Gene expression profile of Ba/F3 variant (#BEB1) cells that have binding ability to Ecrg4
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA416768 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Esophageal cancer-related gene 4 (Ecrg4) encodes a hormone-like peptide, and is thought to be involved in a variety of physiological phenomena including tumor suppressor function. Recent progress of Ecrg4 reveals that Ecrg4 peptides are pro-inflammatory and induce the expression of several cytokines and chemokines. However, detailed molecular mechanisms of Ecrg4 signaling, especially the receptors for Ecrg4 peptides, remain poorly understood. Here, using retrovirus-mediated expression cloning, we identified lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) as a membrane protein bound for amino acid residues 71-132 of Ecrg4, Ecrg4(71-132). Moreover, not only LOX-1 but also several scavenger receptors such as Scarf1, Cd36 and Stabilin-1 efficiently internalized Ecrg4(71-132) into cells. The broad scavenger receptor competitive inhibitor polyinosinic acid reduced both the internalization of Ecrg4(71-132) and activation of NF-kB in microglia. In addition, this activation is dependent on Myd88, an adaptor protein to recruit signaling proteins to TLR and IL-1R receptors with induction of several immune response. These data suggest that multiple scavenger receptors recognize Ecrg4(71-132) and transduce its signals along with TLR/IL-1R receptors in microglia.
2018-03-23 | GSE106400 | GEO
Project description:Transcriptional profiling of transformed Ba/F3 cells by myeloproliferative neoplasm-associated JAK2 V617F mutant comparing control Ba/F3 cells expressing wild type JAK2.
2013-10-31 | GSE34239 | GEO
Project description:Transcriptional profiling of transformed Ba/F3 cells by myeloproliferative neoplasm-associated JAK2 V617F mutant comparing control Ba/F3 cells expressing wild type JAK2. Two-condition experiment, WT cells vs. VF cells. One replicate per array.
2013-10-31 | E-GEOD-34239 | biostudies-arrayexpress
Project description:SPAG9-JAK2 is a novel fusion gene identified in a pediatric patient with Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL). In this study, we performed functional analysis of the SPAG9-JAK2 fusion to establish molecular targeted therapy. Ba/F3 cells expressing SPAG9-JAK2 generated by retroviral transduction (Ba/F3-SPAG9-JAK2), proliferated in the absence of IL-3, and exhibited constitutive phosphorylation of the tyrosine residues in the JAK2 kinase domain of the fusion protein and STAT3/STAT5. Mutation of tyrosine residues in the JAK2 kinase domain (SPAG9-JAK2 mut) abolished IL-3 independence, but had no influence on STAT3/STAT5 phosphorylation levels. Gene expression analysis revealed that Stat1 was significantly up-regulated in Ba/F3-SPAG9-JAK2 cells. STAT1 was also phosphorylated in Ba/F3-SPAG9-JAK2 but not SPAG9-JAK2 mut cells, suggesting that STAT1 is key for SPAG9-JAK2-mediated cell proliferation. Consistently, STAT1 induced expression of the anti-apoptotic proteins, BCL-2 and MCL-1, as did SPAG9-JAK2, but not SPAG9-JAK2 mut. Ruxolitinib abrogated Ba/F3-SPAG9-JAK2-mediated proliferation in vitro, but was insufficient in vivo. Venetoclax (a BCL-2 inhibitor) or AZD5991 (an MCL-1 inhibitor) enhanced the effects of ruxolitinib on Ba/F3-SPAG9-JAK2 in vitro. These findings suggest that activation of the JAK2-STAT1-BCL-2/MCL-1 axis contributes to SPAG9-JAK2-related aberrant growth promotion. BCL-2 or MCL-1 inhibition is a potential therapeutic option for B-ALL with SPAG9-JAK2 fusion.
2021-05-18 | GSE174578 | GEO
Project description:Taking a series of oncogenic protein tyrosine kinases and constitutively expressing them in Ba/F3 cells, proteomic analysis was utilised in order to identify common protein changes.
