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)
- Mucociliary clearance is an airway defense mechanism driven by the coordinated function of mucus and motile cilia. Although ciliary beat frequency (CBF) reflects the motile function of ciliated cells, the generation and maintenance of ciliated cells are also essential for sustained airway epithelial defense. Although short-term treatment with ginsenoside Rd (Rd) increases CBF, its long-term effects on the differentiation of human airway epithelial cells remain unclear. We investigated the effects of Rd on primary normal human bronchial epithelial cells cultured under air-liquid interface conditions. On day 10, Rd increased the percentage of acetylated α-tubulin (Ac-α-tubulin)-positive cells, whereas the percentage of MUC5AC-positive cells remained unchanged. Rd promoted the time-dependent increase in Ac-α-tubulin-positive cells, while LDH release or total cell number were not significantly altered. Long-term Rd treatment did not affect baseline CBF. Furthermore, perfusion with Rd increased CBF independent of differentiation conditions. These observations suggest that the increase in Ac-α-tubulin-positive cells by long-term Rd treatment and the increase in CBF by short-term Rd treatment may be functionally separable. The increase in the percentage of Ac-α-tubulin-positive cells was suppressed by ERβ inhibitors and CREB-dependent transcription inhibitors. Rd also increased the expression of FOXJ1 mRNA transcripts. These findings suggest that Rd may modulate the expression of ciliated cell markers, such as acetylated α-tubulin and FOXJ1, and ciliary motility in human airway epithelial cells. - Source: PubMed
Publication date: 2026/09/23
Noriyama KoutaNakamura SeikouTamiya NobuyoToda YukiHosogi ShigekuniAshihara Eishi - Intratumoral heterogeneity and tumor-microenvironment interactions limit prognostic stratification in breast cancer, but the prognostic relevance and cellular context of recurrent transcriptional meta-programs remain unclear. We aimed to derive a meta-program-related prognostic signature and characterize its component transcripts at single-cell resolution. Six paired institutional tumors and adjacent non-tumor tissues served as a proof-of-concept comparison. Univariable Cox screening and least absolute shrinkage and selection operator Cox regression were used to derive a five-gene score from a prespecified meta-program-related candidate set in The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA) training cohort; the score was tested internally and assessed in GSE20685 using fixed coefficients and cohort-specific median cutoffs. GSE161529 single-cell transcriptomic data were used to map signature transcripts across 136,526 quality-controlled cells, while donor-aware pseudobulk analysis compared upper- and lower-quartile TFPI expression states in annotated myofibroblasts. The score comprised TCN1, FOXJ1, PIGR, SLAIN1, and TFPI and was associated with overall survival in the training, testing, and external cohorts, with concordance indices of 0.782, 0.756, and 0.721, respectively. TFPI transcripts were detected across endothelial, fibroblast, and myofibroblast compartments. TFPI-high myofibroblasts showed transcriptional enrichment of extracellular matrix and collagen fibril organization, transforming growth factor beta signaling, epithelial-mesenchymal transition, and myogenesis, together with lower oxidative phosphorylation and fatty acid metabolism programs. In bulk TCGA-BRCA tissue, TFPI expression correlated positively with stromal (r = 0.48), immune (r = 0.25), and composite microenvironment scores (r = 0.40; all p < 0.001). These findings identify a hypothesis-generating five-gene bulk-tissue prognostic signature and an expression-associated TFPI-high myofibroblast state but do not establish a discrete lineage, the cellular source of bulk TFPI, a TFPI-dependent mechanism, or clinical utility. Independent prospective cohorts, spatial and protein-level validation, and functional perturbation studies are required. - Source: PubMed
Publication date: 2026/09/10
