ArticleProceedings of the National Academy of Sciences of the United States of America2004
The promyelocytic leukemia zinc finger protein down-regulates apoptosis and expression of the proapoptotic BID protein in lymphocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- Blood gene expression profiling of an early acetaminophen response.The pharmacogenomics journal · 2017Trial
- Old versus new: upstream and downstream of promyelocytic leukemia zinc finger protein.Cancer gene therapy · 2025Review
- Glucocorticoid-mediated induction of ZBTB16 affects insulin secretion in human islets and EndoC-βH1 β-cells.iScience · 2023Article
- Progranulin regulates the development and function of NKT2 cells through EZH2 and PLZF.Cell death and differentiation · 2022Article
- Expression of the PTEN/FOXO3a/PLZF signalling pathway in pancreatic cancer and its significance in tumourigenesis and progression.Investigational new drugs · 2020Article
- Differential Skewing of Circulating MR1-Restricted and γδ T Cells in Human Psoriasis Vulgaris.Frontiers in immunology · 2020Article
- Far-infrared protects vascular endothelial cells from advanced glycation end products-induced injury via PLZF-mediated autophagy in diabetic mice.Scientific reports · 2017Article
- Increase of zinc finger protein 179 in response to CCAAT/enhancer binding protein delta conferring an antiapoptotic effect in astrocytes of Alzheimer's disease.Molecular neurobiology · 2015Article
- Role of promyelocytic leukemia zinc finger (PLZF) in cell proliferation and cyclin-dependent kinase inhibitor 1A (p21WAF/CDKN1A) gene repression.The Journal of biological chemistry · 2014Article
- PLZF expression during colorectal cancer development and in normal colorectal mucosa according to body size, as marker of colorectal cancer risk.TheScientificWorldJournal · 2013Article
- Zinc finger protein ZBTB20 expression is increased in hepatocellular carcinoma and associated with poor prognosis.BMC cancer · 2011Article
- Understanding PLZF: two transcriptional targets, REDD1 and smooth muscle α-actin, define new questions in growth control, senescence, self-renewal and tumor suppression.Cell cycle (Georgetown, Tex.) · 2011Article
- The promyelocytic leukemia zinc finger (PLZF) protein exerts neuroprotective effects in neuronal cells and is dysregulated in experimental stroke.Brain pathology (Zurich, Switzerland) · 2011Article
- The BTB-zinc finger transcriptional regulator PLZF controls the development of invariant natural killer T cell effector functions.Nature immunology · 2008Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.