TFF2 (Human) Recombinant Protein (P01)
- Known as:
- TFF2 (Human) Recombinant Protein (P01)
- Catalog number:
- H00007032-P01-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- TFF2 (Human) Recombinant Protein (P01)
Related genes to: TFF2 (Human) Recombinant Protein (P01)
- Gene:
- BZW2 NIH gene
- Name:
- basic leucine zipper and W2 domains 2
- Previous symbol:
- -
- Synonyms:
- HSPC028, MST017, MSTP017
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-05
- Date modifiied:
- 2016-10-05
- Gene:
- C2CD3 NIH gene
- Name:
- C2 calcium dependent domain containing 3
- Previous symbol:
- -
- Synonyms:
- DKFZP586P0123
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2007-10-17
- Date modifiied:
- 2016-06-08
- Gene:
- MBTD1 NIH gene
- Name:
- mbt domain containing 1
- Previous symbol:
- -
- Synonyms:
- SA49P01, FLJ20055
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-01-15
- Date modifiied:
- 2015-04-21
- 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
- Gene:
- TMEM63C NIH gene
- Name:
- transmembrane protein 63C
- Previous symbol:
- C14orf171
- Synonyms:
- DKFZp434P0111, CSC1, hsCSC1
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-10
- Date modifiied:
- 2017-10-17
Related products to: TFF2 (Human) Recombinant Protein (P01)
Related articles to: TFF2 (Human) Recombinant Protein (P01)
- Eosinophilic gastritis (EoG) is a chronic inflammatory disease characterized by infiltration of eosinophils and mast cells, epithelial remodeling, and fibrosis. Although EoG is increasingly recognized as a distinct type 2 inflammatory disease, the cellular and molecular events that drive disease pathogenesis remain poorly understood. This is due in part to the absence of robust and physiologically relevant experimental models that recapitulate human disease METHODS: Experimental EoG was induced in wild-type and Il13ra1 mice by repeated intragastric oxazolone challenges in skin-sensitized mice. IL-4Rα was neutralized using antibodies. Gastric histopathology was determined by H&E, anti-Ki67, chloroacetate esterase, and anti-MBP staining. Gastric RNA was subjected to RNA sequencing. - Source: PubMed
Publication date: 2026/06/18
Dsilva AnishSharma ShraddhaBarakey ShireenWagner ArielKeisar AliceBar-On TaliItan MichalMunitz Ariel - The pathogenesis of gallbladder adenocarcinoma(GBC) remains inadequately elucidated. While its association with intestinal metaplasia (IM) has been acknowledged, there is a paucity of evidence connecting GBC to the most prevalent metaplastic type-pseudopyloric metaplasia (PPM). Given the morphological similarities between PPM and spasmolytic polypeptide-expressing metaplasia (SPEM), a recognized gastric precancerous condition, we propose that trefoil factor 2 (TFF2)-positive PPM may represent a cellular origin of GBC. Furthermore, we examine the role of the emerging therapeutic target claudin-18 (CLDN18) in this context. Through immunohistochemistry (IHC) analysis of 37 GBC, 30 biliary intraepithelial neoplasia (BilIN), 20 intracholecystic papillary neoplasm (ICPN), 26 IM, and 20 PPM samples, we observed an inverse correlation between CLDN18 expression and vascular invasion, whereas TFF2 expression was positively associated with tumor differentiation. CLDN18 overexpression(a staining intensity ≥ 2 + in ≥ 75% of tumour cells) was identified in 18.9% of GBC cases. This study provides the first evidence that CLDN18 is specifically activated at the precursor stage of gallbladder carcinogenesis, being strictly confined to lesions with an intestinal phenotype (IM, BilIN, ICPN) while remaining entirely negative in normal epithelium and PPM. This "all or none" expression pattern establishes CLDN18 as an ideal biomarker for identifying high risk gallbladder precursor lesions, particularly for recognizing PPM that has undergone malignant prone intestinal differentiation. Furthermore, the subset of GBCs with high CLDN18 expression identifies patients who may benefit from CLDN18 targeted therapies. - Source: PubMed
Publication date: 2026/05/26
Min QinqinJiang XuCheng YaoYu XuewenYang TingtingGu GuiyuanMei KaiyongShao Mumin - Spasmolytic polypeptide-expressing metaplasia (SPEM) arises in the gastric corpus in response to oxyntic atrophy, but its cellular origin and role in gastric cancer remain unclear. - Source: PubMed
Publication date: 2026/04/14
Tu RuhongZheng Hua-LongZheng BiyunZhong QingQian JinYu QianWu FeijingShiokawa ToshiroOchiai YosukeKobayashi HirokiWaterbury Quin TZamechek LeahGao YouxinTakahashi SatoruMizuno SeiyaHuang Chang MingLi PingHayakawa YokuWang Timothy C - Chronic atrophic gastritis (CAG) severity risk assessment remains challenging due to limitations of current static histologic/endoscopic tools. We evaluated the leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5)/trefoil factor 2 (TFF2) ratio - quantifying gastric stem cell niche imbalance- as a dynamic biomarker for high-risk CAG (OLGA/OLGIM III-IV). - Source: PubMed
Publication date: 2026/04/09
Zhang QingqingWu DiGuo FengyunYang ShengnanBao LijingZhang RuiyingWang Ping - In clinical practice, Hezi Qingyou Formula (HZQYF) has been observed to effectively alleviate clinical symptoms associated with gastri ulcers, though its precise mechanism of action remains unclear. To investigate the effects of HZQYF on gastric ulcers, we established a rat model of gastric ulcer and examined its impact on ulcer area, pathological changes, inflammatory cytokines, gastric repair factors, levels of T-superoxide dismutase (SOD), and malondialdehyde (MDA), as well as metabolites in gastric tissue and feces. The results demonstrated that HZQYF significantly reduced the gastric ulcer area and promoted gastric tissue repair in rats. It downregulated the phosphorylation of P-P38, P-JNK1/2, and ERK1/2 proteins in the mitogen-activated protein kinases (MAPKs) pathway, inhibited pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α), enhanced the expression of gastric repair factors including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), trefoil factor family 2 (TFF2), and prostaglandin E2 (PGE2), reduced MDA content, and increased the activity of the antioxidant enzyme T-SOD, thereby suppressing inflammatory responses and ameliorating gastric mucosal damage. Metabolomic studies revealed that HZQYF effectively normalized 40 metabolites in gastric tissue through four key metabolic pathways and 39 metabolites in feces through five key metabolic pathways. Notably, it regulated taurine and hypotaurine metabolism, as well as phenylalanine metabolism, restoring metabolite levels to normal and ameliorating metabolic disorders in diseased rats. In conclusion, HZQYF promotes the healing of experimental gastric ulcers in rats through anti-inflammatory effects, activation of gastric repair factors, and normalization of gastric tissue metabolites, suggesting its potential therapeutic role in the treatment of gastric ulcers. - Source: PubMed
Feng ZhongWei RuixiaTian JunhaoLi HuiChen HaoboHao YajieChen MeiyunSu BingmeiLai YuqianXun MingjinZhang GuiminYao Meicun