ArticleCell death & disease2013
B-Myb switches from Cyclin/Cdk-dependent to Jnk- and p38 kinase-dependent phosphorylation and associates with SC35 bodies after UV stress.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- JNK Inhibition Overcomes Resistance of Metastatic Tetraploid Cancer Cells to Irradiation-Induced Apoptosis.International journal of molecular sciences · 2025Article
- Activation of the oncogenic transcription factor B-Myb via multisite phosphorylation and prolyl cis/trans isomerization.Nucleic acids research · 2019Article
- Interplay with the Mre11-Rad50-Nbs1 complex and phosphorylation by GSK3β implicate human B-Myb in DNA-damage signaling.Scientific reports · 2017Article
- Cefradine blocks solar-ultraviolet induced skin inflammation through direct inhibition of T-LAK cell-originated protein kinase.Oncotarget · 2016Article
- PDIP38 is translocated to the spliceosomes/nuclear speckles in response to UV-induced DNA damage and is required for UV-induced alternative splicing of MDM2.Cell cycle (Georgetown, Tex.) · 2013Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B-Myb is a highly conserved member of the Myb transcription factor family that has essential roles in cell-cycle progression. Recent work has suggested that B-Myb is also involved in the cellular DNA-damage response. Here, we have investigated the fate of B-Myb in UV-irradiated cells. UV stress leads to the appearance of phosphorylated B-Myb in nuclear SC35 speckles during transcriptional shutdown. Furthermore, we show that UV irradiation leads to a change of the phosphorylation pattern of B-Myb, which is caused by a switch from Cyclin/Cdk-dependent to Jnk and p38 kinase-dependent phosphorylation. Taken together, we have identified Jnk and p38 kinase as novel regulators of B-Myb and established the localization of phosphorylated B-Myb in SC35 speckles as a potential novel regulatory mechanism for B-Myb in UV irradiated cells.
Indexed as
Identifiers
What OpenQuestion holds
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.