Ansclgene product lacking the transactivation domain induces bony abnormalities and cooperates with LMO1 to generate T-cell malignancies in transgenic mice-Reference-Cited by-同舟云学术

Ansclgene product lacking the transactivation domain induces bony abnormalities and cooperates with LMO1 to generate T-cell malignancies in transgenic mice

Published:1997-05-01 Issue:9 Volume:16 Page:2408-2419
ISSN:0261-4189
Container-title:The EMBO Journal
language:en
Short-container-title:

Author:

Aplan Peter D.¹²³,Jones Craig A.⁴,Chervinsky David S.¹²,Zhao XianFeng¹²,Ellsworth MaryKay⁴,Wu Chuanzen⁴,McGuire Elizabeth A.⁵,Gross Kenneth W.⁴

Affiliation:

1. Department of Pediatrics, Roswell Park Cancer Institute; Buffalo NY 14263 USA

2. Department of Molecular Medicine, Roswell Park Cancer Institute; Buffalo NY 14263 USA

3. Department of Pediatrics, State University of New York at Buffalo; Buffalo NY 14222 USA

4. Department of Cellular and Molecular Biology, Roswell Park Cancer Institute; Buffalo NY 14263 USA

5. University of Pittsburgh Cancer Institute; Pittsburgh PA USA

Publisher

Wiley

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Molecular Biology,General Neuroscience

Reference58 articles.

1. The SCL gene is formed from a transcriptionally complex locus;Aplan;Mol Cell Biol,1990a

2. Disruption of the human SCL locus by ‘illegitimate’ V(D)J recombinase activity;Aplan;Science,1990b

3. Structural chracterization of SIL, a gene frequently disrupted in T-cell acute lymphoblastic leukemia;Aplan;Mol Cell Biol,1991

4. The SCL gene product: a positive regulator of erythroid differentiation;Aplan;EMBO J,1992

5. Does activation of the TAL1 gene occur in a majority of patients with T-cell acute lymphoblastic leukemia?;Bash;Blood,1995

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