Mouse Epstein-Barr Virus Induced Gene 3
- Known as:
- Mouse Epstein-Barr Virus Induced Gene 3
- Catalog number:
- GEM-300-302P1
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- SeraLab
- Gene target:
- Mouse Epstein-Barr Virus Induced Gene 3
Related genes to: Mouse Epstein-Barr Virus Induced Gene 3
- Gene:
- FOXD3 NIH gene
- Name:
- forkhead box D3
- Previous symbol:
- -
- Synonyms:
- Genesis, HFH2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: Mouse Epstein-Barr Virus Induced Gene 3
Related articles to: Mouse Epstein-Barr Virus Induced Gene 3
- KRAS G12C mutation is a clinically relevant driver in non-small cell lung cancer (NSCLC), yet the signaling networks that modulate malignant behavior in this context remain incompletely defined. In this study, we examined the functional role of FOXD3 and its relationship with NF-κB signaling in KRAS G12C-mutant NSCLC models. Stable FOXD3 overexpression was established in SW1573 and LU65 cells. FOXD3 reduced cell viability, migration, and invasion while increasing caspase 3/7 activity in both cell lines. Transcriptomic profiling in LU65 cells followed by Hallmark enrichment analysis identified TNFα signaling via NF-κB as a prominently altered pathway associated with FOXD3 overexpression. Consistently, NF-κB dual-luciferase assays showed reduced basal NF-κB transcriptional activity in FOXD3-overexpressing cells. TNFα stimulation partially reversed the inhibitory effects of FOXD3 on proliferation, migration, and invasion and attenuated FOXD3-induced apoptosis. In addition, stable FOXD3 overexpression suppressed xenograft growth in vivo. Collectively, these findings support a functional association between FOXD3 overexpression and reduced NF-κB-related transcriptional activity in KRAS G12C-mutant NSCLC models, although the present data do not establish direct causal mediation by NF-κB. - Source: PubMed
Publication date: 2026/08/28
Xu PengzhenPeng JieGuo ChaoLiu ZhuCao YufengSheng QingXu WenfeiLi Xuhui - Diabetic cataract (DC) is a lens-opacity complication of diabetes driven by hyperglycemia-related oxidative, apoptotic, metabolic, and epithelial-mesenchymal transition (EMT) pathways. This review evaluated the expression and mechanistic roles of long non-coding RNAs (lncRNAs) and lncRNA-related epitranscriptomic regulators in DC. - Source: PubMed
Publication date: 2026/08/12
Chen Kai-YangChan Hoi-ChunChan Chi-Ming - Body color brightness is a key determinant of ornamental value in koi, yet nutritional strategies targeting structural coloration mediated by iridophores remain underexplored. Fish scale meal (FSM), an abundant fishery by-product, contains guanine and collagen, which may contribute to structural coloration and body brightness. This study evaluated the effects of partial replacement of fish meal with FSM on growth performance, body color parameters, pigment accumulation, iridophore density, and iridophore-related gene expression in koi. A total of 384 koi with an initial body weight of 19.02 ± 0.18 g were randomly assigned to six dietary treatments for 8 weeks, with FSM inclusion levels ranging from 0% to 9.55%, corresponding to 0-100% replacement of dietary fish meal. Growth performance, including final body weight, weight gain rate, and specific growth rate, decreased with increasing FSM inclusion. Body lightness (L*) and scale guanine content increased progressively with FSM level and reached their highest values at 9.55% FSM, whereas redness (a*), yellowness (b*), and total carotenoid content showed the opposite trend. Iridophore density was significantly higher in the 3.82-5.73% FSM groups than in the other treatments. The expression of iridophore-related genes, including , , , , and , showed non-linear responses and generally reached higher levels at moderate FSM inclusion, whereas showed an opposite transcript pattern. Overall, dietary FSM inclusion elicited trait-dependent responses in koi. Low or no FSM inclusion was preferable for maintaining growth, intermediate inclusion was more favorable for iridophore development, whereas higher FSM inclusion enhanced brightness-related traits. These findings suggest that FSM should be used according to the intended production objective, with inclusion levels adjusted for growth maintenance, iridophore-related coloration improvement, or brightness enhancement. - Source: PubMed
Publication date: 2026/07/19
Gao ShengyuXu XiaolongDing TongCheng YunxinZhang JiayueZheng HuiyiZhou ZuoqinLiu EnXu GaoxiaoHe Chaofan - The unique nature of neural crest cells has encouraged the characterization of the dorsal neural tube as distinct from the rest of the neural tube. Yet the dorsal and ventral neural tube have several similarities during neurulation, both acting as hinge points and opposing signaling centers. Furthermore, we find that the neural crest marker gene FOXD3, is expressed in both the dorsal and ventral neural tube, indicating shared roles unrelated to neural crest specification. This project aimed to identify genes coexpressed in the dorsal and ventral neural tube and characterize ventral FOXD3 function. - Source: PubMed
Publication date: 2026/07/06
Rees JenaidTaroc Ed ZandroBarbosa-Sabanero KarlaKirkland JamiyaMehedincu StefaniaSchiffmacher AndrewKerosuo Laura - SIX1 variants underlying branchio-oto-renal syndrome occur in the SIX domain (SD) or homeodomain (HD). We tested whether different variants - V17E (SD), Y129C (HD) - cause distinct developmental phenotypes in Xenopus embryos with reduced Six1 in comparison to wild-type Six1 (Six1WT). In Six1 morphants, Six1WT restored neural crest and preplacodal gene expression; V17E restored foxd3 and irx1 better than Y129C, and Y129C restored sox11 better than V17E. In six1-null otic vesicles, Six1WT partially restored tbx1 and sobp, V17E was less effective and Y129C was least effective; all three restored dlx5. In six1 heterozygotes, Six1WT and Y129C had similar pleiotropic effects on tbx1, whereas V17E had no effect; Six1WT restored dlx5 expression, V17E was less effective and Y129C was most deficient. In six1-null tadpoles, reduced cranial cartilage volume and individual cartilage abnormalities were rescued by Six1WT, less so by V17E and not by Y129C. In heterozygotes and wild types, Y129C caused a higher frequency of abnormal cartilages compared to Six1WT or V17E. Thus, variants with different functional deficits have distinguishable effects in both nulls and heterozygotes on the formation of the tissues affected in branchio-oto-renal syndrome. - Source: PubMed
Publication date: 2026/07/06
Coppenrath KelseyShaidani Nikko-IdeenNaert ThomasMajumdar Himani DHorb MarkoLienkamp Soeren SKlein Steven LMoody Sally A