Huang YuWu XianminLi XiangnanZhu XuetingHuang XiaoyunHuang AnLiu HaitaoYang YanZhou GuanghuiZhang YiningLong JingpeiFeng Qingjing - Per- and polyfluoroalkyl substances (PFASs) are implicated in respiratory diseases, yet systematic toxicity data and mechanistic understanding for most compounds remain critically lacking. To address this gap, we established human 3D airway organoids that recapitulate native epithelial architecture and function to assess the respiratory toxicity of 10 PFAS compounds. At 0.1 μM, a concentration relevant to high-exposure, PFASs induced a cascade of effects, including mitochondrial dysfunction, barrier disruption, and inflammation. These events converged on epithelial differentiation imbalance, characterized by a 21-66% reduction in ciliated cells marker FOXJ1 and a 1.2-2.3-fold upregulation of goblet cells marker MUC5AC. Multiend point Toxicological Priority Index ranking revealed that emerging substitutes, particularly sodium p-perfluorinated noneoxybenzenesulfonate (OBS) and fluorotelomer alcohols (FTOHs), exhibited higher toxicity potency than legacy compounds. In vivo validation confirmed perfluorooctanesulfonic acid (PFOS)-induced airway obstruction and mucus hypersecretion, supporting the in vivo relevance of organoid-derived airway injury phenotypes. Single-cell transcriptomics implicated Notch-related signaling in PFOS-associated differentiation disturbance, supported by inhibitor intervention. These findings provide functional and mechanistic evidence relevant to obstructive airway disease; establish an adverse outcome pathway for PFASs' respiratory toxicity; and provide a sensitive, predictive platform for hazard identification and regulatory prioritization of emerging PFASs. - Source: PubMed
Niu YuxinZhu SiruiLang YuemingZhang LeiZhang BoCui WeiXing LiguoZhang XuanLiu Wei - Ependymal cells are specialized multiciliated epithelial cells that line the brain ventricles. Their coordinated ciliary beating contributes to cerebrospinal fluid circulation and neural homeostasis. Hydrocephalus, a severe neurological condition affecting ∼1-3 per 1000 births worldwide, can arise from defects in ciliary motility, ependymal cell differentiation, planar cell polarity (PCP), and cytoskeletal organization. Mutations in genes that regulate these processes have been identified in patients with congenital hydrocephalus and related ciliopathies, establishing the clinical relevance of these pathways. This review summarizes the recent advances in the molecular mechanisms underlying ependymal cell biology. We describe the structural and functional organization of the ependymal cilia and discuss how ciliary defects range from severe developmental disruptions causing neonatal hydrocephalus to subtle maintenance defects underlying late-onset forms of the disease. We then examine the hierarchical transcriptional programs controlling ependymal differentiation, from master regulators such as GemC1 and Multicilin to downstream effectors, including FoxJ1 and Regulatory Factor X proteins. The core PCP pathway, comprising Vangl, Celsr, Frizzled, and Dishevelled proteins, coordinates tissue-wide ciliary orientation. Recent cryo-electron microscopy studies have provided structural insights into core components. Finally, we discuss the role of cytoskeletal networks in ependymal maintenance. Actin networks support structural integrity through mechanosensitive feedback loops and transduce mechanical forces into transcriptional activation of multiciliogenesis. In parallel, microtubule-based systems coordinate the planar polarized ciliary orientation via the Daple-dynein axis. Taken together, these molecular insights advance our understanding of the pathogenesis of hydrocephalus and may inform future diagnostic and therapeutic strategies. - Source: PubMed
Ohata ShinyaTakagishi Maki - Intervertebral disc (IVD) degeneration, a leading cause of chronic lower back pain, is associated with loss of vacuolated notochordal cells (NCs) and fibrotic remodeling of the nucleus pulposus. Emerging therapies increasingly focus on NCs, which are rare but therapeutically relevant cells for regenerating degenerated IVDs. In this study, we used CRISPR-based transactivation (CRISPRa) to direct the differentiation of human induced pluripotent stem cells (iPSCs) into the NC lineage. We tested CRISPRa-mediated activation of NOTO, TBXT, FOXA2, SOX5, SOX6, and SOX9, coupled with single-cell sequencing of Aggrecan-2A-mScarlet reporter iPSCs. This approach identified the SOX5/6/9 combination (SOX-trio) as critical for promoting NC lineage commitment. The SOX-trio yielded the largest cell population expressing a range of genes previously associated with NC identity, including SHH, FOXA1, FOXA2, FOXJ1, FN1, ALCAM, KRT8, and KRT18. Our study demonstrates the integration of CRISPRa with single-cell technologies as a powerful platform for investigating and enriching iPSC-derived NCs, supporting future regenerative strategies across various fields. - Source: PubMed
Publication date: 2026/08/27
Tong XiaoleVisscher MariekeRiemers Frank MVersluis DanielleGeijsen NielsShang PengTryfonidou Marianna APoramba-Liyanage Deepani W