ArticleMolecular and cellular biology2002
Critical residues within the BTB domain of PLZF and Bcl-6 modulate interaction with corepressors.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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91 citing papers in PubMed, 212 citations in OpenAlex.
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- Sibling rivalry among the ZBTB transcription factor family: homodimers versus heterodimers.Life science alliance · 2022Article
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- The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by repressing pro-differentiation genes.Cell reports · 2022Article
- B cell lymphoma 6A regulates immune development and function in zebrafish.Frontiers in cellular and infection microbiology · 2022Article
- KCTD19 and its associated protein ZFP541 are independently essential for meiosis in male mice.PLoS genetics · 2021Article
- Dual targeting of brain region-specific kinases potentiates neurological rescue in Spinocerebellar ataxia type 1.The EMBO journal · 2021Article
- BCL6 confers KRAS-mutant non-small-cell lung cancer resistance to BET inhibitors.The Journal of clinical investigation · 2021Article
- Structural analysis of the PATZ1 BTB domain homodimer.Acta crystallographica. Section D, Structural biology · 2020Article
- Expression of the PTEN/FOXO3a/PLZF signalling pathway in pancreatic cancer and its significance in tumourigenesis and progression.Investigational new drugs · 2020Article
- Identifying Genome-Wide Sequence Variations and Candidate Genes Implicated in Self-Incompatibility by ResequencingInternational journal of molecular sciences · 2019Article
31 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
The PLZF (promyelocytic leukemia zinc finger) transcriptional repressor, when fused to retinoic acid receptor alpha (RARalpha), causes a refractory form of acute promyelocytic leukemia. The highly conserved N-terminal BTB (bric a brac, tramtrack, broad complex)/POZ domain of PLZF plays a critical role in this disease, since it is required for transcriptional repression by the PLZF-RARalpha fusion protein. The crystal structure of the PLZF BTB domain revealed an obligate homodimer with a highly conserved charged pocket formed by apposition of the two monomers. An extensive structure-function analysis showed that the charged pocket motif plays a major role in transcriptional repression by PLZF. We found that mutations of the BTB domain that neutralize key charged pocket residues did not disrupt dimerization, yet abrogated the ability of PLZF to repress transcription and led to the loss of interaction with N-CoR, SMRT, and histone deacetylases (HDACs). We extended these studies to the Bcl-6 protein, which is linked to the pathogenesis of non-Hodgkin's lymphomas. In this case, neutralizing the charged pocket also resulted in loss of repression and corepressor binding. Experiments with purified protein showed that corepressor-BTB interactions were direct. A comparison of the PLZF, Bcl-6, and the FAZF (Fanconi anemia zinc finger)/ROG protein shows that variations in the BTB pocket result in differential affinity for corepressors, which predicts the potency of transcriptional repression. Thus, the BTB pocket represents a molecular structure involved in recruitment of transcriptional repression complexes to target promoters.
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