CHES
- Known as:
- CHES
- Catalog number:
- CB0115
- Product Quantity:
- 50G
- Category:
- -
- Supplier:
- BioBasic
- Gene target:
- CHES
Related genes to: CHES
- Gene:
- FOXN3 NIH gene
- Name:
- forkhead box N3
- Previous symbol:
- C14orf116, CHES1
- Synonyms:
- -
- Chromosome:
- 14q31.3-q32.11
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-16
- Date modifiied:
- 2018-02-13
Related products to: CHES
Related articles to: CHES
- The reproductive performance of roosters is an important factor influencing production efficiency and genetic progress in the poultry industry. Leydig cells (LCs) support male reproductive function through testosterone synthesis and secretion; however, the post-transcriptional mechanisms regulating chicken LCs function remain incompletely understood. Previous studies have shown that testicular miR-182-5p expression is higher in 200-day-old than in 500-day-old roosters, suggesting a possible association with age-related changes in testicular function. This study aims to investigate the role of miR-182-5p in vitro. miR-182-5p overexpression promoted proliferation, inhibited senescence, and elevated testosterone levels in chicken LCs, whereas miR-182-5p inhibition produced the opposite effects. A dual-luciferase reporter assay performed in the chicken fibroblast cell line (DF-1 cells) demonstrated that miR-182-5p targets the 3'untranslated region (3'UTR) of FOXN3. FOXN3 knockdown produced effects consistent with those of miR-182-5p overexpression, supporting FOXN3 as a functional downstream mediator of miR-182-5p. Moreover, miR-182-5p enhanced Wnt/β-catenin signaling, and co-transfection with FOXN3 overexpression, which inhibited this pathway, attenuated the miR-182-5p-induced increases in proliferation and testosterone levels as well as the decrease in senescence. These findings support a miR-182-5p/FOXN3/Wnt/β-catenin regulatory axis that modulates proliferation, senescence, and testosterone levels in chicken LCs in vitro. Further age-comparative and in vivo studies are warranted to determine whether this mechanism contributes to natural reproductive aging or influences reproductive performance in roosters. - Source: PubMed
Publication date: 2026/09/11
Zhao Xin-YueChen Yu-QiZhang YaoYin Hua-Dong - YTH N6-Methyladenosine RNA Binding Protein F2 (YTHDF2) had been implicated in nasopharyngeal carcinoma (NPC) progression. Increasing evidence indicated that numerous circular RNAs (circRNAs) were involved in regulating tumor progression. However, how the regulation of circRNAs by YTHDF2 contributes to NPC progression remains to be uncovered. In this study, we aimed to elucidate the role and mechanism of YTHDF2-mediated circRNA regulation in NPC migration and invasion. YTHDF2 expression in NPC was assessed using GEO datasets and immunohistochemistry. Functional experiments were performed in HNE1 and 5-8F cells, with migration/invasion evaluated by wound healing and transwell assays, and epithelial-mesenchymal transition (EMT) markers by Western blotting. CircRNA candidates were screened through circRNA sequencing. CircRNA m6A modification was assessed by methylated RNA immunoprecipitation-quantitative PCR (MeRIP-qPCR). The SELECT method (single-base elongation- and ligation-based qPCR amplification) was used to identify the specific m6A modification site. RNA stability was measured by actinomycin D assay. circRNA-miRNA and miRNA-target interactions were validated by luciferase reporter assays. YTHDF2 expression was upregulated in NPC tissues and was found to promote migration and invasion phenotypes. Mechanistically, m6A-modified was recognized and degraded by YTHDF2. YTHDF2-mediated pro-migration and pro-invasion effects were reversed by . was identified as a target of . was found to sequester , thereby de-repressing expression. In this study, a potential oncogenic pathway was delineated in which NPC migration and invasion were facilitated by YTHDF2 via degradation of , thereby the sponging effect of was abolished and expression was suppressed. - Source: PubMed
