Ask about this productRelated genes to: GFOD1 antibody
- Gene:
- GFOD1 NIH gene
- Name:
- glucose-fructose oxidoreductase domain containing 1
- Previous symbol:
- C6orf114
- Synonyms:
- FLJ20330, ADG-90
- Chromosome:
- 6p24.1-p23
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-19
- Date modifiied:
- 2018-02-13
Related products to: GFOD1 antibody
Related articles to: GFOD1 antibody
- Acute and chronic high-temperature stress negatively impact olive flounder (Paralichthys olivaceus) aquaculture, weakening immune function and increasing mortality. This study conducted a genome-wide association study (GWAS) to identify genetic markers linked to thermal stress resilience. A total of 384 fish were exposed to acute stress (29 °C for 30 min and 1 h) and chronic stress (19.8-30 °C for 16 days). Genomic DNA from 329 deceased and 55 surviving fish was genotyped using a 70 K SNP chip, yielding 57,638 SNPs from 376 fish after quality filtering. GWAS identified 34 SNPs associated with both acute and chronic thermal stress on chromosomes 4, 10, 11, 15, 18, 19, and 23, surpassing the suggestive (p < 1 × 10) and Bonferroni-corrected (p < 8.6 × 10) thresholds. Genes myhc, nlrc5, hydin, and gfod1 were linked to thermal stress. These findings may support marker-assisted selection for thermal stress resilience strains, promoting sustainable aquaculture. - Source: PubMed
Publication date: 2025/09/30
Hanchapola H A C RGong PoKim GaeunLiyanage D SOmeka W K MKim JeongeunKodagoda Yasara KavindiDilshan M A HRodrigo D C GGanepola G A N PiyumikaMassault CecileJerry Dean RLee JihunLee Jehee - The potential of inhibiting hsa-miR-19b-3p as a therapeutic approach for triple-negative breast cancer (TNBC) was investigated. To explore this, we studied the function of hsa-miR-19b-3p in TNBC cells, specifically the MDA-MB-231 cell line. We transfected these cells with LNA-anti-miR to inhibit the miRNA and then used qRT-PCR to measure the level of inhibition. Interestingly, we observed over 95 % inhibition at 24 h, and even at 48 h, the inhibition remained high at over 75 %. Upon closer examination, we determined the impact of this inhibition on cell viability using MTT assays, which showed a significant decrease in cell numbers following treatment with LNA-anti-miR-19b-3p. Furthermore, our apoptosis analysis, using Annexin V/Propidium iodide staining, revealed an increased apoptosis rate in the transfected cells compared to the controls. Alongside these experimental studies, we employed computational methods to investigate hsa-miR-19b-3p in greater detail, including RNA-Seq analysis of TCGA data, which identified 2585 upregulated and 4251 downregulated genes. Cross-referencing downregulated genes with target genes from miRTarBase, RNAInter, and miRWalk led to the identification of four potential hsa-miR-19b-3p targets: TMTC1, MBNL3, FAT3, and GFOD1, with TMTC1 and MBNL3 showing statistically significant downregulation. Additionally, we screened for potential small molecule inhibitors, identifying four promising candidates, including Dovitinib, S-Adenosylmethionine, Guanosine-5',3'-tetraphosphate, and Neomycin, which exhibited favorable drug-like characteristics. In conclusion, our multifaceted approach demonstrates the significant potential of LNA-anti-miR-19b-3p as a therapeutic option for TNBC patients, and the small molecule inhibitors we've uncovered could open new avenues for treating this aggressive form of breast cancer. - Source: PubMed
Publication date: 2025/07/14
Kamali Mohammad JavadSaeedi FatemehKhoshghiafeh AzinMir Mahsa AghajaniAram CenaAhmadifard Mohamadreza - The goal of this research was to examine the expression levels of Glucose-Fructose Oxidoreductase Domain Containing 1 (GFOD1) and to explore how it influences the proliferation, migration, and invasion of cancer cells in clear cell renal cell carcinoma (ccRCC, also known as KIRC). - Source: PubMed
