TFF2_MOUSE Tff2 ELISA tesk kit
- Known as:
- TFF2_MOUSE Tff2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen10946
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TFF2_MOUSE Tff2 ELISA tesk kit
Related genes to: TFF2_MOUSE Tff2 ELISA tesk kit
- Gene:
- TFF2 NIH gene
- Name:
- trefoil factor 2
- Previous symbol:
- SML1
- Synonyms:
- -
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-13
- Date modifiied:
- 2015-08-26
Related products to: TFF2_MOUSE Tff2 ELISA tesk kit
Related articles to: TFF2_MOUSE Tff2 ELISA tesk kit
- Ascaris roundworms impair human and swine health. While treatments using anthelmintic drugs are generally effective in eliminating worms, their effects on the gut microenvironment remain poorly understood. Here we applied integrated multi-omics to characterize infection- and treatment-associated alterations in the pig-Ascaris system. anaerobic cultures were conducted as supportive validation of selected observations. infection altered microbial composition and dysregulated 182 serum and fecal metabolites, including histamine and p-cresol sulfate. Compared with time-matched uninfected controls, infected pigs treated with fenbendazole showed marked differences in gut microbial composition 13 days after confirmed worm clearance. Eleven microbial pathways were enriched in successfully treated pigs, including peptidoglycan biosynthesis and histidine metabolism, indicating that infection-associated alterations may persist after treatment. co-exposure of to fenbendazole and proteins increased histamine production by approximately 79% at 48 h ( < 0.05), serving as supportive evidence of a microbiome contribution. Collectively, our findings support that host-microbiota-parasite interactions are multifaceted. Microbiota-derived metabolites were associated with regulation of host gene expression, such as and . Microbiota plasticity allows the exploitation of the niche differentiated upon infection, resulting in the proliferation of certain strains in treated animals. Nevertheless, interpretations of treatment effects are made cautiously given the absence of an uninfected drug-only group and the cross-sectional design. Understanding these complex interactions will be important for the design of next-generation functional anthelmintics. - Source: PubMed
Publication date: 2026/09/11
Liu FangStreett HannahSolano-Aguilar GloriaSmith Allen DCarbaugh DonaldUrban Joseph FLi Robert W - Invasive mucinous adenocarcinoma (IMA) of the lung is a distinct subtype of lung adenocarcinoma with unique clinicopathologic features; however, its histogenesis remains incompletely understood. Although mucinous metaplasia has been suspected as a precursor lesion, direct molecular evidence supporting this progression is limited. In this study, we applied morphology-guided spatial transcriptomics to investigate epithelial lineage relationships across the mucinous spectrum of lung lesions. Formalin-fixed, paraffin-embedded lung tissues from 26 patients were analyzed using the GeoMx digital spatial profiling platform. A total of 118 cytokeratin-positive regions of interest representing normal bronchioles, bronchiolar metaplasia, mucinous metaplasia, mucinous dysplasia, IMA, nonmucinous terminal respiratory unit-type adenocarcinoma, squamous metaplasia/dysplasia, and squamous cell carcinoma were profiled. Spatial transcriptomic data were integrated with two independent public cohorts and mapped to the Human Lung Cell Atlas for epithelial cell-type assignment. Unsupervised clustering identified a distinct mucinous cluster comprising IMA and most mucinous dysplasia regions, characterized by enrichment of gastric-type differentiation markers, including MUC5AC, MUC6, TFF1, TFF2, and CLDN18. Label-transfer analysis demonstrated that mucinous metaplasia and dysplasia were predominantly associated with club and goblet cell identities, whereas IMAs showed enrichment of club and goblet signatures. In contrast, nonmucinous adenocarcinomas consistently aligned with alveolar type 2 cell identity across all datasets. Immunohistochemistry confirmed uniform CLDN18 expression in IMAs and its absence in nonmucinous adenocarcinomas. These findings provide spatial transcriptomic evidence supporting a club cell-associated mucinous pathway in lung tumorigenesis and identify CLDN18 as a defining molecular feature of IMA. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/09/08
Park Joon YoungKim Do YeonLee Hyun JungLee Jung HeePark Hae RyounShin Dong Hoon - This research sought to investigate the therapeutic efficacy and underlying mechanisms of Shengjiang Powder (SJP) in the context of chronic gastritis. - Source: PubMed
Publication date: 2026/08/14
Liu YihuangLi XiaofengZhang XiaCao HuaZhang NailinSun JianhuiChen Pingping - The article "Identification of LGR5 and TFF2 as Biomarkers in High-Risk Chronic Atrophic Gastritis: From Multi-Omics Mining to Clinical Validation" [Digestion. 2026; https://doi.org/10.1159/000549887] by Qingqing Zhang, Di Wu, Fengyun Guo, Shengnan Yang, Lijing Bao, Ruiying Zhang and Ping Wang has been retracted by the Publisher and the Editor.Post-publication concerns were raised regarding the integrity of the clinical cohort data reported in the article. The data presented in Table 1 shares the same subgroup size, gender distributions and H. pylori infection rates across all three subgroups to those reported in a previously published article by the same research group [1]. Additionally, the images in Figure 4b and d of this article are published as Figure 2a and b in [1]. The previous publication was not cited in this article.When asked about the similarities between the cohorts, the authors stated that they were two independent cohorts and that the similarities were coincidental. The Editors did not find the authors' explanation sufficient to resolve their concerns, and as a result have lost confidence in the reliability and originality of the reported cohort data.The authors did not respond to our correspondence about the retraction of this article within the timeframe specified. - Source: PubMed
Publication date: 2026/07/31
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Publication date: 2026/07/18
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