Arabidopsis thaliana wild-type and ire1a/ire1b double mutant plants were treated with tunicamycin. RNA was extracted and subjected to microarray analysis.
Arabidopsis IRE1 catalyses unconventional splicing of bZIP60 mRNA to produce the active transcription factor.
No sample metadata fields
View SamplesArabidopsis seedlings of wildtype or ire1a ire1b double mutant were treated with or without tunicamycine in the presence of actinomycin D (ActD).
Defects in IRE1 enhance cell death and fail to degrade mRNAs encoding secretory pathway proteins in the Arabidopsis unfolded protein response.
Treatment
View SamplesInitially, ATL cell lines (MT-1 or KK-1) were stably transfected with reporter plasmid for HTLV-1 Tax expression, and single clones were isolated . This reporter in composed of Tax responsive element upstream of d2EGFP fluorescent protein. d2EGFP is expressed upon Tax expression in any individual cell. To compare transcriptomes of Tax(-) and Tax(+) cells, FACS sorting was done for d2EGFP(-) and d2EGFP(+) populations and RNA sequencing was performed. Overall design: Two ATL reporter cell lines were used in this study (MT1GFP and KK1GFP). For Each cell line, two samples were analyzed: d2EGFP(-) and d2EGFP(+). In total 4 samples were used in this study.
Sporadic on/off switching of HTLV-1 Tax expression is crucial to maintain the whole population of virus-induced leukemic cells.
Specimen part, Subject
View SamplesWe previously reported that human T cell lymphotropic virus 1 (HTLV-1) Tax oncoprotein constitutively activates TAK1. Here, we established Tax-positive HuT-102 cells stably downregulated TAK1 expression by short-hairpin RNA (HuT-shTAK1 cells), and investigated the physiological function of TAK1. Microarray analysis demonstrated that several interferon (IFN)-inducible genes including chemokines such as CXCL10 and CCL5 were significantly downregulated in HuT-shTAK1 cells. In contrast, Tax-mediated constitutive activation of NF-kB was intact in HuT-shTAK1 cells. IRF3, a critical transcription factor in innate immunity to viral infection, was constitutively activated in a Tax-dependent manner. Activation of IRF3 and IRF3-dependent gene expression were dependent on TAK1 and TBK1. On the other hand, IRF4, another IRF family of transcription factor overexpressed in a Tax-independent manner, negatively regulated the TAK1-dependent IRF3 transcriptional activity. Together, HTLV-1 manipulates IFN signaling by regulating both positive and negative IRFs.
Human T cell lymphotropic virus 1 manipulates interferon regulatory signals by controlling the TAK1-IRF3 and IRF4 pathways.
Specimen part, Cell line
View SamplesThe microarray analysis showed an interesting up-regulation in the set of genes controlling the development of Th1, mainly IFN-gamma, and other type 1 interferon response genes including CXCL10 in IRF4 knocked-down HuT-102 cells.
Distinct roles of transforming growth factor-beta-activated kinase 1 (TAK1)-c-Rel and interferon regulatory factor 4 (IRF4) pathways in human T cell lymphotropic virus 1-transformed T helper 17 cells producing interleukin-9.
Specimen part
View SamplesTo understand molecular mechanisms by which JunB regulates Treg function, we performed RNA-seq analysis of JunB-deficient and control Treg cells (CD4+ CD25hi). Overall design: Gene expresson profiles in WT and JunB-deficient Treg cells.
JunB regulates homeostasis and suppressive functions of effector regulatory T cells.
Specimen part, Cell line, Subject
View SamplesNCCs and NCC-derived MSCs were induced from FOP-iPSCs and control iPSCs, and their expresion profiles were compared.
Derivation of mesenchymal stromal cells from pluripotent stem cells through a neural crest lineage using small molecule compounds with defined media.
Specimen part
View SamplesWe developed simple, robust, efficient, and serum-free/feeder-free induction protocol for neural crest cells from human pluripotent stem cells. To characterize the hNCCs and hNCC-derived MSCs, we performed gene expression profiling experiments.
Derivation of mesenchymal stromal cells from pluripotent stem cells through a neural crest lineage using small molecule compounds with defined media.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of MMP1 as a novel risk factor for intracranial aneurysms in ADPKD using iPSC models.
Sex, Specimen part, Disease stage, Subject
View SamplesCardiovascular complications are the leading cause of death in autosomal dominant polycystic kidney disease (ADPKD), and intracranial aneurysm (ICA) causing subarachnoid hemorrhage is among the most serious complications. The diagnostic and therapeutic strategies for ICAs in ADPKD have not been fully established. We here generated induced pluripotent stem cells (iPSCs) from seven ADPKD patients, including four with ICAs. The vascular cells differentiated from ADPKD-iPSCs showed altered Ca2+ entry and gene expression profiles compared with those from control-iPSCs. We found that the expression level of a metalloenzyme gene, matrix metalloproteinase (MMP) 1, was specifically elevated in the iPSC-derived endothelia from ADPKD patients with ICAs. Furthermore, we confirmed a statistically significant correlation between the serum MMP1 levels and the development of ICAs in 354 ADPKD patients, indicating that the serum MMP1 levels may be a novel risk factor and become more beneficial when combined with other risk factors. These results suggest that cellular disease models with ADPKD-specific iPSCs can be used to study the disease mechanisms and to identify novel disease-related molecules or risk factors.
Identification of MMP1 as a novel risk factor for intracranial aneurysms in ADPKD using iPSC models.
Sex, Specimen part, Disease stage, Subject
View Samples