CHES
- Known as:
- CHES
- Catalog number:
- 101-103-47-9
- Product Quantity:
- 50kg
- Category:
- -
- Supplier:
- MDBIONIC
- 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
- - Source: PubMed
Dai YuediWang MeixingWu HaixiaXiao MiLiu HoubaoZhang Dexiang - To investigate the mechanism of FOXN3 in acute leukemia. - Source: PubMed
Publication date: 2026/03/24
Zhang JinjingJiang QiaoLiu TongLi HongLiang YingLu XianglanPang HuiLi ShiboLi YanZhang Rui - Monocyte-derived macrophages are usually recruited and play pivotal roles in establishing an immunosuppressive tumor microenvironment, and the interplay between tumor cells and tumor-associated macrophages (TAMs) is crucial for tumor development. However, the detailed mechanisms remain largely unelucidated in certain aggressive human cancers, such as melanoma. Here, through miRNA sequencing analysis, we found the microRNA miR-708-5p was highly enriched in melanoma exosomes, which was dependent on SFRS1. Treatment by melanoma exosomes facilitated M2 polarization of macrophages, while the polarized macrophages in turn promoted melanoma progression and metastasis both in vitro and in vivo. Mechanistically, miR-708-5p directly targets FOXN3, a member of the fork head/winged helix transcription factor family, and subsequently activates the PI3K/AKT/mTOR pathway in macrophages. Conversely, re-expression of FOXN3 in macrophages stably expressing miR-708-5p could reverse the impact on macrophages. In addition, downregulation of FOXN3 by miR-708-5p in macrophages reduced their phagocytic capacity and increased the secretion of IL-10 and TGF-β. Interestingly, we found that cellular retention of miR-708-5p could inhibit the proliferation and promote the apoptosis of melanoma cells, suggesting the necessity for secretion of this microRNA. In summary, our findings provide novel insights into the mechanism of melanoma-derived miR-708-5p in facilitating the formation of an immunosuppressive tumor microenvironment and indicate the potential of miR-708-5p and FOXN3 as therapeutic targets for the treatment of melanoma. - Source: PubMed
Publication date: 2026/03/24
Xu MengHe BincanZhou XiaofengShu LiMa Dan - Retinas from mice with a targeted disruption of the gene encoding forkhead transcription factor Foxn3 contained additional displaced amacrine interneurons and retinal astrocytes in the inner plexiform and ganglion cell layers, as well as ectopic primary cilia on bipolar and amacrine interneurons. Foxn3 is a transcriptional repressor and numerous genes linked to cilia structure or assembly were upregulated in embryonic retinas with disrupted Foxn3. CUT&RUN analysis revealed that many upregulated retinal genes were bound by the Foxn3 and Rfx3 proteins. A short hydrophobic motif (LXXLXWL) shared by Foxn3, Foxn4 and Foxj1 was required for association with Rfx3 and for full transcriptional repression by Foxn3, as well as for full transcriptional activation by Foxj1 or Foxn4. AlphaFold 3 predicted interaction between the hydrophobic motif and the Rfx3 dimerization domain. Mutations in Rfx3 at the predicted interaction site disrupted association of Rfx3 with Foxn3, Foxn4 or Foxj1. These results reveal a new layer of transcriptional regulation of genes required for cilia, with Foxn3 functioning as a repressor of cilia genes and limiting primary cilia formation in the developing retina. - Source: PubMed
Publication date: 2026/03/10
Zhang HuanqingNair ThejasMeng FanTurner David L - The sterol regulatory element-binding transcription factor 1 (SREBP-1) plays a crucial role in the transcriptional regulation of lipogenic response genes, thereby contributing to the development of non-alcoholic fatty liver disease (NAFLD). However, the modulation of SREBP-1 transcriptional activity remains incompletely understood. Here, we report that the transcription factor FOXN3 interacts with the KU70/KU80/SREBP-1 complex, facilitating the recruitment of SREBP-1 for the transcriptional activation of lipogenic response genes. Hepatocyte-specific knockout of FOXN3 significantly alleviates the pathological progression of NAFLD by suppressing fatty acid and cholesterol synthesis. Furthermore, phosphorylation of FOXN3 at the S83 and S85 residues disrupts the stability of the KU70/KU80/FOXN3/SREBP-1 complex, which is required for SREBP-1 transcriptional activity. This disruption consequently impedes the progression of NAFLD. Clinical investigations reveal that FOXN3, KU80, and SREBP-1 co-target the promoters of lipogenic response genes in fatty liver tissues from patients. Notably, phosphorylation levels of FOXN3 at S83 and S85 are significantly reduced in fatty liver tissues compared to normal samples. This reduction enhances the enrichment of the FOXN3/SREBP-1 complex at the promoters of lipogenic response genes during the progression of NAFLD. Our study underscores the critical role of FOXN3 in maintaining the intact KU70/KU80/FOXN3/SREBP-1 complex, which is essential for SREBP-1-mediated metabolic disorders. - Source: PubMed
Du JiangJin LeleWang SuhuiHu XinghongYu JinjinYu JingyuHuo QingyangWu NanLiu XiaotianYang YanZhang YongHuang SizhouZhou JihongZheng Song GuoZheng ChunfuZhu Xinxing