ArticleMolecular and cellular biology2001
Nuclear localization of CBF1 is regulated by interactions with the SMRT corepressor complex.
Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 116 citations in OpenAlex.
- EN2 Regulates Pancreatic Cancer Initiation, Progression, and Epithelial-Mesenchymal Transition Through the Notch Signalling Pathway.Journal of cellular and molecular medicine · 2026Article
- Novel Genome-EngineeredGenes · 2024Article
- MicroRNAs as the pivotal regulators of cisplatin resistance in head and neck cancers.Cancer cell international · 2023Review
- OptIC-Notch reveals mechanism that regulates receptor interactions with CSL.Development (Cambridge, England) · 2023Article
- Review
- The Binding of CSL Proteins to Either Co-Activators or Co-Repressors Protects from Proteasomal Degradation Induced by MAPK-Dependent Phosphorylation.International journal of molecular sciences · 2022Article
- Review
- Nucleo-cytoplasmic shuttling of murine RBPJ by Hairless protein matches that of Su(H) protein in the model system Drosophila melanogaster.Hereditas · 2021Article
- An RBPJ-Cells · 2019Article
- Long non-coding RNA AFAP1-AS1/miR-320a/RBPJ axis regulates laryngeal carcinoma cell stemness and chemoresistance.Journal of cellular and molecular medicine · 2018Article
- Consequences of early life stress on genomic landscape of H3K4me3 in prefrontal cortex of adult mice.BMC genomics · 2018Article
- Hairless-binding deficient Suppressor of Hairless alleles reveal Su(H) protein levels are dependent on complex formation with Hairless.PLoS genetics · 2017Article
- Notch1-promoted TRPA1 expression in erythroleukemic cells suppresses erythroid but enhances megakaryocyte differentiation.Scientific reports · 2017Article
- Transcription factors, transcriptional coregulators, and epigenetic modulation in the control of pulmonary vascular cell phenotype: therapeutic implications for pulmonary hypertension (2015 Grover Conference series).Pulmonary circulation · 2016Review
- Negative control of CSL gene transcription by stress/DNA damage response and p53.Cell cycle (Georgetown, Tex.) · 2016Article
- Structure and Function of the Su(H)-Hairless Repressor Complex, the Major Antagonist of Notch Signaling in Drosophila melanogaster.PLoS biology · 2016Article
- Article
- The CSL proteins, versatile transcription factors and context dependent corepressors of the notch signaling pathway.Cell division · 2016Review
- Loss of the Notch effector RBPJ promotes tumorigenesis.The Journal of experimental medicine · 2015Article
- Nuclear receptor corepressor complexes in cancer: mechanism, function and regulation.American journal of clinical and experimental urology · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The CSL family protein CBF1 is a nuclear mediator of Notch signaling and has been predicted to contain an N-terminal nuclear localization signal in exon 4. Surprisingly, we found that CBF1 carrying mutations at codon 233 or 249 within exon 7 was restricted to the cytoplasm. In mammalian and yeast two-hybrid assays, these mutations were also associated with a loss of CBF1-mediated transcriptional repression and a severely impaired interaction with the corepressors SMRT and CIR. Overexpression of SMRT rescued the ability of mutant CBF1 to target to the nucleus of transfected cells and similarly rescued nuclear targeting of enhanced green fluorescent protein (EGFP)-CBF1 exons 6 to 9 CBF1(6-9)carrying the codon 233 or 249 mutations. Carboxy-terminally truncated SMRT with amino acids (aa) 1291 to 1495 deleted was unable to rescue the nuclear targeting of mutant EGFP-CBF1(6-9). In yeast two-hybrid assays, the SMRT aa 1291 to 1495 domain interacted with SKIP and SMRT aa 1291 to 1495 colocalized with SKIP within the nuclei of cotransfected cells. Comparison of the intracellular localization of CBF1(6-9) with that of CBF1(5-9) further supported the suggestion that nuclear targeting of CBF1 is dependent on the formation of a CBF1-SMRT-SKIP corepressor complex. These observations suggest that nuclear targeting of CBF1 is itself a component of CBF1-mediated gene regulation and that in the absence of signaling, CBF1 enters the nucleus precommitted to a transcriptional repression function. The activators NotchIC (the intracellular domain of Notch) and Epstein-Barr virus EBNA2 also mediated nuclear targeting of mutant CBF1, consistent with the competition model for activator versus corepressor binding to CBF1.
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