Easy blot Mini SKit HGH, Qualitative Protein Detection-Skit
- Known as:
- Easy blot Mini SKit HGH, Qualitative Protein Detection-Skit
- Catalog number:
- RF0084
- Category:
- -
- Supplier:
- Agren
- Gene target:
- Easy blot Mini SKit HGH Qualitative Protein Detection-Skit
Related genes to: Easy blot Mini SKit HGH, Qualitative Protein Detection-Skit
- Gene:
- GKN2 NIH gene
- Name:
- gastrokine 2
- Previous symbol:
- -
- Synonyms:
- TFIZ1, PRO813, VLTI465, blottin, GDDR, BRICD1B
- Chromosome:
- 2p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2007-01-29
- Date modifiied:
- 2016-10-05
Related products to: Easy blot Mini SKit HGH, Qualitative Protein Detection-Skit
Related articles to: Easy blot Mini SKit HGH, Qualitative Protein Detection-Skit
- infection is the main risk factor for gastric cancer. easily develop antibiotic resistance and evade host defenses. In-depth knowledge of the first barrier that encounter, the gastric surface mucus-producing epithelial cells (SMCs), may enable improved treatment and prevention. This study aimed to characterize SMC gene expression, mucus glycosylation, and identify how colonization affects these parameters. The glycosylation of eight -infected and eight sham control mice was characterized by mass spectrometry. SMCs from five infected and five sham control mice were extracted with laser microdissection (LCM) and sequenced with RNA sequencing (RNA-Seq). SMCs were characterized by high gene expression for proteins secreted into mucus (, , , , and , mitoribosome RNA, and cytoskeleton proteins. Mucin glycans were large, complex, heavily fucosylated, and dense with H-antigen motifs. Two main glycosylation pathways ending in H-antigen glycans were identified and corroborated with glycosyltransferase expression. Glycosylation was consistent between -infected and sham control mice. RNA-Seq data was analysed for differential gene expression, gene set enrichment analysis, and network analysis of functionally-related genes. The analyses revealed that genes required for protein synthesis and oxidative phosphorylation were down-regulated in infected mice. Most up-regulated genes were either interferon-stimulated genes or able to induce interferon production themselves. Depletion of Nkx6-3 occurred in the infected mice, indicating initiation of a pre-cancerous cascade. LCM RNA-Seq of SMCs was thus feasible and enabled characterization of the SMC and definition of a gene set showing how infection affects SMCs. - Source: PubMed
Publication date: 2026/03/25
Erhardsson MattiasSantos LicíniaBenktander JohnSharba SinanThorell KaisaLindén Sara - Accumulating evidence has revealed that epithelial-mesenchymal transition (EMT) plays a crucial role in tumor progression and the immune microenvironment, which further results in a high rate of recurrence and metastasis. The EMT immune signaling pathway provides a great perspective for designing personalized therapies. - Source: PubMed
Publication date: 2026/01/19
Liang WeiWang Zi-YingShao Quan-FengLi Yuan-YuanZhu BeiQin Xi-HuChen Wei-Xian - For small ruminants, meat quality-an economically significant characteristic-results from the combined effects of genetic, dietary, and physiological elements. However, the contribution of gastrointestinal (GI) tract gene expression to meat quality remains unclear. - Source: PubMed
Publication date: 2025/10/29
Chen BinlongHuang ZhiyingCai ZhongkunLi SiyuYan GuangwenChang WeihuaZhang YiYang Shizhong - The stomach has been a highly conserved organ throughout vertebrate evolution; however, there are now over 20 lineages composed of monotremes, lungfish and teleost fish displaying a secondary loss of stomach function and morphology. This "agastric phenotype" has evolved convergently and is typified by a loss of gastric glands and gastric acid secretion and a near-to-complete loss of storage capacity of the stomach. All agastric species have lost the genes for gastric enzymes ( and ) and proton pump subunits ( and ), and gastrin () has been lost in monotremes. As a key gastric hormone, the conservation of gastrin has not yet been investigated in the lungfish or agastric teleosts, and it is unclear how the loss of gastrin affects the evolution and selection of the native receptor (), gastrin-releasing peptide () and gastrin-releasing peptide receptor () in vertebrates. Furthermore, there are still many genes implicated in gastric development and function which have yet to be associated with the agastric phenotype. We analysed the evolution, selection and conservation of the gastrin pathway and a novel gastric gene repertoire (, , , , and ) to determine the correlation with the agastric phenotype. We found that the loss of gastrin or its associated genes does not correlate with the agastric phenotype, and their conservation is due to multiple pleiotropic roles throughout vertebrate evolution. We found a loss of the gastric gene repertoire in the agastric phenotype, except in the echidna, which retained several genes (, and ). Our findings suggest that the gastrin physiological pathway evolved differently in pleiotropic roles throughout vertebrate evolution and support the convergent evolution of the agastric phenotype through shared independent gene-loss events. - Source: PubMed
Publication date: 2025/08/05
Dann JacksonGrützner Frank - Intestinal metaplasia (IM) represents a precancerous condition associated with an increased risk of gastric cancer. A better understanding of whether and how precancerous lesions progress to gastric cancer is crucial for patient stratification and personalized prevention. In this study, we reconstruct evolutionary trajectories of genomic alterations in 330 multiregion matched samples of IM and tumors from 93 patients with gastric cancer. Intestinal-type gastric cancer (IGC) exhibited a higher mutation burden than diffuse-type gastric cancer (DGC), notably in genomically stable patients. IM from genomically stable patients carried more mutations associated with alcohol consumption. The 20 significantly mutated genes identified were classified into three evolutionary patterns. "Maintained" genes (TP53, APC, and PIK3CA) were commonly altered in IM and matched gastric cancer samples in both IGC and DGC, whereas CDH1 mutations were specific to DGC. "Maintained" mutations in IM accelerated gastric cancer progression. Alterations in "IM-favored" genes (MUC6, CFTR, BMP6, and MTRR) were associated with IM development but were negatively selected in gastric cancer. Interestingly, MUC6 mutations were enriched in specific pit cells with upregulation of GKN1 and GKN2. The remaining genes were "gastric cancer-favored" and showed high heterogeneity in gastric cancer. These findings illuminate the genomic evolution from IM to IGC or DGC, providing insights that could guide precancerous lesion surveillance and early prevention strategies. - Source: PubMed
Xu XianfengYan CaiwangBian LijunLi ZheYu YuhuiZhu XiaGao YunXu HaoLi FengyuanLiu YaoSun PingWang ZhengFu YaoJiang YueDai JunchengMa HongxiaHu ZhibinShen HongbingLi GangWang ChengJin Guangfu