NDLI: The promyelocytic leukemia zinc finger protein down-regulates apoptosis and expression of the proapoptotic BID protein in lymphocytes

Content Provider	PubMed Central
Author	Parrado, Antonio Robledo, Macarena Rosa, Moya-quiles M. Marín, Luis A. Christine, Chomienne Padua, Rose Ann Álvarez-lópez, M. Rocío
Copyright Year	2004
Abstract	The promyelocytic leukemia zinc finger (PLZF) gene, involved in rare cases of acute promyelocytic leukemia, encodes a Krüppel-type zinc finger transcription factor. It has been reported that PLZF affects myeloid cell growth, differentiation, and apoptosis. However, the function of PLZF in the lymphoid compartment, where PLZF is also expressed, remains largely unknown. To investigate a potential relationship between PLZF expression in lymphocytes and programmed cell death, an inducible model of stable clones of the lymphoid Jurkat cell line was created by using the tet-off system. Although induction of PLZF expression by itself did not produce changes in the basal levels of apoptosis, PLZF had a significant anti-apoptotic effect in Jurkat cells cultured in conditions of serum starvation, as measured by annexin V staining and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling. In addition, retarded loss of mitochondrial transmembrane potential was observed in the PLZF-expressing clones, suggesting that PLZF protects from cell death through a mitochondrial-dependent mechanism. To identify apoptosis-related targets of PLZF, a screen for differential expression identified BID, a proapoptotic member of the Bcl2 family, as significantly down-regulated by PLZF. Furthermore, a high-affinity PLZF-binding site element was identified upstream of the BID transcriptional start site, as assessed by electrophoretic mobility-shift assays. These results suggest that BID is a target of PLZF repression and a candidate gene to mediate the PLZF-induced resistance to apoptosis.
Related Links	http://dx.doi.org/10.1073/pnas.0308358100
Ending Page	1903
Page Count	6
Starting Page	1898
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	7
Volume Number	101
Language	English
Publisher	National Academy of Sciences
Publisher Date	2004-02-17
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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