ArticlePloS one2011
Dynamic regulation of Oct1 during mitosis by phosphorylation and ubiquitination.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- A non-transcriptional mitotic function of POU/Oct factors ensures spindle assembly and chromosome segregation.Journal of cell science · 2026Article
- Review
- 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
- In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022Review
- Moonlighting in Mitosis: Analysis of the Mitotic Functions of Transcription and Splicing Factors.Cells · 2020Review
- Oct1/Pou2f1 is selectively required for colon regeneration and regulates colon malignancy.PLoS genetics · 2019Article
- MicroRNA-451 Inhibits Migration of Glioblastoma while Making It More Susceptible to Conventional Therapy.Non-coding RNA · 2019Article
- Article
- The POU/Oct Transcription Factor Nubbin Controls the Balance of Intestinal Stem Cell Maintenance and Differentiation by Isoform-Specific Regulation.Stem cell reports · 2018Article
- Diversity among POU transcription factors in chromatin recognition and cell fate reprogramming.Cellular and molecular life sciences : CMLS · 2018Review
- BRCA1 through Its E3 Ligase Activity Regulates the Transcription Factor Oct1 and Carbohydrate Metabolism.Molecular cancer research : MCR · 2018Article
- Stress-induced release of Oct-1 from the nuclear envelope is mediated by JNK phosphorylation of lamin B1.PloS one · 2017Article
- 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 telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence.Open biology · 2016Article
- Increased level of Oct-1 protein in tumor cells modulates cellular response to anticancer drugs.Doklady. Biochemistry and biophysics · 2016Article
- The Oct1 transcription factor and epithelial malignancies: Old protein learns new tricks.Biochimica et biophysica acta · 2016Review
- Aurkb/PP1-mediated resetting of Oct4 during the cell cycle determines the identity of embryonic stem cells.eLife · 2016Article
- Glucose-based regulation of miR-451/AMPK signaling depends on the OCT1 transcription factor.Cell reports · 2015Article
- "Stop Ne(c)king around": How interactomics contributes to functionally characterize Nek family kinases.World journal of biological chemistry · 2014Review
- Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTranscription factor Oct1 regulates multiple cellular processes. It is known to be phosphorylated during the cell cycle and by stress, however the upstream kinases and downstream consequences are not well understood. One of these modified forms, phosphorylated at S335, lacks the ability to bind DNA. Other modification states besides phosphorylation have not been described. METHODOLOGY/PRINCIPAL
findingsWe show that Oct1 is phosphorylated at S335 in the Oct1 DNA binding domain during M-phase by the NIMA-related kinase Nek6. Phospho-Oct1 is also ubiquitinated. Phosphorylation excludes Oct1 from mitotic chromatin. Instead, Oct1(pS335) concentrates at centrosomes, mitotic spindle poles, kinetochores and the midbody. Oct1 siRNA knockdown diminishes the signal at these locations. Both Oct1 ablation and overexpression result in abnormal mitoses. S335 is important for the overexpression phenotype, implicating this residue in mitotic regulation. Oct1 depletion causes defects in spindle morphogenesis in Xenopus egg extracts, establishing a mitosis-specific function of Oct1. Oct1 colocalizes with lamin B1 at the spindle poles and midbody. At the midbody, both proteins are mutually required to correctly localize the other. We show that phospho-Oct1 is modified late in mitosis by non-canonical K11-linked polyubiquitin chains. Ubiquitination requires the anaphase-promoting complex, and we further show that the anaphase-promoting complex large subunit APC1 and Oct1(pS335) interact. CONCLUSIONS/SIGNIFICANCE: These findings reveal mechanistic coupling between Oct1 phosphorylation and ubquitination during mitotic progression, and a role for Oct1 in mitosis.
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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.