AHR Gene aryl hydrocarbon receptor
- Known as:
- AHR Gene aryl hydrocarbon receptor
- Catalog number:
- AHSA1
- Category:
- -
- Supplier:
- Transposagen
- Gene target:
- AHR Gene aryl hydrocarbon receptor
Related genes to: AHR Gene aryl hydrocarbon receptor
- Gene:
- FOXD3 NIH gene
- Name:
- forkhead box D3
- Previous symbol:
- -
- Synonyms:
- Genesis, HFH2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: AHR Gene aryl hydrocarbon receptor
"Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP ""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP""Recombinant Human Interleukin-18 receptor accessory protein_IL18RAP"α - Calcitonin Gene Related Peptide, α - CGRP, rat(Ala1)-PAR-4 (1-6) (mouse)
(Ala1)-Thrombin Receptor-Like 3 (1-6) (mouse), (Ala1)-Proteinase Activated Receptor 4 (1-6) (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) (mouse), AYPGKF 98%(Ala1)-PAR-4 (1-6) amide (mouse)
AYPGKFamide, (Ala1)-Thrombin Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Coagulation Factor II Receptor-Like 3 (1-6) amide (mouse), (Ala1)-Proteinase Activated Recepto(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II(Ala1)_PAR_4 (1_6) (mouse) Salt Trifluoroacetate Binding _ Synonym (Ala1)_Thrombin Receptor_Like 3 (1_6) (mouse), (Ala1)_Proteinase Activated Receptor 4 (1_6) (mouse), (Ala1)_Coagulation Factor II Related articles to: AHR Gene aryl hydrocarbon receptor
- Body color brightness is a key determinant of ornamental value in koi, yet nutritional strategies targeting structural coloration mediated by iridophores remain underexplored. Fish scale meal (FSM), an abundant fishery by-product, contains guanine and collagen, which may contribute to structural coloration and body brightness. This study evaluated the effects of partial replacement of fish meal with FSM on growth performance, body color parameters, pigment accumulation, iridophore density, and iridophore-related gene expression in koi. A total of 384 koi with an initial body weight of 19.02 ± 0.18 g were randomly assigned to six dietary treatments for 8 weeks, with FSM inclusion levels ranging from 0% to 9.55%, corresponding to 0-100% replacement of dietary fish meal. Growth performance, including final body weight, weight gain rate, and specific growth rate, decreased with increasing FSM inclusion. Body lightness (L*) and scale guanine content increased progressively with FSM level and reached their highest values at 9.55% FSM, whereas redness (a*), yellowness (b*), and total carotenoid content showed the opposite trend. Iridophore density was significantly higher in the 3.82-5.73% FSM groups than in the other treatments. The expression of iridophore-related genes, including , , , , and , showed non-linear responses and generally reached higher levels at moderate FSM inclusion, whereas showed an opposite transcript pattern. Overall, dietary FSM inclusion elicited trait-dependent responses in koi. Low or no FSM inclusion was preferable for maintaining growth, intermediate inclusion was more favorable for iridophore development, whereas higher FSM inclusion enhanced brightness-related traits. These findings suggest that FSM should be used according to the intended production objective, with inclusion levels adjusted for growth maintenance, iridophore-related coloration improvement, or brightness enhancement. - Source: PubMed
Publication date: 2026/07/19
Gao ShengyuXu XiaolongDing TongCheng YunxinZhang JiayueZheng HuiyiZhou ZuoqinLiu EnXu GaoxiaoHe Chaofan - The unique nature of neural crest cells has encouraged the characterization of the dorsal neural tube as distinct from the rest of the neural tube. Yet the dorsal and ventral neural tube have several similarities during neurulation, both acting as hinge points and opposing signaling centers. Furthermore, we find that the neural crest marker gene FOXD3, is expressed in both the dorsal and ventral neural tube, indicating shared roles unrelated to neural crest specification. This project aimed to identify genes coexpressed in the dorsal and ventral neural tube and characterize ventral FOXD3 function. - Source: PubMed
Publication date: 2026/07/06
