRNA processing among the most significantly affected biological processes. During the ARF6-GFP-AAV vs GFP-AAV treated WT iEC comparison we found 1106 vs 1218 proteins significantly down- and upregulated, respectively. Enrichment analyses of significantly upregulated proteins revealed endocytic recycling, retrograde transport (endosome to Golgi), and ER-Golgi vesicle-mediated transport among the most significantly affected biological processes. Specifically, ARF6 and its binding-protein GGA2, DNM1L and several subunits of the Conserved oligomeric Golgi complex (COG) were upregulated. Our approach uncovered changes not picked up by transcriptomic studies such as accumulation of vesicle cargo and receptor ligands including Apoe, a major regulator of brain lipid metabolism. Proteomic analysis of BECs from Apoe deficient mice revealed a signature of accelerated aging. To explore the role of APOE in human endothelial cells, in this experiment we compared human iECs differentiated from APOE-KO and WT iPSCs and found 326 significantly altered proteins. Enrichment analyses of significantly downregulated proteins revealed vesicle-mediated transport and vesicle fusion to be among the most significantly affected biological processes. Specifically, among the 34 significantly altered vesicle-mediated transport proteins 26 were downregulated. Accordingly, we found reduced levels of endocytosis of FM1-43FX in newly formed vesicles in APOE-KO iECs.
2024-02-15 | PXD045026 | Pride
Project description:Background: PIM1 is a constitutively active serine-threonine kinase regulating cell survival and proliferation. Increased PIM1 expression has been correlated with cancer metastasis by facilitating migration and anti-adhesion. Endothelial cells play a pivotal role in these processes by contributing a barrier to the blood stream. Here, we investigated whether PIM1 regulates mouse aortic endothelial cell (MAEC) monolayer integrity. Methods: Pim1-/-MAEC were isolated from Pim1 knockout mice and used in trypsinization-, wound closure assays, electrical cell-substrate sensing, immunostaining, cDNA transfection and as RNA source for microarray analysis. Results: Pim1-/-MAEC displayed decreased migration, slowed cell detachment and increased electrical resistance across the endothelial monolayer. Reintroduction of Pim1- cDNA into Pim1-/-MAEC significantly restored wildtype adhesive characteristics. Pim1-/--MAEC displayed enhanced focal adhesion and adherens junction structures containing vinculin and M-NM-2-catenin, respectively. Junctional molecules such as Cadherin 13 and matrix components such as Collagen 6a3 were highly upregulated in Pim1-/- cells. Intriguingly, extracellular matrix deposited by Pim1-/- cells alone was sufficient to induce the hyperadhesive phenotype in wildtype endothelial cells. Conclusion: Loss of Pim1 induces a strong adhesive phenotype by enhancing endothelial cell-cell and cell-matrix adhesion by the deposition of a specific extracellular matrix. Targeting PIM1 function therefore might be important to promote endothelial barrier integrity. Pim-1-/- mouse aortic endothelial cells were compared to wildtype cells
2012-10-29 | E-GEOD-32059 | biostudies-arrayexpress