ArticleCell cycle (Georgetown, Tex.)2013
FMN2 is a novel regulator of the cyclin-dependent kinase inhibitor p21.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 33 citations in OpenAlex.
- High expression of formin-2 can promote ovarian cancer chemoresistance via immunosuppressive macrophages.Functional & integrative genomics · 2025Article
- Personalized identification and characterization of genome-wide gene expression differences between patient-matched intracranial and extracranial melanoma metastasis pairs.Acta neuropathologica communications · 2024Article
- Transcriptome Profile in the Mouse Brain of Hepatic Encephalopathy and Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Heterozygous FMN2 missense variant found in a family case of premature ovarian insufficiency.Journal of ovarian research · 2022Article
- Article
- Impact of Disseminated Neuroblastoma Cells on the Identification of the Relapse-Seeding Clone.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Article
- Genomic regulation of senescence and innate immunity signaling in the retinal pigment epithelium.Mammalian genome : official journal of the International Mammalian Genome Society · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
We have identified the human FMN2 gene as a novel target regulated by induction of p14ARF and by multiple other stress responses, including DNA damage and hypoxia, which have in common activation of cell cycle arrest. We showed that increased expression of the FMN2 gene following p14ARF induction is caused, at the transcriptional level, by relief of repression by RelA and E2F1, which, under non-induced conditions, bind the FMN2 promoter. Increased FMN2 protein levels promote cell cycle arrest by inhibiting the degradation of p21, and our data show that control of p21 stability is a key part of the mechanism that regulates p21 induction. Consistent with this model, we have shown that transient expression of exogenous FMN2 protein alone is sufficient to increase p21 protein levels in cells, without altering p21 mRNA levels. Here, we provide additional evidence for the role of the N terminus of FMN2 as being the important domain required for p21 stability. In addition, we also investigate the role of RelA's threonine 505 residue in the control of FMN2. Our results identify FMN2 as a crucial protein involved in the control of p21.
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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.