Sheep Trefoil Factor 3, Intestinal ELISA , TFF3
- Known as:
- Sheep Trefoil Factor 3, Intestinal Enzyme-linked immunosorbent assay test , TFF3
- Catalog number:
- E14T0133
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Sheep Trefoil Factor 3 Intestinal ELISA TFF3
Related genes to: Sheep Trefoil Factor 3, Intestinal ELISA , TFF3
- Gene:
- TFF3 NIH gene
- Name:
- trefoil factor 3
- Previous symbol:
- -
- Synonyms:
- HITF, ITF
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-22
- Date modifiied:
- 2016-04-25
Related products to: Sheep Trefoil Factor 3, Intestinal ELISA , TFF3
Related articles to: Sheep Trefoil Factor 3, Intestinal ELISA , TFF3
- - Source: PubMed
Publication date: 2026/07/14
Ross-Innes Caryn SSomerset TimothyHadjinicolaou Andreas VBabbage AnneFreeman AdamFitzgerald Rebecca C - Ulcerative colitis (UC) is characterized by mucosal barrier erosion, a process exacerbated by bacterial sialidases. We investigated the therapeutic efficacy of the sialidase inhibitor (SI) in UC. In a pilot randomized clinical trial, SI intervention significantly improved clinical symptoms and endoscopic outcomes in mild-to-moderate UC patients. This improvement correlated with an enrichment of butyrate-producing taxa and beneficial metabolic pathways. In a dextran sulfate sodium-induced colitis mouse model, SI attenuated inflammation and restored mucus layer integrity, accompanied by increased expression of and . Crucially, unlike broad-spectrum antibiotics, SI preserved microbial community resilience while specifically enriching beneficial mucolytic commensals, and . These findings identify SI as a promising therapeutic strategy that targets sialidase activity to reinforce the mucosal barrier and restore gut homeostasis.IMPORTANCEThe gut microbiota plays a pivotal role in maintaining mucosal integrity and intestinal homeostasis; however, dysbiosis-driven mucus layer degradation remains a hallmark of ulcerative colitis (UC). Current interventions like antibiotics often disrupt microbial diversity, exacerbating dysbiosis and failing to address mucosal thinning, which is a critical factor in UC progression. Developing strategies to reinforce the mucus barrier without compromising microbial balance is urgently needed, but such approaches remain underexplored. Our study demonstrates that sialidase inhibitors (SIs) uniquely preserve mucosal thickness by curbing microbial mucin degradation while selectively enriching beneficial taxa and butyrate-producing bacteria. Unlike antibiotics, SIs enhance mucosal protection without destabilizing microbial communities, offering a dual-action therapeutic strategy. This work bridges a critical knowledge gap, providing evidence for microbiota-targeted therapies that synergistically restore mucosal health and microbial ecology in UC.CLINICAL TRIALSThis study was registered with the Chinese Clinial Trial Registry as ChiCTR2000028767. - Source: PubMed
Publication date: 2026/07/10
Zhao YimingChen LuluLi ChunyanXu YiHuang JingChen ShuijiaoYu ZhengLiu Xiaowei - Transcription activation of genes by estrogen is driven by enhancers, which are often located within the same topologically associating domain (TAD) as non-targeted promoters. We investigated how acute enhancer-driven activation affects neighbouring non-target genes within the same TAD. Using single-molecule RNA FISH (smFISH), we tracked the transcription of TFF1 (enhancer-target gene) and TFF3 (non-target gene) during estrogen stimulation. We observed mutually exclusive expression patterns: TFF1 expression peaked at 1 hr, while TFF3 reached its peak at 3 hr after TFF1 activation had diminished. Chromatin looping data indicated that the enhancer loops with the TFF1 gene but not TFF3, suggesting that TFF3 upregulation is not due to direct enhancer-promoter interactions. CRISPR deletion of the enhancer affected TFF1 transcription more acutely than TFF3. 1,6-hexanediol (HD) exposure suggested that the TFF1 enhancer:promoter undergoes a potential ERĪ±-mediated condensate formation, which sequesters the transcriptional machinery and inhibits TFF3 expression. As estrogen signaling fades at 3 hr, TFF1 expression declines while TFF3 expression increases. Our findings reveal that enhancer-driven activation can indirectly repress neighboring genes within the same TAD, highlighting a dynamic shift in gene expression as signaling progresses. - Source: PubMed
Publication date: 2026/07/07
Bohra DarshikaIslam ZubairulNidharshan SundarrajMazumder AprotimNotani Dimple - Organic thin-film transistor (OTFT)-based biosensors have garnered significant attention in life and health monitoring due to their rapid response, label-free detection, and ease of integration. However, in high ionic strength physiological fluids (e.g., blood, saliva), the charges of target biomolecules are shielded by counterions in the solution, resulting in the electrostatic Debye shielding effect. Herein, a unique concave-convex film composed of a Dy-Cu(OH) nanomaterial and a conjugated polymer was developed. The convex regions were used to enhance field penetration, and the concave regions were used to suppress the Debye shielding effect, enabling ultrasensitive dual-mode signal responses to TFF3 at the zeptomolar (zM) level. Besides, the detection reliability enhanced by four machine learning algorithms, offering a potential way toward ultraearly diagnosis of cancer biomarkers. - Source: PubMed
Publication date: 2026/07/01
Guo DeWang JunhuaiYang LeiSun ChenfangZhou YidiCheng Shanshan - While trefoil factor 3 (TFF3) has been linked to cardiovascular disease, its role in peripheral artery disease (PAD) remains largely unexplored. In this prospective study, we assessed three pre-selected circulating biomarkers and found that TFF3 demonstrated the strongest association with the presence of PAD. Building on this finding, we integrated plasma TFF3 concentrations with clinical characteristics to construct predictive models aimed at identifying individuals with PAD and estimating their risk of major adverse limb events (MALE) over a two-year follow-up period. - Source: PubMed
Publication date: 2026/06/17
Li BenKhan HamzahShaikh FarahZamzam AbdelrahmanRaphael RavelSyed Muzammil HAbdin RawandQadura Mohammad