ArticleEndocrine1998
c-Fos dimerization with c-Jun represses c-Jun enhancement of androgen receptor transactivation.
Article in Endocrine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Integrated single-cell analysis defines the epigenetic basis of castration-resistant prostate luminal cells.Cell stem cell · 2024Article
- JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression.Molecular cancer · 2024Article
- Intrinsically disordered proteins and conformational noise: The hypothesis a decade later.iScience · 2023Review
- Protein conformational dynamics and phenotypic switching.Biophysical reviews · 2021Review
- PAGE4 and Conformational Switching: Insights from Molecular Dynamics Simulations and Implications for Prostate Cancer.Journal of molecular biology · 2018Article
- Phenotypic Plasticity, Bet-Hedging, and Androgen Independence in Prostate Cancer: Role of Non-Genetic Heterogeneity.Frontiers in oncology · 2018Review
- Phenotypic Plasticity and Cell Fate Decisions in Cancer: Insights from Dynamical Systems Theory.Cancers · 2017Review
- Cancer/Testis Antigens: "Smart" Biomarkers for Diagnosis and Prognosis of Prostate and Other Cancers.International journal of molecular sciences · 2017Review
- Phosphorylation-induced conformational dynamics in an intrinsically disordered protein and potential role in phenotypic heterogeneity.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Androgen receptor phosphorylation: biological context and functional consequences.Endocrine-related cancer · 2014Review
- Repression of NF-kappaB and activation of AP-1 enhance apoptosis in prostate cancer cells.International journal of cancer · 2009Article
- c-Fos as a proapoptotic agent in TRAIL-induced apoptosis in prostate cancer cells.Cancer research · 2007Article
- c-Jun enhancement of androgen receptor transactivation is associated with prostate cancer cell proliferation.Oncogene · 2006Article
- Makorin RING finger protein 1 (MKRN1) has negative and positive effects on RNA polymerase II-dependent transcription.Endocrine · 2006Article
- c-Jun targets amino terminus of androgen receptor in regulating androgen-responsive transcription.Endocrine · 2000Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional activity of the human androgen receptor (hAR), like other nuclear receptors, is dependent on accessory factors. One such factor is c-Jun, which has been shown to have a selective function of mediating androgen receptor-dependent transactivation. This c-Jun activity is inhibited by c-Fos, another protooncoprotein that can dimerize with c-Jun to form the transcription factor AP-1. Here we show that c-jun mediates hAR-induced transactivation from the promoter of the androgen-regulated gene, human kallikrein-2 (hKLK2), and c-Fos blocks this activity. Using c-Fos truncation mutants and measuring hKLK2-dependent transcription, we have determined that the bZIP region of c-Fos is required and sufficient for inhibiting c-Jun enhancement of hAR transactivation. Further truncation analysis of the bZIP shows that the c-Fos dimerization function, mediated through the leucine zipper, is essential for the negative activity, whereas DNA binding, mediated through the basic region, is dispensable. These results suggest that heterodimerization by c-Fos with c-Jun blocks c-Jun's ability to enhance hAR-induced transactivation.
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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.