ArticleOncogene2007
DNA-PK phosphorylation sites on Oct-1 promote cell survival following DNA damage.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Trial
- Review
- DNA-PKcs, a player winding and dancing with RNA metabolism and diseases.Cellular & molecular biology letters · 2025Review
- Secrets of DNA-PKcs beyond DNA repair.NPJ precision oncology · 2024Review
- High expression of transcription factor POU2F1 confers improved survival on smokers with lung adenocarcinoma: a retrospective study of two cohorts.Translational lung cancer research · 2023Article
- Article
- The POU-Domain Transcription Factor Oct-6/POU3F1 as a Regulator of Cellular Response to Genotoxic Stress.Cancers · 2019Article
- Diversity among POU transcription factors in chromatin recognition and cell fate reprogramming.Cellular and molecular life sciences : CMLS · 2018Review
- Different N-terminal isoforms of Oct-1 control expression of distinct sets of genes and their high levels in Namalwa Burkitt's lymphoma cells affect a wide range of cellular processes.Nucleic acids research · 2016Article
- The Oct1 transcription factor and epithelial malignancies: Old protein learns new tricks.Biochimica et biophysica acta · 2016Review
- Oct-2 forms a complex with Oct-1 on the iNOS promoter and represses transcription by interfering with recruitment of RNA PolII by Oct-1.Nucleic acids research · 2015Article
- Regulation of Oct1/Pou2f1 transcription activity by O-GlcNAcylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Oct transcription factors in development and stem cells: insights and mechanisms.Development (Cambridge, England) · 2013Review
- Octamer-binding transcription factors: genomics and functions.Frontiers in bioscience (Landmark edition) · 2013Review
- Systematic analysis of somatic mutations in phosphorylation signaling predicts novel cancer drivers.Molecular systems biology · 2013Article
- Article
- Cdx2 homeoprotein inhibits non-homologous end joining in colon cancer but not in leukemia cells.Nucleic acids research · 2012Article
- Ku regulates signaling to DNA damage response pathways through the Ku70 von Willebrand A domain.Molecular and cellular biology · 2012Article
- RanBPM is an inhibitor of ERK signaling.PloS one · 2012Article
- Lymphocyte development: integration of DNA damage response signaling.Advances in immunology · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Octamer transcription factor-1 (Oct-1) has recently been shown to function as a stress sensor that promotes cell survival subsequent to DNA damage. Here, we show that the survival signal imparted by Oct-1 following exposure to ionizing radiation (IR) is dependent upon DNA-dependent protein kinase (DNA-PK)-dependent phosphorylation of a cluster of 13 specific ser/thr residues within the N-terminal transcriptional regulatory domain of Oct-1. Although IR treatment did not affect the recruitment of Oct-1 to the histone H2B promoter, the recruitment of RNA polymerase II, TATA-binding protein and histone H4 acetylation were strongly reduced, consistent with a decrease in Oct-1 transcriptional regulatory potential following IR exposure. Ser/Thr-Ala substitution of 13 sites present in Oct-1 transcriptional regulatory domain eliminated Oct-1 phosphorylation subsequent to IR exposure. Further, these substitutions prevented Oct-1 from rescuing the survival of IR-treated Oct-1-/- murine embryonic fibroblasts, providing a direct link between DNA-PK-dependent phosphorylation and the contribution of Oct-1 to cell survival. These results implicate Oct-1 as a primary effector in a DNA-PK-dependent cell survival pathway that is activated by double-stranded DNA breaks.
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.