Rees JenaidTaroc Ed ZandroBarbosa-Sabanero KarlaKirkland JamiyaMehedincu StefaniaSchiffmacher AndrewKerosuo Laura - SIX1 variants underlying branchio-oto-renal syndrome occur in the SIX domain (SD) or homeodomain (HD). We tested whether different variants - V17E (SD), Y129C (HD) - cause distinct developmental phenotypes in Xenopus embryos with reduced Six1 in comparison to wild-type Six1 (Six1WT). In Six1 morphants, Six1WT restored neural crest and preplacodal gene expression; V17E restored foxd3 and irx1 better than Y129C, and Y129C restored sox11 better than V17E. In six1-null otic vesicles, Six1WT partially restored tbx1 and sobp, V17E was less effective and Y129C was least effective; all three restored dlx5. In six1 heterozygotes, Six1WT and Y129C had similar pleiotropic effects on tbx1, whereas V17E had no effect; Six1WT restored dlx5 expression, V17E was less effective and Y129C was most deficient. In six1-null tadpoles, reduced cranial cartilage volume and individual cartilage abnormalities were rescued by Six1WT, less so by V17E and not by Y129C. In heterozygotes and wild types, Y129C caused a higher frequency of abnormal cartilages compared to Six1WT or V17E. Thus, variants with different functional deficits have distinguishable effects in both nulls and heterozygotes on the formation of the tissues affected in branchio-oto-renal syndrome. - Source: PubMed
Publication date: 2026/07/06
Coppenrath KelseyShaidani Nikko-IdeenNaert ThomasMajumdar Himani DHorb MarkoLienkamp Soeren SKlein Steven LMoody Sally A - BACKGROUND: Cancer stemness-related long non-coding RNAs (lncRNAs) play a crucial role in tumor initiation and progression. This study aimed to identify stemness-related lncRNAs in cervical cancer (CESC) and evaluate the prognostic significance, clinical relevance, and biological functions. MATERIALS & METHODS: Transcriptome data from the Cancer Genome Atlas were used to construct a co-expression network of cancer stemness-related genes and CESC-specific lncRNAs, focusing on cervical squamous cell carcinoma and endocervical adenocarcinoma. Identified stemness-related lncRNAs were used to develop a prognostic model through univariate, LASSO, and multivariate Cox regression analyses. Quantitative real-time PCR and in situ hybridization were performed to measure EMX2OS expression in normal and cancerous cervical tissues. Statistical tests were applied to analyze the association between EMX2OS expression and clinicopathological features. The effects of EMX2OS overexpression on cell proliferation, migration, and invasion were investigated using using the Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2’-deoxyuridine (EdU) assay, plate cloning assay, wound healing assay, and transwell assays. RESULTS: A prognostic model comprising five lncRNAs (FOXD3-AS1, KCNMB2-AS1, EMX2OS, LINC02446, SOCS2-AS1) was developed, demonstrating robust prognostic performance. EMX2OS expression was significantly down-regulated in CESC tissues compared to normal tissues. In situ hybridization showed a marked association between EMX2OS expression and tumor size (P = 0.005), depth of stromal invasion (P = 0.009), and 5-year survival status (P = 0.003). The 5-year survival rate was significantly lower in the low expression group (P = 0.006). Overexpression of EMX2OS significantly suppressed cell proliferation, migration, and invasion. CONCLUSIONS: The prognostic model based on 5 lncRNAs reflecting the stemness of CESC stem cells can reliably predict the prognosis of patients with CESC. Additionally, EMX2OS serves as a significant tumor suppressor marker in CESC. - Source: PubMed
Publication date: 2026/04/20
Liu XiaochenLiao YuandongLiu YunyunHuang HuaZhang ChunyuHuang ShiyingQin ShuhangChen MingXia MengLiu TianyuLiang YanchunYao Shuzhong - Docetaxel (DTX) is a standard chemotherapy agent for castration-resistant prostate cancer (CRPC); however, DTX resistance remains a major clinical challenge, and the underlying molecular mechanisms are not fully understood. In our study, it was found that OTUB2 was highly expressed in DTX-resistant CRPC and could be served as a key driver of DTX resistance. Mechanistically, OTUB2 stabilizes the m5C reader ALYREF by removing its K48-linked polyubiquitin chains, leading to increased ALYREF protein levels. And then, ALYREF enhances the mRNA stability and expression of ABCG4, thereby promoting ATP-dependent efflux of DTX. Moreover, the expression of OTUB2 mRNA and protein could be regulated by FOXD3-AS1 derived from cancer-associated fibroblasts (CAFs). More importantly, treatment with OTUB2 inhibitor (OTUB2-IN-1) resensitized resistant CRPC to DTX. Together, our findings establish OTUB2 as a novel driver of DTX resistance in CRPC and highlight the role of CAFs-derived FOXD3-AS1 and OTUB2/ALYREF/ABCG4 axis in modulating DTX resistance of CRPC. - Source: PubMed
Publication date: 2026/03/17
Ke Zhi-BinChen Jia-YinLin BinChen Chao-RanXue Yu-TingSun Jiang-BoYan Zi-HengZhao Yu-XuanLiu Meng-XinWang ZhenXue Xue-YiZheng Qing-ShuiWei YongXu Ning