2016-06-03 | PXD001505 | Pride
Project description:ETV6::FRK is a rare kinase-related fusion gene which was identified only in AML but not in ALL. Herein, we firstly identified ETV6::FRK fusion gene in a patient with pediatric B-ALL. Because FRK is Src family tyrosine kinase, we performed functional analysis of ETV6::FRK to establish molecular targeting therapy. Our case with B-ALL was refractory to conventional chemotherapy and received allogeneic bone marrow transplantation following administration of blinatumomab. Cytogenetic analysis demonstrated 46,XY,t(6;12)(q21;p13) and target capture mRNA sequencing revealed ETV6::FRK. Ba/F3 cells expressing ETV6::FRK generated by retroviral transduction (Ba/F3-ETV6::FRK) and analyzed for IL-3 independent growth. Gene expression analysis using whole transcriptome sequencing and gene set enrichment analysis (GSEA) was performed for comprehensive analysis of gene expression profile related to ETV6::FRK. It was also analyzed whether dasatinib, which is Src-kinase inhibitor, suppressed the growth of Ba/F3-ETV6::FRK in vitro and in vivo. Ba/F3-ETV6::FRK proliferated without IL-3, suggesting ETV6::FRK had proliferation activity. Western blot revealed that constitutive phosphorylation of tyrosine residue of ETV6::FRK and STAT3/STAT5, suggesting constitutive activation of FRK-STAT3/STAT5 pathway. GSEA of oncogenic gene sets (C6) from the GSEA Molecular Signatures Database revealed that, compared with control cells, Ba/F3-ETV6::FRK cells were enriched for up-regulation of SNF5 target genes and down-regulation of RB target genes involved in cell cycle regulation. In vitro killing assay showed that dasatinib killed efficiently Ba/F3-ETV6::FRK. Dasatinib also suppressed the growth of Ba/F3-ETV6::FRK in vivo and extended the survival time of the xenografted NSG mice. These findings suggest that activation of FRK-STAT3/STAT5 pathway contributes aberrant growth promotion of Ba/F3-ETV6::FRK. Our study demonstrated that dasatinib might be effective for the patient with B-ALL harboring ETV6::FRK.
2022-12-31 | GSE220610 | GEO
Project description:Gene expression profiles in Ba/F3 cells expressing ETV6-PDGFRB, FIP1L1-PDGFRA or a control vector, treated or not with imatinib (Glivec) Ba/F3 cells expressing FIP1L1-PDGFRA or ETV6-PDGFRB were cultured in the presence or absence of imatinib for 4 hours before RNA extraction followed by hybridization on Affymetrix microarrays. In a control condition Ba/F3 cells were cultured in the presence of IL3 in the absence or in the presence of imatinib for 4 hours before RNA extraction. 4 hours treatment with imatinib in Ba/F3 cells expressing ETV6-PDGFRB, FIP1L1-PDGFRA or a control vector
2014-03-21 | E-GEOD-44810 | biostudies-arrayexpress
Project description:The aim of the study is to analyse whether the Sorafenib renders FLT3-ITD-positive acute myeloid leukemia (AML) cells more immunogenic . We used Ba/F3-ITD cells as a model cell line to study the effect of Sorafenib on FLT3-ITD-positive AML cells. Ba/F3-ITD cells are murine pro-B cell lines with a stable FLT3-ITD expression. Ba/F3-ITD cells were treated with DMSO or 10nM sorafenib for 24 hours. Cells were harvested and total RNA was isolated
2018-02-01 | E-MTAB-4487 | biostudies-arrayexpress
Project description:Ba/F3 cells were transformed after transfection with CRISPR/CAS9 + gRNA vs target gene. Oligoclonal cell population was flow sorted into single cells and processes for RNAseq.
2014-12-09 | E-ERAD-298 | biostudies-arrayexpress
Project description:Gene expression profiles in Ba/F3 cells expressing ETV6-PDGFRB, FIP1L1-PDGFRA or a control vector, treated or not with imatinib (Glivec)
2014-03-21 | GSE44810 | GEO