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Microarray gene expression analysis of mouse fetal liver erythroblasts after plek2 knockdown

ABSTRACT: The goal of this experiment is to determine the expression levels of the genes that are influenced by the downregulation of plek2.

ORGANISM(S): Mus musculus

PROVIDER: GSE48332 | GEO | 2013/06/28

SECONDARY ACCESSION(S): PRJNA209973

REPOSITORIES: GEO

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Microarray gene expression analysis of mouse fetal liver erythroblasts after plek2 knockdown

Project description:The goal of this experiment is to determine the expression levels of the genes that are influenced by the downregulation of plek2. TER119 negative mouse fetal liver erythroblasts were purified and infected with control and plek2 shRNA retroviruses and cultured in Epo free medium for 24 hours followed by Epo medium for 24 hours. Microarray gene expression profile analysis was performed using an Illumina platform with a biological triplicate of the same experiment.

2013-06-28 | E-GEOD-48332 | biostudies-arrayexpress

PLEK2 functions as a co-factor of YTHDF2 to enhance TYMS mRNA stability in colorectal cancer

Project description:High expression of nucleotide synthetic enzyme thymidylate synthase (TYMS) is responsible for the resistance to fluorouracil (FU) treatment and worse survival in colorectal cancer. Herein, we revealed that Pleckstrin-2 (PLEK2), highly expressed in CRC, enhanced TYMS mRNA stability via its interaction with YTHDF2 in a m6A-dependent manner. Silencing of PLEK2 led to the downregulation of TYMS, and consequent inhibition of CRC cell proliferation via the cellular senescence. Additionally, PLEK2 is also required for CRC cell migration, invasion and stemness-like properties. PLEK2 inhibition is sufficient to ameliorate the progression of CRC. Moreover, loss of PLEK2 inhibited AOM/DSS-induced colonic tumorigenesis in vivo. Together, our study identified PLEK2 as a key regulator for the progress of CRC via the regulation of TYMS expression, and demonstrated that PLEK2 is a novel therapeutic target for CRC.

2025-07-23 | GSE252234 | GEO

Quantitative Analysis of JAK2V617F/+ Plek2+/+ and JAK2V617F/+ Plek2-/- erythroblast and hematopoietic stem cells/ progenitor cells Transcriptomes

Project description:V617F driver mutation of JAK2 is the leading cause of the Philadelphia-chromosome-negative myeloproliferative neoplasms (MPNs). Loss of Plek2 ameliorated JAK2V617F-induced myeloproliferative phenotypes including erythrocytosis, neutrophilia, thrombocytosis, and splenomegaly, thereby reverting the widespread vascular occlusions and lethality of JAK2V617F knockin mice. To reveal the role of Plek2 in the pathogenesis of JAK2V617F-induced MPNs and the detail mechanisms of its rescue, we performed RNA sequencing to analyze the gene expression profiles change between JAK2V617F/+ Plek2+/+ and JAK2V617F/+ Plek2-/- erythroblasts and hematopoietic stem/progenitor cells.

2019-04-11 | GSE97658 | GEO

Effect of PLEK2 knockdown on the gene expression of HCT116 cells

Project description:To investigate the effect of PLEK2 in the regulation of HCT116 cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of HCT116 cells.

2025-07-23 | GSE252372 | GEO

Effects of over-expression of PLEK2 on gene expression in 22RV1 cells

Project description:We previously found that loss of Plek2 decreased Akt activity and reverted disease phenotypes in hematopoietic system specific Pten knockout mice. Pten knockout mice also show prostate cancer phenotype. Using a well known Pten prostate-specific knockout mouse model, we found that loss of Plek2 also reverted tumorigenesis of prostate cancer via decreasing Akt pathway activity. Furthermore, we found that PLEK2 over-expression increased AKT pathway activity and promoted proliferation in 22RV1 cells which is a kind of prostate cancer cell line. To explore additional pathway which PLEK2 may involve in prostate cancer, we performed RNA sequencing in PLEK2 over-expressed and control 22RV1 cells.

2024-07-09 | GSE253449 | GEO

Reactivating Fetal Hemoglobin Expression in Human Adult Erythroblasts Through BCL11A Knockdown Using Targeted Endonucleases.

