ArticleThe Journal of cell biology2008
Fast regulation of AP-1 activity through interaction of lamin A/C, ERK1/2, and c-Fos at the nuclear envelope.
Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 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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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.
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Who cites it
90 citing papers in PubMed, 172 citations in OpenAlex.
- Article
- Deep Invaginations of Nuclear Envelope Coordinate Spatial Organization of Chromatin in Epithelium.bioRxiv : the preprint server for biology · 2026Article
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- Multi-omics analysis reveals the effects of prenatal nutrition on carcass-related tissues in beef cattle.Scientific reports · 2025Article
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- Rare Variation in LMNA Underlies Polycystic Ovary Syndrome Pathogenesis in 2 Independent Cohorts.The Journal of clinical endocrinology and metabolism · 2025Article
- Identifying the IntergenicMedComm · 2025Article
- Nuclear envelope proteins, mechanotransduction, and their contribution to breast cancer progression.npj biological physics and mechanics · 2025Review
- Mouse polyomavirus infection induces lamin reorganisation.The FEBS journal · 2024Article
- Role of lamin A/C on dendritic cell function in antiviral immunity.Cellular and molecular life sciences : CMLS · 2024Article
- Perinuclear damage from nuclear envelope deterioration elicits stress responses that contribute toScience advances · 2024Article
- Targeting c-Myc transactivation by LMNA inhibits tRNA processing essential for malate-aspartate shuttle and tumour progression.Clinical and translational medicine · 2024Article
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- c-Fos regulated by TMPO/ERK axis promotes 5-FU resistance via inducing NANOG transcription in colon cancer.Cell death & disease · 2024Article
- Prolonged Inhibition of the MEK1/2-ERK Signaling Axis Primes Interleukin-1 Beta Expression through Histone 3 Lysine 9 Demethylation in Murine Macrophages.International journal of molecular sciences · 2023Article
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- Functions and clinical significance of mechanical tumor microenvironment: cancer cell sensing, mechanobiology and metastasis.Cancer communications (London, England) · 2022Review
- Review
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- The Sky's the LEMit: New insights into nuclear structure regulation of transcription factor activity.Current opinion in cell biology · 2021Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sequestration of c-Fos at the nuclear envelope (NE) through interaction with A-type lamins suppresses AP-1-dependent transcription. We show here that c-Fos accumulation within the extraction-resistant nuclear fraction (ERNF) and its interaction with lamin A are reduced and enhanced by gain-of and loss-of ERK1/2 activity, respectively. Moreover, hindering ERK1/2-dependent phosphorylation of c-Fos attenuates its release from the ERNF induced by serum and promotes its interaction with lamin A. Accordingly, serum stimulation rapidly releases preexisting c-Fos from the NE via ERK1/2-dependent phosphorylation, leading to a fast activation of AP-1 before de novo c-Fos synthesis. Moreover, lamin A-null cells exhibit increased AP-1 activity and reduced levels of c-Fos phosphorylation. We also find that active ERK1/2 interacts with lamin A and colocalizes with c-Fos and A-type lamins at the NE. Thus, NE-bound ERK1/2 functions as a molecular switch for rapid mitogen-dependent AP-1 activation through phosphorylation-induced release of preexisting c-Fos from its inhibitory interaction with lamin A/C.
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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.