Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reduced Representation Bisulphite Sequencing of WT and AICDA KO iPCS clones

ABSTRACT: We report AICDA facilitates naïve pluripotency of mouse iPSCs by suppressing FGF/ERK signaling. In the absence of AICDA iPSCs fail to achive naïve pluripotent state and display chracteristics of EpiSCs and are primed for differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE129187 | GEO | 2019/04/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA sequencing of WT and AICDA KO iPCS clones

Project description:We report AICDA facilitates naïve pluripotency of mouse iPSCs by suppressing FGF/ERK signaling. In the absence of AICDA iPSCs fail to achive naïve pluripotent state and display chracteristics of EpiSCs and are primed for differentiation.

2019-04-03 | GSE129186 | GEO

Reduced Representation Bisulphite Sequencing of WT and AICDA KO iPCS clones

Project description:Reduced Representation Bisulphite Sequencing of WT and AICDA KO iPCS clones

| PRJNA530408 | ENA

Differential programming of B cells in Aicda-/- mice [MethylCap-Seq]

Project description:We determined CpG methylation load from GC B cells obtained from both Aicda-/- and Aicda+/+ mice. Examination of methylation load of Aicda-/- and Acida+/+ GC B cells.

2013-06-07 | E-GEOD-47704 | biostudies-arrayexpress

GY118F downstream effect in EpiSCs

Project description:This microarray was performed to gain insight in the effect of GY118F stimulation in EpiSCs. This array is part of the following paper to be published in Nature Communications: “JAK/STAT3 signalling is sufficient and dominant over antagonistic cues for the establishment of naïve pluripotency” by Anouk L. van Oosten, Yael Costa, Austin Smith & José C.R. Silva Gy0 a, gy0 b, gy0 c (triplicate samples for GY118F EpiSCs in N2B27+Activin+Fgf) c0 a, c0 b, c0 c (triplicate samples for Control EpiSCs in N2B27+Activin+Fgf) gy3 b, gy3 c (duplicate samples for GY118F EpiSCs in N2B27+Activin+Fgf stimulated with GCSF for 3 hours) c3 a, c3 b, c3 c (triplicate samples for Control EpiSCs in N2B27+Activin+Fgf stimulated with GCSF for 3 hours) Within the manucript genes of interest were defined as those that were significantly upregulated (P<0.01) above a 1.4 fold change threshold in GCSF stimulated GY118F EpiSCs as compared to those not stimulated, but for which the expression did not significantly change upon GCSF stimulation in the control. The fold change in expression was calculated by 2^absolute value of subtracted normalised data.

2012-04-30 | E-GEOD-36817 | biostudies-arrayexpress

Differential programming of B cells in Aicda-/- mice [RNA-Seq]

Project description:We sequenced mRNA from naive, in vitro activated, and GC B cells obtained from both Aicda-/- and Aicda+/+ mice. Examination of mRNA levels in naive, in vitro activated, and GC B cells.

2013-06-07 | E-GEOD-47703 | biostudies-arrayexpress

Differential programming of B cells in Aicda-/- mice [MethylCap-Seq]

Project description:We determined CpG methylation load from GC B cells obtained from both Aicda-/- and Aicda+/+ mice.

2013-06-07 | GSE47704 | GEO

AICDA-induced epigenetic plasticity accelerates germinal center-derived lymphomagenesis

Project description:Epigenetic heterogeneity is emerging as a significant phenotypic feature of tumors. In diffuse large B-cell lymphomas (DLBCLs), increased cytosine methylation heterogeneity is associated with poor clinical outcome, yet the biological mechanisms driving epigenetic heterogeneity remain unclear. Activation-induced cytidine deaminase (AICDA), an enzyme that deaminates and facilitates demethylation of DNA methyl-cytosines in germinal center (GC) B-cells, is required for DLBCL pathogenesis and linked to inferior clinical outcomes. Here, we show that overexpression of AICDA causes more aggressive disease and worse outcome in BCL2-driven murine lymphomas. This phenotype was associated with significantly increased focal inter-tumor and intra-tumor cytosine methylation heterogeneity as compared to control lymphomas, but not with increased mutational burden. AICDA-mediated epigenetic heterogeneity was accompanied by DNA hypomethylation. Reciprocally, we observed that the focal inter-individual and intra-individual cytosine methylation heterogeneity characteristic of normal GC B-cells was lost upon depletion of AICDA. There was significant overlap of AICDA-induced methylation heterogeneity foci in GC B-cells and murine lymphomas. These observations are relevant to human patients, since DLBCLs with high AICDA expression likewise manifest extensive increases in focal inter-patient and intra-patient heterogeneity as compared to DLBCLs with low AICDA expression. Affected regions significantly overlapped with those found in murine AICDA-overexpressing lymphomas. Our results identify AICDA as a novel source of epigenetic plasticity and heterogeneity in B-cell lymphomas with potential significance for other tumors that express cytosine deaminases.

2018-01-19 | GSE95013 | GEO

The Cytosine Deaminase AICDA Regulates FGF/ERK Signaling to Achieve the Naïve Pluripotent State During Reprogramming.

Project description:The Cytosine Deaminase AICDA Regulates FGF/ERK Signaling to Achieve the Naïve Pluripotent State During Reprogramming.

| PRJNA530550 | ENA

Differential programming of B cells in Aicda-/- mice [RNA-Seq]

Project description:We sequenced mRNA from naive, in vitro activated, and GC B cells obtained from both Aicda-/- and Aicda+/+ mice.

2013-06-07 | GSE47703 | GEO

RNA sequencing of WT and AICDA KO iPCS clones

Project description:RNA sequencing of WT and AICDA KO iPCS clones

| PRJNA530409 | ENA