ArticleMolecular cancer2011
PIAS1 interacts with FLASH and enhances its co-activation of c-Myb.
Article in Molecular cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP).Translational oncology · 2024Article
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- The E3 Ligase PIAS1 Regulates p53 Sumoylation to Control Stress-Induced Apoptosis of Lens Epithelial Cells Through the Proapoptotic Regulator Bax.Frontiers in cell and developmental biology · 2021Article
- Dissecting the transactivation domain (tAD) of the transcription factor c-Myb to assess recent models of tAD function.FEBS open bio · 2020Article
- The SUMO protease SENP1 and the chromatin remodeler CHD3 interact and jointly affect chromatin accessibility and gene expression.The Journal of biological chemistry · 2018Article
- Review
- FLASH protects ZEB1 from degradation and supports cancer cells' epithelial-to-mesenchymal transition.Oncogenesis · 2016Article
- SUMOylation by the E3 ligase TbSIZ1/PIAS1 positively regulates VSG expression in Trypanosoma brucei.PLoS pathogens · 2014Article
- Novel strategies to enforce an epithelial phenotype in mesenchymal cells.Cancer research · 2014Article
- SUMO regulates proteasome-dependent degradation of FLASH/Casp8AP2.Cell cycle (Georgetown, Tex.) · 2013Article
- Article
- Poly-small ubiquitin-like modifier (PolySUMO)-binding proteins identified through a string search.The Journal of biological chemistry · 2012Article
- Systems-wide RNAi analysis of CASP8AP2/FLASH shows transcriptional deregulation of the replication-dependent histone genes and extensive effects on the transcriptome of colorectal cancer cells.Molecular cancer · 2012Article
- FLASH knockdown sensitizes cells to Fas-mediated apoptosis via down-regulation of the anti-apoptotic proteins, MCL-1 and Cflip short.PloS one · 2012Article
- Identification of c-Myb Target Genes in K562 Cells Reveals a Role for c-Myb as a Master Regulator.Genes & cancer · 2011Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFLASH is a huge nuclear protein involved in various cellular functions such as apoptosis signalling, NF-κB activation, S-phase regulation, processing of histone pre-mRNAs, and co-regulation of transcription. Recently, we identified FLASH as a co-activator of the transcription factor c-Myb and found FLASH to be tightly associated with active transcription foci. As a huge multifunctional protein, FLASH is expected to have many interaction partners, some which may shed light on its function as a transcriptional regulator.
resultsTo find additional FLASH-associated proteins, we performed a yeast two-hybrid (Y2H) screening with FLASH as bait and identified the SUMO E3 ligase PIAS1 as an interaction partner. The association appears to involve two distinct interaction surfaces in FLASH. We verified the interaction by Y2H-mating, GST pulldowns, co-IP and ChIP. FLASH and PIAS1 were found to co-localize in nuclear speckles. Functional assays revealed that PIAS1 enhances the intrinsic transcriptional activity of FLASH in a RING finger-dependent manner. Furthermore, PIAS1 also augments the specific activity of c-Myb, and cooperates with FLASH to further co-activate c-Myb. The three proteins, FLASH, PIAS1, and c-Myb, are all co-localized with active RNA polymerase II foci, resembling transcription factories.
conclusionsWe conclude that PIAS1 is a common partner for two cancer-related nuclear factors, c-Myb and FLASH. Our results point to a functional cooperation between FLASH and PIAS1 in the enhancement of c-Myb activity in active nuclear foci.
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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.