FOXJ1 antibody - N-terminal region (ARP38038_P050)
- Known as:
- FOXJ1 (anti-) - N-terminal region (ARP38038_P050)
- Catalog number:
- arp38038_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FOXJ1 antibody - N-terminal region (ARP38038_P050)
Related genes to: FOXJ1 antibody - N-terminal region (ARP38038_P050)
- Gene:
- FOXJ1 NIH gene
- Name:
- forkhead box J1
- Previous symbol:
- FKHL13
- Synonyms:
- HFH-4, HFH4
- Chromosome:
- 17q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-11-13
- Date modifiied:
- 2015-08-25
Related products to: FOXJ1 antibody - N-terminal region (ARP38038_P050)
Related articles to: FOXJ1 antibody - N-terminal region (ARP38038_P050)
- Ciliated epithelial change in endometrial lesions is a recognized morphologic finding, but its immunophenotypic correlates and biological significance remain insufficiently defined. We investigated whether endometrial lesions with ciliated epithelial change show reproducible immunohistochemical alterations across benign, premalignant, and malignant diagnostic categories. We performed a retrospective immunohistochemical study of 315 formalin-fixed paraffin-embedded eutopic uterine endometrial specimens (no endometriotic/ectopic lesions included) collected between 2019 and 2024 and distributed equally across seven diagnostic categories ( = 45 each): normal endometrium, endometrial polyp, hyperplasia with cystic/disordered glands, hyperplasia with crowded glands, atypical hyperplasia/EIN, endometrioid carcinoma, and serous carcinoma. Marker expression was quantified by digital image analysis and compared between lesions with and without ciliated epithelial change, including lesions with ciliated epithelial change showing cytological atypia. Ciliated epithelial change (CEC) was identified in 86/315 cases (27.3%), including 41 cases (13.0%) with atypical CEC. In benign categories, lesions with CEC showed lower E-cadherin expression and higher β-catenin expression, including more frequent nuclear β-catenin localization. In carcinomas, these patterns were not recapitulated and instead showed an opposite or attenuated profile, supporting a context-dependent rather than linear model. Vimentin was consistently reduced in lesions with CEC across diagnostic categories. p53 and CD44 showed heterogeneous findings and were less informative than the adhesion- and phenotype-related markers. Endometrial lesions with CEC show reproducible, context-dependent immunohistochemical alterations, most consistently involving E-cadherin, β-catenin, and vimentin. In particular, nuclear β-catenin reactivity in this setting should not be interpreted as evidence of canonical Wnt-pathway activation in the absence of CTNNB1 sequencing or validated downstream readouts, and the carcinoma findings cannot be assigned to a specific TCGA/ProMisE molecular subgroup using immunohistochemistry alone. The observations should therefore be regarded as exploratory and warrant validation in studies incorporating molecular classification, direct ciliogenesis markers (FOXJ1, acetylated α-tubulin, basal body markers), and outcome data. - Source: PubMed
Publication date: 2026/05/27
Turashvili TeonaTevdorashvili GeorgeBurkadze George - Airway hyperresponsiveness (AHR) is a clinically important feature of chronic pediatric inflammatory airway disease, but its cellular architecture remains incompletely resolved. Because bulk transcriptomic approaches can mask signals from rare or state-specific cell populations, single-cell RNA sequencing (scRNA-seq) offers a useful framework for examining epithelial and immune cell diversity in hyperresponsive airways. - Source: PubMed
Publication date: 2026/06/09
Yang WeimingMao ShunfengZhou Liuyang - Eosinophilic chronic rhinosinusitis (ECRS) is characterized by refractory nasal polyps and severely impaired mucociliary clearance (MCC). The molecular mechanisms underlying the modulation of mucociliogenesis following IL-4/13 blockade with dupilumab remain poorly understood, notwithstanding its proven clinical efficacy. - Source: PubMed
Publication date: 2026/05/15
Fujita RikutoIshino TakashiOda TakashiKawasumi TomohiroNishida ManabuHoribe YuichiroChikuie NobuyukiTaruya TakayukiHamamoto TakaoUeda TsutomuTakeno Sachio - The respiratory toxicity of heated tobacco products (HTPs) remains incompletely characterized, and traditional models often fail to capture human-specific responses. Here, we established a human pluripotent stem cell (hPSC)-derived airway organoid (AO) platform and systematically compared the toxicological profiles of two HTP aerosols using an integrated framework encompassing conventional cytotoxicity assays, lineage-specific analysis, network perturbation modeling and multi-omics profiling. Both HTPs induced time- and concentration-dependent cytotoxicity, oxidative stress, DNA damage, and apoptosis in AOs. Exposure also triggered epithelial chemokine response characterized by elevated IL-8, MCP-1, MIP-1β, GM-CSF, and RANTES, with concomitant suppression of IP-10, indicating epithelial-derived inflammatory alarm signals. Lineage-specific transcriptional changes revealed mucociliary dysfunction characterized by goblet cell hyperplasia (MUC5AC upregulation) and ciliated cell impairment (FOXJ1 downregulation), key features of airway remodeling in chronic respiratory diseases. To delineate underlying mechanisms, we employed Network Perturbation Amplitude (NPA) analysis, which uncovered qualitatively distinct toxicity architectures: HTP-1 exhibited higher overall toxicity and elicited broad-spectrum network perturbations involving cell stress, proliferation, and immune regulation, correlating with greater apoptotic induction; HTP-2 triggered focused activation of damage-sensing pathways, consistent with its earlier membrane disruption and more pronounced genotoxicity. Multi-omics analysis further linked these mechanistic perturbations to human disease-relevant pathways, with HTP-1 showing stronger enrichment for COPD-associated expression patterns and HTP-2 for lung cancer-related signatures, suggesting the acute molecular response to each product exhibits similarity to specific pulmonary disease-associated molecular signatures. These findings establish human-derived airway organoids as a sensitive, human-relevant platform within the New Approach Methodologies (NAMs) framework for qualitative comparison and mechanistic interrogation of product-specific toxicity. - Source: PubMed
Publication date: 2026/05/25
Li XiaoTian YushanWu YujuanJiang YuanyuanWang HongjuanHan ShuleiCui LiliSong ZhengChen HuanHou Hongwei - - Source: PubMed
Publication date: 2026/05/11
Hao MeihuaYuan Feng