ArticleBMC molecular biology2009
Interaction of ZEB and histone deacetylase with the PLDLS-binding cleft region of monomeric C-terminal binding protein 2.
Article in BMC molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 62 citations in OpenAlex.
- Obesity Disrupts CtBP2-Mediated Maintenance of Transcriptional Equilibrium in Hypothalamic Feeding Circuitry.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Variant characterization in the intrinsically disordered human proteome.Nature structural & molecular biology · 2026Article
- Locus-specific proteomics identifies novel regulators of Epstein-Barr virus lytic reactivation.Journal of virology · 2026Article
- Identification and characterization of Eco-miR 169-EcNF-YA13 gene regulatory network reveal their role in conferring tolerance to dehydration and salinity stress in finger millet.Scientific reports · 2025Article
- Phosphorylation-mediated disassembly of C-terminal binding protein 2 tetramer impedes epigenetic silencing of pluripotency in mouse embryonic stem cells.Nucleic acids research · 2024Article
- Decline in corepressor CNOT1 in the pregnant myometrium near term impairs progesterone receptor function and increases contractile gene expression.The Journal of biological chemistry · 2024Article
- Master corepressor inactivation through multivalent SLiM-induced polymerization mediated by the oncogene suppressor RAI2.Nature communications · 2024Article
- Review
- ZEB1 promotes non-homologous end joining double-strand break repair.Nucleic acids research · 2023Article
- Aldolase B attenuates clear cell renal cell carcinoma progression by inhibiting CtBP2.Frontiers of medicine · 2023Article
- Metabolic modulation of CtBP dimeric status impacts the repression of DNA damage repair genes and the platinum sensitivity of ovarian cancer.International journal of biological sciences · 2023Article
- The CtIP-CtBP1/2-HDAC1-AP1 transcriptional complex is required for the transrepression of DNA damage modulators in the pathogenesis of osteosarcoma.Translational oncology · 2022Article
- Circular RNA circHERC4 as a novel oncogenic driver to promote tumor metastasis via the miR-556-5p/CTBP2/E-cadherin axis in colorectal cancer.Journal of hematology & oncology · 2021Article
- The transrepression and transactivation roles of CtBPs in the pathogenesis of different diseases.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Review
- Proteomic Analysis of Zeb1 Interactome in Breast Carcinoma Cells.Molecules (Basel, Switzerland) · 2021Article
- p53 is regulated by aerobic glycolysis in cancer cells by the CtBP family of NADH-dependent transcriptional regulators.Science signaling · 2020Article
- ZEB1/NuRD complex suppresses TBC1D2b to stimulate E-cadherin internalization and promote metastasis in lung cancer.Nature communications · 2019Article
- A pathogenic CtBP1 missense mutation causes altered cofactor binding and transcriptional activity.Neurogenetics · 2019Article
- Oligomeric form of C-terminal-binding protein coactivates NeuroD1-mediated transcription.FEBS letters · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProteins of the C-terminal binding protein (CtBP) family, CtBP1 and CtBP2 are closely related transcriptional regulators that are coded by two different gene loci in the vertebrate genomes. They perform redundant and unique functions during animal development. CtBP proteins mediate their transcriptional function through interaction with various DNA-binding repressors that contain PLDLS-like motifs and chromatin modifying enzymes, such as class I histone deacetylases (HDAC) that do not contain such motifs. The N-terminal region of CtBP1/2 forms a hydrophobic cleft and is involved in interaction with both PLDLS-containing factors and non-PLDLS factors. CtBP proteins function as dimers to mediate transcriptional repression and dimerization is modulated by specific binding to NAD/NADH.
resultsIn this study, we have investigated the role of dimerization of CtBP2 in recruitment of PLDLS-motif cofactors and non-PLDLS cofactors. Our results indicate that mutations in CtBP2 that interfere with dimerization abolish CtBP2 interaction with most cellular factors, except the PLDLS-motif factor zinc-finger E-box binding homeobox (ZEB) and the non-PLDLS factor HDAC2. Unlike most PLDLS-containing CtBP-binding proteins, ZEB contains three PLDLS-like motifs and all three contribute to the interaction with the CtBP2 monomer. Despite the ability to interact with ZEB and HDAC, the CtBP2 monomer fails to mediate ZEB-dependent transcriptional repression. The lack of repression activity of the CtBP2 monomer is correlated with the competition between ZEB and HDAC for interaction with the CtBP2 monomer.
conclusionThese results suggest a competition between the canonical PLDLS-motif factors such as E1A and non-PLDLS factor HDAC for interaction with CtBP. They also indicate that the affinity for the CtBP monomer may be determined by the number as well as amino acid sequence compositions of the PLDLS-like motifs. Our results are consistent with a model that the CtBP2 dimer may interact with a PLDLS-containing repressor through one monomer and recruit HDAC and other chromatin modifying enzymes through the second monomer in the CtBP2 dimer.
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