|
||
Articles |


Department of Cell Biology and Kaplan Cancer Center, New York University Medical Center, New York 10016; and the
Department of Molecular Pharmacology and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305
Two models have been proposed for the molecular mechanism by which the Tal1 oncogene causes T cell acute lymphoblastic leukemia (T-ALL). The activation model suggests that Tal1 as heterodimers with the E2A transcription factor activates the expression of oncogenes. The inhibition model postulates that Tal1 interferes with the tumor-suppressing function of E2A. In the Jurkat T cell line, originally derived from a patient with T-ALL, Tal1 is complexed with E2A proteins and the transcriptional activity of E2A is very low. When E2A activity was restored by expressing an E2A–Tal1 fusion protein, E-T/2, the Jurkat cells underwent growth arrest and subsequently apoptosis, thus supporting the inhibition model and suggesting that E2A loss may contribute to leukemic progression.
Key Words: Tal1 E2A apoptosis growth inhibition leukemogenesis
Abbreviations used: bHLH, basic helix-loop-helix; BrdU, bromodeoxyuridine; EMSA, electrophoretic mobility shift assay; GFP, green fluorescent protein; PI, propidium iodide; T-ALL, T cell acute lymphoblastic leukemia; zVAD, zVAD-fluoromethylketone.
![]()
CiteULike
Complore
Connotea
Del.icio.us
Digg
Facebook
Reddit
Technorati
Twitter What's this?
| TABLE OF CONTENTS |
|