publication_authors:Orkin SH Results

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Organism

Mus musculus (264)

Homo sapiens (88)

Technology

Microarray (258)

Platform

Affymetrix Mouse Genome 430 2.0 Array (mouse4302) (176)

Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2) (89)

Includes Publication

GSE21056

Differential roles of Sall4 isoforms in ES cell pluripotency

Mus musculus
8 Downloadable Samples

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.

Alternate Accession IDs

E-GEOD-21056

Sample Metadata Fields

Specimen part, Cell line

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GSE21054

Differential roles of Sall4 isoforms in ES cell pluripotency: expression

Mus musculus
8 Downloadable Samples

Description

Murine embryonic stem cells (ESCs) are defined by continuous self-renewal and pluripotency. A diverse repertoire of protein isoforms arising from alternative splicing are expressed in ES cells without defined biological roles. Sall4, a transcription factor essential for pluripotency, exists as two isoforms (Sall4a and Sall4b). By genome-wide location analysis, we have determined that Sall4b, and not Sall4a, binds preferentially to highly expressed loci in ES cells. Sall4a and Sall4b binding sites are distinguished by both epigenetic marks at target loci and their clustering with binding sites of other pluripotency factors. When ESCs expressing a single isoform of Sall4 are generated, Sall4b alone could maintain the pluripotent state, although it could not completely suppress all differentiation markers. Sall4a and Sall4b collaborate in maintenance of the pluripotent state, but play distinct roles. Our work is novel in establishing such isoform-specific differences in ES cells.

Publication Title

Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.

Alternate Accession IDs

E-GEOD-21054

Sample Metadata Fields

Specimen part, Cell line

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GSE16655

Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis

Mus musculus, Homo sapiens
47 Downloadable Samples

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Alternate Accession IDs

E-GEOD-16655

Sample Metadata Fields

Specimen part, Disease, Cell line, Treatment

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GSE16676

Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1

Mus musculus
11 Downloadable Samples

Description

In this project, we studied a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the GATA1 transcription factor (called GATA1s mutation). The model was generated through retroviral insertional mutagenesis in Gata1s mutant fetal liver progenitors. In this study, we analyzed the dependency of these leukemic cells on the Gata1s mutant protein.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Alternate Accession IDs

E-GEOD-16676

Sample Metadata Fields

Specimen part, Cell line, Treatment

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GSE16679

Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia

Mus musculus
8 Downloadable Samples

Description

The goal of this study is to develop a Plag1 signature and determine how its overexpression contributes to leukemogenesis.

Publication Title

Developmental stage-specific interplay of GATA1 and IGF signaling in fetal megakaryopoiesis and leukemogenesis.

Alternate Accession IDs

E-GEOD-16679

Sample Metadata Fields

Cell line

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GSE16684

Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling

Mus musculus
6 Downloadable Samples

Description

The goal of this study is to derive a mouse model of human Down Syndrome (DS) megakaryocytic leukemia involving mutations in the hematopoietic transcription factor, GATA1 (called GATA1s mutation). We achieved this through transduction of Gata1s mutant fetal progenitors by MSCV-based retrovirus expressing a GFP marker, followed by in vitro selection (for immortalized cell lines), and then in vivo selection (for transformed cell lines) through transplantation.