ArticleInternational journal of molecular sciences2014
Aryl hydrocarbon receptor repressor and TiPARP (ARTD14) use similar, but also distinct mechanisms to repress aryl hydrocarbon receptor signaling.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Mechanistic Insights into Regulation of the Aryl Hydrocarbon Receptor Expression in Mouse and Human Hepatoma Cells.International journal of molecular sciences · 2026Article
- AHR-Responsive Carbon Dots Orchestrate Skin Wound Healing and Colonic Mucosal Repair via Treg-Mediated Macrophage Efferocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Correlation of AHR Activation-Induced Suppression of PWM-Stimulated IgG and IgG-Triggered Signaling in Human PBMCs.Antibodies (Basel, Switzerland) · 2026Article
- Aryl hydrocarbon receptor pharmacology-mechanisms, ligands, and therapeutic potential.Pharmacological reviews · 2026Review
- PARP7 as a new target for activating anti-tumor immunity in cancer.EMBO molecular medicine · 2025Review
- Article
- Aryl hydrocarbon receptor restricts axon regeneration of DRG neurons in response to injury.bioRxiv : the preprint server for biology · 2024Article
- The AHR repressor limits expression of antimicrobial genes but not AHR-dependent genes in intestinal eosinophils.Journal of leukocyte biology · 2024Article
- Differential cell type-specific function of the aryl hydrocarbon receptor and its repressor in diet-induced obesity and fibrosis.Molecular metabolism · 2024Article
- Article
- Bioluminescence imaging of Cyp1a1-luciferase reporter mice demonstrates prolonged activation of the aryl hydrocarbon receptor in the lung.Communications biology · 2024Article
- Aberrant gene expression yet undiminished retinal ganglion cell genesis in iPSC-derived models of optic nerve hypoplasia.Ophthalmic genetics · 2024Article
- Dose-dependent exposure to indoxyl sulfate alters AHR signaling, sirtuins gene expression, oxidative DNA damage, and bone mineral status in rats.Scientific reports · 2024Article
- The complex biology of aryl hydrocarbon receptor activation in cancer and beyond.Biochemical pharmacology · 2023Review
- Modulating AHR function offers exciting therapeutic potential in gut immunity and inflammation.Cell & bioscience · 2023Review
- Hexokinase 2 is a transcriptional target and a positive modulator of AHR signalling.Nucleic acids research · 2022Article
- Are PARPs promiscuous?Bioscience reports · 2022Review
- The aryl hydrocarbon receptor: A predominant mediator for the toxicity of emerging dioxin-like compounds.Journal of hazardous materials · 2022Review
- Reduced Colonic Mucosal Injury in 2,3,7,8-Tetrachlorodibenzo-International journal of molecular sciences · 2022Article
- The aryl hydrocarbon receptor as a model PAS sensor.Toxicology reports · 2022Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The aryl hydrocarbon receptor (AHR) regulates the toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The AHR repressor (AHRR) is an AHR target gene and functions as a ligand-induced repressor of AHR; however, its mechanism of inhibition is controversial. Recently, we reported that TCDD-inducible poly (ADP-ribose) polymerase (TiPARP; ARTD14) also acts as a repressor of AHR, representing a new player in the mechanism of AHR action. Here we compared the ability of AHRR- and TiPARP-mediated inhibition of AHR activity. TCDD increased AHRR mRNA levels and recruitment of AHRR to cytochrome P450 1A1 (CYP1A1) in MCF7 cells. Knockdown of TiPARP, but not AHRR, increased TCDD-induced CYP1A1 mRNA and AHR protein levels. Similarly, immortalized TiPARP(-/-) mouse embryonic fibroblasts (MEFs) and AHRR(-/-) MEFs exhibited enhanced AHR transactivation. However, unlike TiPARP(-/-) MEFs, AHRR(-/-) MEFs did not exhibit increased AHR protein levels. Overexpression of TiPARP in AHRR(-/-) MEFs or AHRRΔ8, the active isoform of AHRR, in TiPARP(-/-) MEFs reduced TCDD-induced CYP1A1 mRNA levels, suggesting that they independently repress AHR. GFP-AHRRΔ8 and GFP-TiPARP expressed as small diffuse nuclear foci in MCF7 and HuH7 cells. GFP-AHRRΔ8_Δ1-49, which lacks its putative nuclear localization signal, localized to both the nucleus and the cytoplasm, while the GFP-AHRRΔ8_Δ1-100 mutant localized predominantly in large cytoplasmic foci. Neither GFP-AHRRΔ8_Δ1-49 nor GFP-AHRRΔ8_Δ1-100 repressed AHR. Taken together, AHRR and TiPARP repress AHR transactivation by similar, but also different mechanisms.
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