Similar to embryo-derived stem cells, application of human induced pluripotent stem cells (iPSCs) is limited by our understanding of lineage specification. Here, we demonstrate the ability to generate progenitors and mature cells of the hematopoietic fate directly from human dermal fibroblasts without establishing pluripotency. POU domain activation of hematopoietic transcription factors by ectopic expression of Oct-4, together with specific cytokine treatment, allowed generation of cells expressing the pan-leukocyte marker CD45. These unique fibroblast-derived cells gave rise to granulocytic, monocytic, megakaryocytic, and
Direct conversion of human fibroblasts to multilineage blood progenitors.
Sex, Specimen part, Time
View SamplesDuring development, lineage specification is controlled by several signaling pathways involving various transcription factors (TFs). Here, we studied the RE1-silencing transcription factor (REST) and identified an important role of this TF in cardiac differentiation. Using mouse embryonic stem cells (ESC) to model development, we analyzed the effect of REST knock-out on the ability to these cells to differentiate into the cardiac lineage. Detailed analysis of specific lineage markers expression showed selective down-regulation of endoderm markers in REST-null cells, thus contributing to a loss of cardiogenic signals.
A Role for RE-1-Silencing Transcription Factor in Embryonic Stem Cells Cardiac Lineage Specification.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.
Cell line, Treatment
View SamplesAnalysis of the expression of KH2 embryonic stem cells inducibly expressing V5 tagged Sox17 protein. Results provide information on the endodermal gene expression program activated after Sox17 expression in ES cells.
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.
Cell line, Treatment
View SamplesAnalysis of the expression of F9 cells after knockdown of Sox7 and Sox17 during their primitive endoderm differnetiation induction with retinoic acid. Results provide information on the endodermal gene expression program regulated by Sox7 and Sox17.
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.
Cell line, Treatment
View SamplesBreast cancer (BRC) is the most invasive cancer in women. Although the survival rate of BRC is gradually increasing due to improved screening systems, development of novel therapeutic targets for inhibition of BRC proliferation, metastasis and recurrence have been constantly needed. Thus, in this study, we identified overexpression of SETDB1, a histone methyltransferase, in RNA-seq data of BRC derived from TCGA portal. In Gene Ontology (GO) analysis, cell migration-related GO terms were enriched, and we confirmed down-regulation of cell migration/invasion and alteration of EMT /MET markers after knockdown of SETDB1. Moreover, gene network analysis showed that SMAD7 expression is regulated by SETDB1 levels, indicating that up-regulation of SMAD7 by SETDB1 knockdown inhibited BRC metastasis. Therefore, development of SETDB1 inhibitors and functional studies may help develop more effective clinical guidelines for BRC treatment
No associated publication
Sex, Age, Specimen part, Disease, Cell line, Treatment
View SamplesNPTX1 is a key inducer of neural lineages from the human ESC.
NPTX1 regulates neural lineage specification from human pluripotent stem cells.
Cell line, Time
View SamplesNicotinamide (NAM) inhibited the expression of Age related macular degeneration (AMD) associated proteins in hiPSC-derived retinal pigment epithelium (RPE).
No associated publication
Disease, Treatment
View SamplesThe goal of this study is to reveal the characters and therapeutic targets of CNS leukemia.
No associated publication
Sex, Age, Specimen part, Disease
View SamplesBuilding the gene expression profiles and identifying the differentially expressed genes in specific comparisons.
No associated publication
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