Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of hepatocyte-like cells generated by doxycycline inducible expression of HNF4A, HNF1A and FOXA3

ABSTRACT: We have generated an immortal fibroblast-derived cell line without malignant traits capable of being efficiently and easily reprogrammable into hepatocyte-like cells under standard culture conditions by combining hTERT expression and a polycistronic vector inducible with doxycycline.

ORGANISM(S): Homo sapiens

PROVIDER: GSE204867 | GEO | 2023/03/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Clinical heterogeneity of hyperinsulinism due to HNF1A and HNF4A mutations.

Project description: Not available

| S-EPMC6030428 | biostudies-literature

Double heterozygous mutations involving both HNF1A/MODY3 and HNF4A/MODY1 genes: a case report.

Project description: Not available

| S-EPMC2963490 | biostudies-literature

Novel presentations of congenital hyperinsulinism due to mutations in the MODY genes: HNF1A and HNF4A.

Project description: Not available

| S-EPMC3674296 | biostudies-literature

Direct conversion of human fibroblasts into hepatocyte-like cells by ATF5, PROX1, FOXA2, FOXA3, and HNF4A transduction.

Project description: Not available

| S-EPMC5709502 | biostudies-other

Transcriptional profiles by deep sequencing (RNA-seq) of in vivo-generated mouse iPSCs, in vitro-generated mouse iPSCs, and mouse ESCs

Project description:We have generated “reprogrammable” transgenic mice that ubiquitously express the four Yamanaka factors in an inducible manner. Transitory induction of the transgene results in multiple teratomas emerging from a variety of organs, thus indicating that full reprogramming into iPSCs can occur in vivo. By performing bone marrow transplant experiments, we demonstrate that both hematopoietic cells, as well as non-hematopoietic cells can be reprogrammed in vivo. Remarkably, reprogrammable mice also present circulating iPSCs in the bloodstream (in vivo-iPSCs) with all the expected properties of bona fide iPSCs. Moreover, in contrast to in vitro-iPSCs or embryonic stem cells (ESCs), in vivo-iPSCs have an increased capacity to undergo trophectoderm lineage differentiation, which suggests that in vivo-iPSCs are more plastic or primitive than in vitro-generated iPSCs or ESCs.

2013-09-12 | GSE48364 | GEO

In vivo Environment Swiftly Restricts Human Pancreatic Progenitors Toward Mono-Hormonal Identity via a HNF1A/HNF4A Mechanism.

Project description: Not available

| S-EPMC7052484 | biostudies-literature

Transgene-free iPSCs generated from small volume peripheral blood nonmobilized CD34+ cells

Project description:A variety of somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs), but the small number of CD34+ hematopoietic stem cells (HSCs) present in non-mobilized peripheral blood (PB) would be a convenient and desirable starting target. We report here a simple method for targeting derivation of iPSC from non-mobilized PB CD34+ HSCs using immunobead purification and 2-4 day culture to achieve enrichment of CD34+ HSCs to 80±9%, followed by reprogramming transduction with loxP-flanked polycistronic (Oct4, Klf4, Sox2, and c-Myc) STEMCCA-loxP lentivector at an MOI of 2. Our yield was 4.7±2.2 iPSC colonies (n=12) per 20 mL non-mobilized peripheral blood, where most colonies had single copy STEMCCA-loxP that was easily excised by transient transfection expression of Cre. Resultant iPSC clones expressed pluripotent cell markers, had genomic methylation pattern closely matching embryonic stem cells, and generated teratomas containing tissues of all three germ lineages in immunodeficient mice. Furthermore, we conclude that these iPSC are derived from the non-mobilized CD34+ HSCs enriched from PB rather than from any lymphocyte or monocyte contaminants because they lacked somatic rearrangements typical of T or B lymphocytes, and because we demonstrated that purified CD14+ monocytes do not yield iPSC colonies under these reprogramming conditions.

2013-04-26 | GSE40790 | GEO

in vivo environment swiftly restricts human pancreatic progenitors towards monohormonal identity via a HNF1A/HNF4A mechanism

Project description:Generating insulin-producing β-cells from human induced pluripotent stem cells is a promising cell replacement therapy aimed at improving or curing certain forms of diabetes. Nevertheless, despite important recent advances, the efficient production of functionally mature β-cells is yet to be achieved, with most current differentiation protocols generating a heterogeneous population comprising of subpopulation of cells expressing different islet hormones, including hybrid polyhormonal entities. A solution to this issue is transplanting end-stages differentiating cells into living hosts, which was demonstrated to majorly improve β-cell maturation. Yet, to date, the cellular and molecular mechanisms underlying the transplanted cells response to the in vivo environment exposure was not yet properly characterized. Here we use global proteomics and large-scale imaging techniques aimed at demultiplexing and filtering cellular processes and molecular signatures modulated by the immediate in vivo effect. We show that in vivo exposure swiftly confines in vitro generated human pancreatic progenitors to single hormone expression. The global proteome landscape of the transplanted cells was closer to the one presented by native human islets, especially in regard to energy metabolism and redox balance. Moreover our study indicates a possible link between these processed and certain epigenetic regulators involved in maintenance and propagation of the islet cells identity. Pathway analysis predicted HNF1A and HNF4A as key regulators controlling the in vivo islet-promoting response, with experimental evidence confirming their involvement in confining islet cell identity. To our knowledge this is the first study demultiplexing the immediate response of the transplanted pancreatic progenitors to in vivo exposure.

2020-02-12 | PXD015955 | Pride

A Comprehensive Analysis of Hungarian MODY Patients-Part I: Gene Panel Sequencing Reveals Pathogenic Mutations in HNF1A, HNF1B, HNF4A, ABCC8 and INS Genes.

Project description: Not available

| S-EPMC8399091 | biostudies-literature

Identification of HNF4A Mutation p.T130I and HNF1A Mutations p.I27L and p.S487N in a Han Chinese Family with Early-Onset Maternally Inherited Type 2 Diabetes.

Project description: Not available

| S-EPMC4766352 | biostudies-literature