Publication date: 2025/07/01
Liu ZhiWu KuiShu QianChen Xin - Emerging evidence supports that angiogenesis is essential for the wound healing of diabetic foot ulcer (DFU), and high glucose (HG)-induced dysfunction of human dermal microvascular endothelial cells is a key factor that hinders angiogenesis. However, the underlying mechanisms by which HG leads to the dysfunction of human dermal microvascular endothelial cells has not been fully elucidated. In the present investigation, we discovered a significant upregulation of the long non-coding RNA GFOD1-AS1(GFOD1-AS1) in the ulcer margin samples of patients with DFU and the HG-induced dysfunction model of human dermal microvascular endothelial cells, attributing its dysregulation to the stabilizing effect of NAT10-mediated ac4C modification, as corroborated by an integrated approach of data mining and experimental validation. Subsequently, a series of in vitro functional analyses showed that ectopic expression of GFOD1-AS1 promoted impaired function of human dermal microvascular endothelial cells. In contrast, knockdown of GFOD1-AS1 significantly alleviated the HG-induced functional impairment in human dermal microvascular endothelial cells, as indicated by the enhanced cell proliferation, migration, and tube formation. Mechanistically, GFOD1-AS1 directly interacts with DNA methyltransferase DNMT1 to block its ubiquitin-proteasome degradation, thereby enhancing the protein stability of DNMT1.This stability elevates DNMT1 protein expression, ultimately inducing HG-induced dysfunction in human dermal microvascular endothelial cells. In summary, our results reveal that GFOD1-AS1 serves as a potential therapeutic target for DFU, and highlight the critical role of the NAT10/GFOD1-AS1/DNMT1 axis in the dysfunction of human dermal microvascular endothelial cells in DFU. - Source: PubMed
Publication date: 2025/05/24
Yuan JingjingLi LushaLv YangYang Wenjun - Attention-deficit/hyperactivity disorder (ADHD) is a mental behavioral disorder that poses a serious health risk. Oxidative stress, which damages the function of neurons and astrocytes, has been discovered as a key factor contributing to ADHD pathology. A newly identified gene, Glucose-fructose oxidoreductase domain 1 (GFOD1), may be linked to the development of ADHD. It plays a role in regulating oxidative stress in ADHD; however, its exact role is unclear. This manuscript investigates the changes of GFOD1 expression and aim to correlate this with oxidative stress induced by NF-κB signaling pathway in the rat brains with ADHD and in vitro astrocytes. Our results revealed an increase in GFOD1 expression in the prefrontal cortex and cerebellar cortex of rats with ADHD, accompanied by neuronal injury and increased glial fibrillary acidic protein (GFAP) expression in astrocytes, concomitant with activation of the NF-κB p65/NOX2 signaling pathway. Along with this, GFOD1 overexpression in astrocytes resulted in an up-regulation of this signaling pathway similarly. Both ADHD rats and astrocytes in overexpressing GFOD1 showed elevated levels of reactive oxygen species (ROS) and Malondialdehyde (MDA), reduced activity of superoxide dismutase (SOD). Furthermore, treatment with the methylphenidate (MPH) did not affect GFOD1 expression. But it impacted the levels of oxidative stress mediated by the NF-κB p65/NOX2 signaling pathway. Overall, it is suggested that GFOD1 may contribute to increased levels of oxidative stress specifically in the prefrontal cortex and cerebellar cortex regions and astrocytes affected by ADHD via up-regulation of the NF-κB p65/NOX2/oxidative stress axis. - Source: PubMed
Publication date: 2025/04/08
Zheng Meng-LingYang Zhi-HongHe BinSun XinZhan Yu-TingShao An-QiHong Yu-ChenYin Cai-XinWang Ming-ZhengBa Ying-ChunYe Pin