ArticleThe Journal of biological chemistry1998
SRC-1 and GRIP1 coactivate transcription with hepatocyte nuclear factor 4.
Article in The Journal of biological chemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 146 citations in OpenAlex.
- Stomach at the crossroads: nuclear receptor signaling at the interface between what we are and what we eat.Physiological reviews · 2026Review
- Review
- Structural insights into the HNF4 biology.Frontiers in endocrinology · 2023Review
- Therapeutic Potential of HNF4α in End-stage Liver Disease.Organogenesis · 2021Review
- LncRNA Lnc-APUE is Repressed by HNF4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Conformational Characterization of the Co-Activator Binding Site Revealed the Mechanism to Achieve the Bioactive State of FXR.Frontiers in molecular biosciences · 2021Article
- Src-1 and SP2 promote the proliferation and epithelial-mesenchymal transition of nasopharyngeal carcinoma.Open medicine (Warsaw, Poland) · 2021Article
- Review
- Hepatocyte Nuclear Factor 4-Alpha Is Essential for the Active Epigenetic State at Enhancers in Mouse Liver.Hepatology (Baltimore, Md.) · 2019Article
- ErbB3-binding protein 1 (EBP1) represses HNF4α-mediated transcription and insulin secretion in pancreatic β-cells.The Journal of biological chemistry · 2019Article
- Role of hepatocyte nuclear factor 4 alpha in cell proliferation and gemcitabine resistance in pancreatic adenocarcinoma.Cancer cell international · 2019Article
- Article
- Nuclear receptor HNF4A transrepresses CLOCK:BMAL1 and modulates tissue-specific circadian networks.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Crosstalk of HNF4Acta pharmaceutica Sinica. B · 2016Review
- The pregnane X receptor down-regulates organic cation transporter 1 (SLC22A1) in human hepatocytes by competing for ("squelching") SRC-1 coactivator.British journal of pharmacology · 2016Article
- Regulation of hepatocyte identity and quiescence.Cellular and molecular life sciences : CMLS · 2015Review
- In pursuit of genes of glucose metabolism.The Journal of biological chemistry · 2015Article
- Role of Nuclear Receptors in Central Nervous System Development and Associated Diseases.Journal of experimental neuroscience · 2015Review
- Role of hepatocyte nuclear factor 4α (HNF4α) in cell proliferation and cancer.Gene expression · 2015Review
- LXXLL peptide converts transportan 10 to a potent inducer of apoptosis in breast cancer cells.International journal of molecular sciences · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hepatocyte nuclear factor-4 (HNF4), a member of the nuclear receptor superfamily, plays an important role in tissue-specific gene expression, including genes involved in hepatic glucose metabolism. In this study, we show that SRC-1 and GRIP1, which act as coactivators for various nuclear receptors, associate with HNF4 in vivo and enhance its transactivation potential. The AF-2 domain of HNF4 is required for this interaction and for the potentiation of transcriptional activity by these coactivators. p300 can also serve as a coactivator with HNF4, and it synergizes with SRC-1 to further augment the activity of HNF4. HNF4 is also a key regulator of the expression of hepatocyte nuclear factor-1 (HNF1). The overexpression of SRC-1 or GRIP1 enhances expression from a HNF1 gene promoter-reporter in HepG2 hepatoma cells, and this requires an intact HNF4-binding site in the HNF1 gene promoter. Type 1 maturity onset diabetes of young (MODY), which is characterized by abnormal glucose-mediated insulin secretion, is caused by mutations of the HNF4 gene. A mutation of the HNF4-binding site in the HNF1 gene promoter has also been associated with MODY. Thus, HNF4 is involved in the regulation of glucose homeostasis at several levels and along with the SRC-1, GRIP1, and p300 may play an important role in the pathophysiology of non-insulin-dependent diabetes mellitus.
Indexed as
Identifiers
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.