ArticleEndocrine2000
c-Jun targets amino terminus of androgen receptor in regulating androgen-responsive transcription.
Article in Endocrine, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
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
8 citing papers in PubMed, 22 citations in OpenAlex.
- Cellular specificity of androgen receptor, coregulators, and pioneer factors in prostate cancer.Endocrine oncology (Bristol, England) · 2022Review
- Phosphorylation of vaccinia-related kinase 1 at threonine 386 transduces glucose stress signal in human liver cells.Bioscience reports · 2020Article
- Factors that influence the androgen receptor cistrome in benign and malignant prostate cells.Molecular oncology · 2019Article
- Androgen receptor phosphorylation: biological context and functional consequences.Endocrine-related cancer · 2014Review
- Transcriptional activity of c-Jun is critical for the suppression of AR function.Molecular and cellular endocrinology · 2013Article
- Interaction between c-jun and androgen receptor determines the outcome of taxane therapy in castration resistant prostate cancer.PloS one · 2013Article
- c-Jun enhancement of androgen receptor transactivation is associated with prostate cancer cell proliferation.Oncogene · 2006Article
- Androgen-independent prostate cancer: potential role of androgen and ErbB receptor signal transduction crosstalk.Neoplasia (New York, N.Y.)Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human androgen receptor (hAR) is a member of the nuclear receptor superfamily and functions as a ligand-inducible transcription factor. We have previously proposed that c-Jun mediates the transcriptional activity of this receptor. The modular nature of hAR was used in this study to generate several fusions with the heterologous DNA-binding domain of the yeast transcription factor GAL4 in an attempt to identify the c-Jun-responsive domains within the receptor. Our results suggest that the target of c-Jun action is the amino terminus (AB region) of the receptor and that hAR amino acids 502-521 are critical for the c-Jun response. Additionally, amino acids 503-555 were shown to harbor an autonomous transactivation that is stimulated by c-Jun. Furthermore, we demonstrated that transcription intermediary factor-2 (TIF-2), a coactivator that acts on the activation function-2, stimulates the full-length hAR. These results suggest that c-Jun and TIF-2 can work together as coactivators on the hAR by targeting distinct portions of the receptor.
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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.