ArticleFrontiers in cell and developmental biology2021
Stimulation of c-Jun/AP-1-Activity by the Cell Cycle Inhibitor p57
Article in Frontiers in cell and developmental biology, 2021. 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, 16 citations in OpenAlex.
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- Ubiquitination and deubiquitination: Implications for the pathogenesis and treatment of osteoarthritis.Journal of orthopaedic translation · 2024Review
- p57International journal of molecular sciences · 2024Article
- Regulation of developmentally controlled enhancer activity by extrinsic signals in normal and malignant cells: AP-1 at the centre.Frontiers in epigenetics and epigenomics · 2024Article
- Comprehensive Analysis of Kisspeptin Signaling: Effects on Cellular Dynamics in Cervical Cancer.Biomolecules · 2024Article
- Molecular mechanisms of human overgrowth and use ofFrontiers in genetics · 2024Review
- The significance of CDT1 expression in non-cancerous and cancerous liver in cases with hepatocellular carcinoma.Journal of clinical biochemistry and nutrition · 2023Article
- Based on Network Pharmacology Tools to Investigate the Mechanism ofFrontiers in medicine · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p57 is a member of the Cip/Kip family of cell cycle inhibitors which restrict the eukaryotic cell cycle by binding to and inhibiting cyclin/CDK complexes. They are considered as tumor suppressors and inactivating genomic mutations of p57 are associated with human overgrowth disorders. Increasing evidence suggests that p57 controls additional cellular processes beyond cell cycle control such as apoptosis, cell migration or transcription. Here we report that p57 can stimulate AP-1 promotor activity. While transactivation by c-Jun is strongly activated by p57, it did not enhance c-Fos induced transcription. This indicates that c-Jun is the target of p57 in the canonical AP-1 heterodimeric transcription factor. We could detect endogenous p57/c-Jun containing complexes in cells by co-immunoprecipitation. The strong stimulation of c-Jun activity is not the consequence of activating phosphorylation in the transactivation domain (TAD) of c-Jun, but rather due to negative interference with c-Jun repressors and positive interference with c-Jun activators. In contrast to full-length p57, the amino- and carboxy-terminal domains of p57 are insufficient for a significant activation of c-Jun induced transcription. When expressed in presence of full length p57, the p57
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