Ask about this productRelated genes to: IRX3 Blocking Peptide
- Gene:
- IRX3 NIH gene
- Name:
- iroquois homeobox 3
- Previous symbol:
- -
- Synonyms:
- IRX-1
- Chromosome:
- 16q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-27
- Date modifiied:
- 2015-08-25
Related products to: IRX3 Blocking Peptide
Related articles to: IRX3 Blocking Peptide
- Dimethyl sulfoxide can be used to promote mature hepatocyte-like differentiation in hepatocellular carcinoma cells and sustain the expression of liver-specific genes, which is considered a potential novel therapy for liver cancer treatment. However, the molecular targets of dimethyl sulfoxide, especially transcription factors, remain largely unknown. In this study, we show that dimethyl sulfoxide treatment significantly downregulates Iroquois-homeobox protein 3 in Hepatocellular carcinoma cells, illustrating that Iroquois-homeobox protein 3 might regulate Hepatocellular carcinoma proliferation positively. Further clinical data reveal that Iroquois-homeobox protein 3 expression is generally elevated in human Hepatocellular carcinoma tissues and correlates with poor patient survival. Consistent with these observations, gain- and loss-of-function studies demonstrate that Iroquois-homeobox protein 3 promotes Hepatocellular carcinoma proliferation both in vitro and in vivo. Mechanistically, Iroquois-homeobox protein 3 binds to the promoter of F2R-like trypsin receptor 1/Protease-Activated Receptor 2, recruits RNA polymerase II and increases Serine 5 phosphorylation of its C-terminal domain (CTD), thereby upregulating F2R-like trypsin receptor 1/Protease-Activated Receptor 2 expression and driving Hepatocellular carcinoma proliferation. Collectively, our findings reveal a critical role for Iroquois-homeobox protein 3 in Hepatocellular carcinoma development and suggest that Iroquois-homeobox protein 3 might be a potential therapeutic target for Hepatocellular carcinoma. - Source: PubMed
Publication date: 2026/05/07
Yang LijuanHuo ZiyeQian XinRen YiLan XiangFan Hui - A major challenge in deciphering the complex genetic landscape of polycystic ovary syndrome (PCOS) lies in the limited understanding of how susceptibility loci drive molecular mechanisms across diverse phenotypes. To address this, we integrated molecular and epigenomic annotations from proposed causal cell types and employed a deep learning (DL) framework to predict cell type-specific regulatory effects of PCOS-risk variants. Our analysis revealed that these variants affect key transcription factor-binding sites, including , , , and , which regulate gonadotropin signaling, folliculogenesis, and steroidogenesis across brain and endocrine cell types. The DL model, which showed strong concordance with reporter assay data, identified enhancer-disrupting activity in ∼20% of risk variants. Notably, many of these variants disrupt transcription factors involved in androgen-mediated signaling, providing molecular insights into hyperandrogenemia in PCOS. Variants prioritized by the model were more pleiotropic and exerted stronger regulatory effects on gene expression compared with other risk variants. Using the locus as a case study, we demonstrate how regulatory disruptions in tissues such as the fetal brain, pancreas, adipocytes, and endothelial cells may link obesity-associated mechanisms to PCOS pathogenesis via neuronal development, metabolic dysfunction, and impaired folliculogenesis. Collectively, our findings highlight the utility of integrating DL models with epigenomic data to uncover disease-relevant variants, reveal cross-tissue regulatory effects, and refine mechanistic understanding of PCOS. - Source: PubMed
Publication date: 2026/04/09
Srivastava JayaOvcharenko Ivan - The Iroquois () family of homeobox genes regulates critical developmental processes, and emerging evidence suggests that their dysregulation contributes to cancer progression, particularly in relation to cancer stemness. Although their expression appears to be influenced by hormonal regulation, their potential roles in hormone-sensitive cancers remain incompletely understood. In this study, we performed a comprehensive, exploratory analysis of all six Iroquois genes (-) across prostate, breast, ovarian, and endometrial cancers. Using large-scale publicly available transcriptomic datasets, we systematically examined gene expression patterns and their associations with tumour progression, prognosis, hormone regulation, drug response, and cancer stemness. and were consistently elevated in estrogen-dependent tumours and 2 and 4 were notably upregulated in prostate cancer. Despite evidence of estrogen receptor 1 (ESR1) and androgen receptor (AR) binding near several promoters, estrogen treatment assays showed that ESR1 binding at promoters alone was insufficient to induce transcription. Clinically, 2 expression was associated with favourable outcomes in breast, endometrial, and ovarian cancers and showed correlations with stemness-related signatures in prostate cancer. Similarly, 4 expression was associated with stemness features in prostate and endometrial cancers. In addition, 6 expression showed associations with reduced sensitivity to abiraterone, suggesting a potential link with therapeutic resistance in these tumours. Collectively, these findings highlight the context-dependent expression patterns and clinical associations of genes across hormone-driven cancers. While largely correlative, this study provides a framework for future functional investigations and suggests that selected s may have potential utility as biomarkers for disease stratification and treatment response in hormone-sensitive cancers. - Source: PubMed
Publication date: 2026/02/24
Thennakoon AmaliFernando AchalaBatra Jyotsna - To analyse the effects of chromatic light (white, blue, red and green) and stimulus size (6/6 and 6/12) on pupil constriction, Zernike coefficients and the accommodative response curve using wavefront aberrometry across a wide age range of healthy subjects. - Source: PubMed
Publication date: 2026/03/09
Cabrera-Guardiola InésOrduna-Hospital ElviraArcas-Carbonell MaríaSanchez-Cano Ana - Pathological cardiac hypertrophy is a major contributor to heart failure and is often accompanied by ferroptosis and mitochondrial dysfunction. However, the upstream transcriptional mechanisms governing these processes remain poorly defined. We performed integrative bioinformatics analysis using transverse aortic constriction (TAC)-induced hypertrophic heart datasets to identify mitochondria-related differentially expressed genes (MitoDEGs), followed by transcription factor prediction and experimental validation in both in vivo and in vitro models. Adeno-associated virus-mediated overexpression and knockdown strategies were used to assess the regulatory effects of Irx3 and its downstream target Etfa. We identified Etfa as a hub MitoDEG directly regulated by the transcription factor Irx3, which was significantly upregulated in hypertrophic hearts. Mechanistically, Irx3 directly bound to the Etfa promoter and restored Etfa expression in hypertrophic cardiomyocytes. Through integrated transcriptomic analysis, an angiotensin II-induced cardiomyocyte hypertrophy model, and a TAC mouse model, we demonstrate that the Irx3-Etfa axis attenuates hypertrophic remodeling by suppressing ferroptosis. In vitro, overexpression of Irx3 or Etfa alleviates cardiomyocyte hypertrophy and ferroptotic injury, whereas Etfa knockdown abolishes the protective effects of Irx3. In vivo, Irx3 overexpression improves cardiac function, reduces ferroptosis, and limits structural remodeling in TAC mice. These findings reveal a novel transcriptional pathway connecting mitochondrial metabolism to ferroptosis regulation and suggest the Irx3-Etfa axis as a promising therapeutic target for pathological cardiac hypertrophy. - Source: PubMed
Li BingZhang YaotingFu YuZheng YangDou KefeiSun Wanqing