ArticleOncogene2001
PARP co-activates B-MYB through enhanced phosphorylation at cyclin/cdk2 sites.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
11 citing papers in PubMed, 29 citations in OpenAlex.
- Analysis of matched primary and recurrent BRCA1/2 mutation-associated tumors identifies recurrence-specific drivers.Nature communications · 2022Article
- Molecular response to PARP1 inhibition in ovarian cancer cells as determined by mass spectrometry based proteomics.Journal of ovarian research · 2021Article
- Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes.Nature communications · 2019Article
- MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis.Cell death & disease · 2017Review
- Functional and prognostic significance of the genomic amplification of frizzled 6 (FZD6) in breast cancer.The Journal of pathology · 2017Article
- B-Myb switches from Cyclin/Cdk-dependent to Jnk- and p38 kinase-dependent phosphorylation and associates with SC35 bodies after UV stress.Cell death & disease · 2013Article
- B-Myb promotes S-phase independently of its sequence-specific DNA binding activity and interacts with polymerase delta-interacting protein 1 (Pdip1).Cell cycle (Georgetown, Tex.) · 2012Article
- Is there an epigenetic component underlying the resistance of triple-negative breast cancers to parp inhibitors?Frontiers in pharmacology · 2012Article
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- Phosphorylation of progesterone receptor serine 400 mediates ligand-independent transcriptional activity in response to activation of cyclin-dependent protein kinase 2.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PARP is a multifunctional protein that can affect genome stability, transcription control, telomere length and cell death. Recently we have reported that PARP binds to and enhances B-MYB transactivating potential. B-MYB is a potentially oncogenic transcription factor involved in mammalian cell proliferation, survival and differentiation. B-MYB gene expression is growth regulated and B-MYB protein is phosphorylated during S phase by cyclin A or E/cdk2 kinase, resulting in augmented transactivating potential. Here we show that PARP induces phosphorylation of B-MYB protein at cdk2 phosphorylation sites, since a B-MYB protein with mutated cdk2 phosphorylation sites is refractory to PARP-induced phosphorylation and co-activation in mammalian cells. We propose that PARP functions as a B-MYB co-factor by promoting cyclin/cdk2-dependent B-MYB phosphorylation. These results highlight a novel role for PARP as a factor that integrates cyclin-dependent kinases signaling with gene transcription.
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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.