Strict in vivo specificity of the Bcl11a erythroid enhancer-Reference-Cited by-同舟云学术

Strict in vivo specificity of the Bcl11a erythroid enhancer

Published:2016-11-10 Issue:19 Volume:128 Page:2338-2342
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Smith Elenoe C.¹²³⁴^ORCID,Luc Sidinh¹²³⁴,Croney Donyell M.¹²³⁴,Woodworth Mollie B.³⁵⁶^ORCID,Greig Luciano C.³⁵⁶,Fujiwara Yuko¹²³⁴⁷^ORCID,Nguyen Minh¹²³⁴,Sher Falak¹²³⁴,Macklis Jeffrey D.³⁵⁶^ORCID,Bauer Daniel E.¹²³⁴^ORCID,Orkin Stuart H.¹²³⁴⁷^ORCID

Affiliation:

1. Division of Hematology/Oncology, Boston Children’s Hospital, Boston, MA;

2. Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA;

3. Harvard Stem Cell Institute, Harvard University, Cambridge, MA;

4. Department of Pediatrics, Harvard Medical School, Boston, MA;

5. Department of Stem Cell and Regenerative Biology and

6. Center for Brain Science, Harvard University, Cambridge, MA; and

7. Howard Hughes Medical Institute, Boston, MA

Abstract

Key Points Deletion of the erythroid enhancer of Bcl11a from the mouse genome does not affect viability or Bcl11a expression in nonerythroid lineages. Elevated levels of γ-globin in Bcl11a enhancer–deleted mice are comparable to those in erythroid-specific Bcl11a gene knockout mice.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/128/19/2338/1396619/2338.pdf

Reference22 articles.

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4. Human fetal hemoglobin expression is regulated by the developmental stage-specific repressor BCL11A.;Sankaran;Science,2008

5. Developmental and species-divergent globin switching are driven by BCL11A.;Sankaran;Nature,2009

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