ArticleMolecular and cellular biology2000
Cell signaling switches HOX-PBX complexes from repressors to activators of transcription mediated by histone deacetylases and histone acetyltransferases.
Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
73 citing papers in PubMed, 195 citations in OpenAlex.
- HDAC1/2-mediated repression of Wnt receptor expression orients asymmetric division polarity in Caenorhabditis elegans.Development (Cambridge, England) · 2026Article
- Nervous system-wide analysis of Hox regulation of terminal neuronal fate specification in Caenorhabditis elegans.PLoS genetics · 2022Article
- The Tomato Transcription Factor SlNAC063 Is Required for Aluminum Tolerance by RegulatingFrontiers in plant science · 2022Article
- Cell-type-specific Hox regulatory strategies orchestrate tissue identity.Current biology : CB · 2021Article
- Combined genomic and proteomic approaches reveal DNA binding sites and interaction partners of TBX2 in the developing lung.Respiratory research · 2021Article
- Article
- Combinatorial action of NF-Y and TALE at embryonic enhancers defines distinct gene expression programs during zygotic genome activation in zebrafish.Developmental biology · 2020Article
- Elevated HOX gene expression in acute myeloid leukemia is associated with NPM1 mutations and poor survival.Journal of advanced research · 2019Article
- The Hox transcription factor Ubx stabilizes lineage commitment by suppressing cellular plasticity ineLife · 2019Article
- Functional testing of a humanDisease models & mechanisms · 2018Article
- TALE factors use two distinct functional modes to control an essential zebrafish gene expression program.eLife · 2018Article
- HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis.Nature communications · 2018Article
- Targeting HOX/PBX dimers in cancer.Oncotarget · 2017Review
- A PBX1 transcriptional network controls dopaminergic neuron development and is impaired in Parkinson's disease.The EMBO journal · 2016Article
- Developmental Patterning as a Quantitative Trait: Genetic Modulation of the Hoxb6 Mutant Skeletal Phenotype.PloS one · 2016Article
- Pbx1-dependent control of VMC differentiation kinetics underlies gross renal vascular patterning.Development (Cambridge, England) · 2015Article
- Estrogen receptor alpha signaling promotes Sle1-induced loss of tolerance and immune cell activation and is responsible for sex bias in B6.Sle1 congenic mice.Clinical immunology (Orlando, Fla.) · 2015Article
- PDX1 binds and represses hepatic genes to ensure robust pancreatic commitment in differentiating human embryonic stem cells.Stem cell reports · 2015Article
- Contrasting roles for MyoD in organizing myogenic promoter structures during embryonic skeletal muscle development.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- The TALE face of Hox proteins in animal evolution.Frontiers in genetics · 2015Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Hoxb1 autoregulatory element comprises three HOX-PBX binding sites. Despite the presence of HOXB1 and PBX1, this enhancer fails to activate reporter gene expression in retinoic acid-treated P19 cell monolayers. Activation requires cell aggregation in addition to RA. This suggests that HOX-PBX complexes may repress transcription under some conditions. Consistent with this, multimerized HOX-PBX binding sites repress reporter gene expression in HEK293 cells. We provide a mechanistic basis for repressor function by demonstrating that a corepressor complex, including histone deacetylases (HDACs) 1 and 3, mSIN3B, and N-CoR/SMRT, interacts with PBX1A. We map a site of interaction with HDAC1 to the PBX1 N terminus and show that the PBX partner is required for repression by the HOX-PBX complex. Treatment with the deacetylase inhibitor trichostatin A not only relieves repression but also converts the HOX-PBX complex to a net activator of transcription. We show that this activation function is mediated by the recruitment of the coactivator CREB-binding protein by the HOX partner. Interestingly, HOX-PBX complexes are switched from transcriptional repressors to activators in response to protein kinase A signaling or cell aggregation. Together, our results suggest a model whereby the HOX-PBX complex can act as a repressor or activator of transcription via association with corepressors and coactivators. The model implies that cell signaling is a direct determinant of HOX-PBX function in the patterning of the animal embryo.
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Registered trials
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.