Analysis of disease-causing GATA1 mutations in murine gene complementation systems-Reference-Cited by-同舟云学术

Analysis of disease-causing GATA1 mutations in murine gene complementation systems

Published:2013-06-27 Issue:26 Volume:121 Page:5218-5227
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Campbell Amy E.¹²,Wilkinson-White Lorna³,Mackay Joel P.³,Matthews Jacqueline M.³,Blobel Gerd A.¹²

Affiliation:

1. Division of Hematology, The Children’s Hospital of Philadelphia, Philadelphia, PA;

2. Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; and

3. School of Molecular Bioscience, University of Sydney, NSW, Australia

Abstract

Key Points Disease-causing mutations in GATA1 impair binding to the cofactors FOG1 or TAL1 but not DNA. Different substitutions at the same residue selectively disrupt FOG1 or TAL1 binding leading to distinct disease phenotypes.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/121/26/5218/1367508/5218.pdf

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4. Transcriptional activation and DNA binding by the erythroid factor GF-1/NF-E1/Eryf 1.;Martin;Genes Dev,1990

5. A palindromic regulatory site within vertebrate GATA-1 promoters requires both zinc fingers of the GATA-1 DNA-binding domain for high-affinity interaction.;Trainor;Mol Cell Biol,1996

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