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Mitchell J. Weiss

Researcher at St. Jude Children's Research Hospital

Publications -  263
Citations -  23376

Mitchell J. Weiss is an academic researcher from St. Jude Children's Research Hospital. The author has contributed to research in topics: Haematopoiesis & Gene. The author has an hindex of 74, co-authored 241 publications receiving 20575 citations. Previous affiliations of Mitchell J. Weiss include Children's Hospital of Philadelphia & University of Pennsylvania.

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An early haematopoietic defect in mice lacking the transcription factor GATA-2.

TL;DR: It is demonstrated that the transcription factor GATA-2 plays a critical role in haematopoiesis, particularly of an adult type, and proposed that it regulates genes controlling growth factor responsiveness or the proliferative capacity of early haem atopoietic cells.
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A comparative encyclopedia of DNA elements in the mouse genome

Feng Yue, +145 more
- 20 Nov 2014 - 
TL;DR: The mouse ENCODE Consortium has mapped transcription, DNase I hypersensitivity, transcription factor binding, chromatin modifications and replication domains throughout the mouse genome in diverse cell and tissue types as mentioned in this paper.
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FOG, a Multitype Zinc Finger Protein, Acts as a Cofactor for Transcription Factor GATA-1 in Erythroid and Megakaryocytic Differentiation

TL;DR: Findings indicate that FOG acts as a cofactor for GATA-1 and provide a paradigm for the regulation of cell type-specific gene expression by GATA transcription factors.
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Novel insights into erythroid development revealed through in vitro differentiation of GATA-1 embryonic stem cells.

TL;DR: An in vitro ES cell differentiation assay is used for the phenotypic analysis of targeted mutations affecting hematopoietic development and finds that arrested GATA-1(-)-definitive proerythroblasts express GATA target genes at normal levels, implying substantial interchangeability of GATA factors in vivo.
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Proximity among Distant Regulatory Elements at the β-Globin Locus Requires GATA-1 and FOG-1

TL;DR: Using chromosome conformation capture (3C), it is shown that the hematopoietic transcription factor GATA-1 and its cofactor FOG-1 are required for the physical interaction between the beta-globin locus control region (LCR) and thebeta-major globin promoter.