Publication date: 2026/09/14
Ma AiyuWang XuLu LuWang ShuaijieZhao QiuyuZhang XuemeiSun YipingMeng XuanZhang YanYang YuzhongZheng JinhuaZheng Xiang - Breast cancer (BC) remains a leading cause of cancer-related mortality among women worldwide. Despite advances in molecular diagnostics, reliable non-invasive biomarkers for early detection and disease staging remain limited. Circulating microRNAs (miRNAs) are promising epigenetic regulators involved in tumor development and progression. - Source: PubMed
Publication date: 2026/09/15
Abdel-Hamed Asmaa RBarsom MarinaKamel Mahmoud MAbo-Elmatty Dina MGibriel Abdullah Ay - Excessive inflammatory responses are a primary driver of acute lung injury, yet the underlying molecular mechanisms remain incompletely understood. In this study, we identify SKP2, an E3 ubiquitin ligase, as a critical negative regulator of pulmonary inflammation during methicillin-resistant (MRSA) infection. Mechanistically, SKP2 promotes the degradation of its direct substrate p27 (p27), which functions as an activator of a noncanonical NF-κB signaling pathway. We further demonstrate that p27 facilitates the recruitment of p38 kinase to heterogeneous nuclear ribonucleoprotein-U (hnRNPU), leading to direct phosphorylation of the transcriptional repressor FOXN3 at serine residues 83 and 85. This dual phosphorylation event triggers subsequent proteasomal degradation of FOXN3, thereby relieving transcriptional repression and enabling NF-κB-driven activation of pro-inflammatory genes. In vivo, genetic ablation of worsens pulmonary inflammatory injury, elevates neutrophil infiltration, and significantly reduces survival in MRSA-infected mice, and these effects are greatly rescued by concurrent p27 depletion. Collectively, our findings uncover the SKP2-p27-FOXN3 axis as a pivotal regulatory module in pulmonary inflammation and suggest that targeting this axis may offer a promising therapeutic strategy for bacterial infection-induced lung injury. - Source: PubMed
Publication date: 2026/09/11
Yu JinjinHu XinghongWang HuanhuanYu JingyuJin LeleLi YingkeZhou JihongZhu XinxingMoses Emmanuel JairajZheng ChunfuZhang YongLi Wei - As a pivotal tumor suppressor, p53 plays a critical role in the progression of lung adenocarcinoma (LUAD). However, the mechanisms through which its interacting partners modulate p53 transcriptional activity remain poorly understood. In this study, we identified the transcription factor FOXN3 as a key partner that recruits p53 for transcriptional responses. FOXN3 directly interacts with p53, and the two factors exhibit extensive genome-wide colocalization in both lung cancer cells and clinical tumor tissues, thereby co-regulating the transcription of numerous genes. Notably, nearly all p53 point mutants with disrupted DNA-binding capacity show markedly reduced association with FOXN3, underscoring the essential role of FOXN3 in facilitating p53 binding to DNA. Conditional knockout of FOXN3 promotes lung cancer cell survival, invasion, and tumorigenesis. Importantly, the regulation of p53 transcriptional activity by FOXN3 requires phosphorylation at the S83 and S85 sites. This phosphorylation induces the dissociation of FOXN3 from chromatin, thereby inhibiting p53 transcriptional recruitment and activation. Ablation of FOXN3 S83 and S85 phosphorylation impedes the progression of LUAD. Furthermore, increased phosphorylation of FOXN3 at S83 and S85 is observed in clinical lung tumor tissues and correlates with poor prognosis in patients with LUAD, highlighting its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/07/07
Yu JinjinYu JingyuWang SuhuiHu XinghongJin LeleWu NanNi YuhanZhang XueyingZhao ChenglingZhou JihongZhang YongSun BaofaZhang HongxingZheng ChunfuZheng Song GuoLi WeiZhu Xinxing