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Kruppel like factor 7 overexpression suppresses hematopoietic stem and progenitor cell function

ABSTRACT: Kruppel like factor 7 overexpression suppresses hematopoietic stem and progenitor cell function

PROVIDER: PRJNA173546 | ENA |

REPOSITORIES: ENA

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Kruppel like factor 7 overexpression suppresses hematopoietic stem and progenitor cell function

Project description:This SuperSeries is composed of the following subset Series: GSE40323: KLF7 KO vs WT HSPC expression array GSE40324: HSC expression array GSE40327: KLF7 overexpression in HSPCs expression array Refer to individual Series

2012-08-24 | E-GEOD-40331 | biostudies-arrayexpress

Kruppel-like factor 7 overexpression suppresses hematopoietic stem and progenitor cell function.

Project description:Increased expression of Kruppel-like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7(-/-) cells was comparable with control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, although resulting in multilineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21(Cip1/Waf1)) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival.

| S-EPMC3471512 | biostudies-literature

Ageing-associated proteome and acetylome of hematopoietic progenitor cells

Project description:Ageing-associated proteome and acetylome of hematopoietic progenitor cells

2020-09-24 | PXD021651 |

Hematopoietic progenitor cells

Project description:Hematopoietic progenitor cells

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Kruppel like factor 7 overexpression suppresses hematopoietic stem and progenitor cell function

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-08-24 | GSE40331 | GEO

Quantitative Proteomic Analysis of Mouse Fetal and Adult Hematopoietic Progenitor Cells

Project description:Quantitative proteomic analysis of mouse fetal and adult hematopoietic progenitor cells using TMT6plex and an SPS-MS3 method.

2020-07-02 | MSV000085672 | MassIVE

Common primitive-definitive hematopoietic precursors vs. Definitve hematopoietic progenitor cells

Project description:Transcriptional profiling of mouse ES cell-derived hemaopoitic cells comparing common primitive-definitive hematopoietic precursors (CD41SP) with definitve hematopoietic progenitor cells (KA45) RNA isolated from two separate experiments was pooled and used for comparison

2013-11-27 | E-GEOD-48189 | biostudies-arrayexpress

KLF7 overexpression in HSPCs expression array

Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 overexpression in HSPCs expression array: Lin- c-Kit+ Sca-1+ cells transduced with a KLF7 expressing or control (empty vector) lentivirus. Expression profiles of KLF7 overexpressing vs controls HSPCs. Cells were harvested 72 hrs post-transduction to compare expression profiles of control vs KLF7 overexpressing HSPCs

2012-08-24 | E-GEOD-40327 | biostudies-arrayexpress

Common primitive-definitive hematopoietic precursors vs. Definitve hematopoietic progenitor cells

2013-11-27 | GSE48189 | GEO

Gene expression of human chord blood hematopoietic progenitor cells and induced hemato-endothelial progenitor cells derived from human iPSC

Project description:Induced pluripotent stem cells (iPSC) offer a promising platform to model early embryonic developmental processes, to create disease models and proof-of-concept experiments for regenerative medicine. However, generation of iPSC derived hemato-endothelial and hematopoietic progenitor cells for these applications is challenging due to variable and limited cell numbers, which necessitates enormous up-scaling or development of demanding protocols. Here, we unravel the function of key transcriptional regulators SCL, LMO2, GATA2, ETV2 (SLGE) on early hemato-endothelial specification and establish a fully inducible and stepwise hemato-endothelial forward programming system, based on SLGE regulated overexpression. Regulated induction of SLGE in stable SLGE-iPSC lines drives very efficient generation of large numbers of hemato-endothelial progenitor cells (HEP) (CD144+/CD73-), which generate hematopoietic progenitor cells (CD45+/CD34+/CD38-/CD45RA-/CD90+/CD49f+) through a gradual process of endothelial-to-hematopoietic transition (EHT).

2019-11-13 | GSE140221 | GEO

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