Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Modeling Down syndrome AML by introducing disese-specific mutations in iPSCs

ABSTRACT: Modeling Down syndrome AML by introducing disese-specific mutations in iPSCs

PROVIDER: PRJNA779425 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16908201_1.fastq.gz	Fastqsanger.gz
	SRR16908201_2.fastq.gz	Fastqsanger.gz
	SRR16908203_1.fastq.gz	Fastqsanger.gz
	SRR16908203_2.fastq.gz	Fastqsanger.gz
	SRR16908205_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

Modeling Down syndrome AML by introducing disese-specific mutations in iPSCs

Project description:Modeling Down syndrome AML by introducing disese-specific mutations in iPSCs

| PRJNA779425 | ENA

Modeling Down syndrome AML by introducing disese-specific mutations in iPSCs

Project description:Down syndrome AML is characterized by the presence of the pathgnonomic mutation in GATA1, which cooperates with other somatic mutations. In this study, we utilzed iPSCs derived from Down syndrome individuals bearing trisomy 21 and introduced disease-specific mutations using CRISPR-Cas9. Hematopoeitic stem and progenitor cells (HSPCs) obtained by hematopoeitic differentiation of these iPSCs, and megakaryocytes generated from the HSPCs (by culturing in megakaryocyte-specific media) were used for RNA sequencing analysis.

2022-03-02 | GSE188568 | GEO

RNA-seq of CN, CN/AML, and CN/AML BAALC KO iPSCs-derived HSPCs

Project description:Severe congenital neutropenia (CN) is a pre-leukemia syndrome that, in the majority of patients, is caused by heterogeneous ELANE mutations encoding neutrophil elastase (NE). To study leukemogenesis associated with CN we generated CN and CN/AML patient-specific induced pluripotent stem cells (iPSCs). Additional mutations in leukemia-relevant genes, CSF3R and RUNX1, were introduced using CRISPR/Cas9 gene-editing. Consequently, we performed in vitro embryoid body (EB)-based hematopoietic and myeloid differentiation of generated iPSC lines. On day 14-17 of EB-based differentiation, iPSC-derived CD45+CD34+ cells were harvested and mRNA was isolated using RNeasy Mini- or Micro Kit (Qiagen). Sequencing libraries were prepared using the TruSeq RNA Sample Prep Kit (Illumina). Poly (A) selected single-read and pair-read sequencing libraries were sequenced on the Illumina platform in order to compare the transcriptomes of CN and CN/AML iPSCs-derived HSPCs from 2 CN/AML patients. Next, we identified that BAALC knockout resulted in a dramatic induction of granulocytic differentiation and a significant reduction in proliferation of CN/AML iPSC-derived HSPCs. To identify BAALC-dependent leukemia-associated gene expression, we compared the transcriptomes of CN/AML iPSCs before and after BAALC KO using a similar approach described above for CN and CN/AML iPSCs-derived HSPCs.

2021-03-08 | E-MTAB-10162 | biostudies-arrayexpress

RNA-seq of CN, CN/AML, and CN/AML BAALC KO iPSCs-derived HSPCs

Project description:RNA-seq of CN, CN/AML, and CN/AML BAALC KO iPSCs-derived HSPCs

| PRJEB43341 | ENA

Introducing cellular senescence in human induced pluripotent stem cells and differentiated neural lineage for modeling of age-associated diseases

Project description:Reprogramming of somatic cells into induced pluripotent stem cells (iPSCs) resets the epigenetic landscapes that mark the aging clock, and consequently cells differentiated from iPSCs resemble fetal cells rather than adult or aged cells. The lack of proper cellular aging in cells differentiated from iPSCs presents a significant problem in iPSC-based disease models to investigate the pathological progression of age-associated diseases such as neurodegeneration. To address this caveat, we introduced cellular senescence into iPSC-based cell models in this study, as senescence has been shown to play a critical role not only in aging but also in neurodegeneration. We created an inducible CRISPR interference (CRISPRi) targeting TERF2, a major component of the telomere protecting Shelterin complex. We demonstrated that suppression of TERF2 robustly activated DNA damage response, the p53/p21 signaling, cellular senescence and inflammatory response in iPSCs. The inducible approach allows the temporal control of senescence activation over the course of differentiation of iPSCs to desired cell types. We applied the CRISPRi-TERF2 system to differentiation of iPSCs into neural progenitor cells (NPCs) and showed that suppression of TERF2 efficiently activated DNA damage response, the p53/p21 signaling and senescence in differentiated NPCs. The inducible cell model of cellular senescence generated in this study has broad application in investigation of cellular senescence in the progression of age-related diseases and improvement of disease modeling with a proper cellular aging context to facilitate drug discovery.

2023-12-25 | GSE251814 | GEO

Modeling Fanconi Anemia pathogenesis and therapeutics using integration-free patient iPSCs

Project description:Modeling Fanconi Anemia pathogenesis and therapeutics using integration-free patient iPSCs

| PRJNA248194 | ENA

Osteochondral Tissue Chip Derived from iPSCs: Modeling OA pathologies and Testing Drugs

Project description:Osteochondral Tissue Chip Derived from iPSCs: Modeling OA pathologies and Testing Drugs

| PRJNA589299 | ENA

Functional neurons generated from T cell-derived iPSCs for neurological disease modeling

Project description:Functional neurons generated from T cell-derived iPSCs for neurological disease modeling

| PRJNA308724 | ENA

Developmental modeling of hepatogenesis using obese iPSCs-hepatocyte differentiation uncovers pathological features

Project description:Developmental modeling of hepatogenesis using obese iPSCs-hepatocyte differentiation uncovers pathological features

| PRJNA814799 | ENA

Footprint-free human fetal foreskin derived iPSCs: a tool for modeling hepatogenesis associated gene regulatory networks

Project description:Induced pluripotent stem cells (iPSCs) are similar to embryonic stem cells and can be generated from somatic cells. We have generated episomal plasmid-based and integration-free iPSCs (E-iPSCs) from human fetal foreskin fibroblast cells (HFF1). E-iPSCs were fully characterized and their transcriptomes are more similar to that of hESCs (R2 = 0.9363) in comparison to viral-derived HFF1-iPSCs (R2 = 0.8176). We used an E-iPSC-line to model hepatogenesis in vitro. The differentiation of iPSCs into hepatocyte-like cells (HLCs) is a three-step process, from the undifferentiated E-iPSC to definitive endoderm (DE), hepatic endoderm (HE) and ultimately HLCs. The HLCs were characterized biochemically, i.e. glycogen storage, ICG uptake and release, UREA and bile acid production, as well as CYP3A4 activity. Ultra-structure analysis by electron microscopy revealed the presence of lipid and glycogen storage, tight junctions and bile canaliculi- all typical features of hepatocytes. Furthermore, the transcriptome of undifferentiated E-iPSC, DE, HE and HLCs were compared to that of fetal liver and primary human hepatocytes (PHH). K-means clustering identified 100 clusters which include developmental stage-specific groups of genes, e.g. OCT4 expression at the undifferentiated stage, SOX17 marking the DE stage, DLK and HNF6 the HE stage, HNF4a and Albumin is specific to HLCs, fetal liver and adult liver (PHH) stage. The lack of viral DNA integrations in these E-iPSCs endow them superior to viral-derived iPSCs for (i) modeling gene regulatory networks associated with hepatogenesis and gastrulation in general, (ii) toxicology studies and (iii) drug screening platforms.

2017-09-06 | GSE66282 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data