Project description:We examined the efficiency, specificity, and mutational signatures of zinc finger nucleases (ZFNs), transcriptional activator-like effector nucleases (TALENs), and clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 systems designed to target the gene encoding the transcriptional repressor BCL11A, in human K562 cells and human CD34+ progenitor cells. ZFNs and TALENs were delivered as in vitro transcribed mRNA through electroporation; CRISPR/Cas9 was codelivered by Cas9 mRNA with plasmid-encoded guideRNA (gRNA) (pU6.g1) or in vitro transcribed gRNA (gR.1). Analyses of efficacy revealed that for these specific reagents and the delivery methods used, the ZFNs gave rise to more allelic disruption in the targeted locus compared to the TALENs and CRISPR/Cas9, which was associated with increased levels of fetal hemoglobin in erythroid cells produced in vitro from nuclease-treated CD34+ cells. Genome-wide analysis to evaluate the specificity of the nucleases revealed high specificity of this specific ZFN to the target site, while specific TALENs and CRISPRs evaluated showed off-target cleavage activity. ZFN gene-edited CD34+ cells had the capacity to engraft in NOD-PrkdcSCID-IL2Rγnull mice, while retaining multi-lineage potential, in contrast to TALEN gene-edited CD34+ cells. CRISPR engraftment levels mirrored the increased relative plasmid-mediated toxicity of pU6.g1/Cas9 in hematopoietic stem/progenitor cells (HSPCs), highlighting the value for the further improvements of CRISPR/Cas9 delivery in primary human HSPCs.

| S-EPMC5023398 | biostudies-literature

Expression profiling of mouse fetal liver late erythroblasts after knockdown of Xpo7

Project description:To determine the transcriptional function (if any) of the presumed nuclear export protein Xpo7 or RanBP16 Murine fetal liver erythroid precursors (Ter119-negative cells) were isolated from C57Bl6 E14.5 embryos by magnetic depletion and infected with retroviruses containing shRNA constructs against Xpo7. They were then cultured in Epo-containing media (2U/mL) for 36hrs until they were fully differentiated and then sorted by FACS for GFP+ (infected) cells in order to isolate total RNA to be used for the profiling.

2014-01-29 | GSE54457 | GEO

Expression profiling of mouse fetal liver late erythroblasts after knockdown of Xpo7

2014-01-29 | E-GEOD-54457 | biostudies-arrayexpress

Microarray analysis of wildtype and Klf1-/- E13.5 fetal liver

Project description:The aim of this experiment was to investigate the role of KLF1 in the fetal liver Affymetrix microarrays were performed on fetal liver cells from E13.5 wildtype and Klf1-/- mice.

2012-02-07 | GSE35594 | GEO

HMGA2 Moderately Increases Fetal Hemoglobin Expression in Human Adult Erythroblasts.

Project description:Induction of fetal hemoglobin (HbF) has therapeutic importance for patients with beta-hemoglobin disorders. Previous studies showed that let-7 microRNAs (miRNAs) are highly regulated in erythroid cells during the fetal-to-adult developmental transition, and that targeting let-7 mediated the up-regulation of HbF to greater than 30% of the total globin levels in human adult cultured erythroblasts. HMGA2 is a member of the high-mobility group A family of proteins and a validated target of the let-7 family of miRNAs. Here we investigate whether expression of HMGA2 directly regulates fetal hemoglobin in adult erythroblasts. Let-7 resistant HMGA2 expression was studied after lentiviral transduction of CD34(+) cells. The transgene was regulated by the erythroid-specific gene promoter region of the human SPTA1 gene (HMGA2-OE). HMGA2-OE caused significant increases in gamma-globin mRNA expression and HbF to around 16% of the total hemoglobin levels compared to matched control transductions. Interestingly, no significant changes in KLF1, SOX6, GATA1, ZBTB7A and BCL11A mRNA levels were observed. Overall, our data suggest that expression of HMGA2, a downstream target of let-7 miRNAs, causes moderately increased gamma-globin gene and protein expression in adult human erythroblasts.

| S-EPMC5115839 | biostudies-literature

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