Easy blot Mini SKit HGH
- Known as:
- Easy blot Mini SKit HGH
- Catalog number:
- rf0084
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Agrenvec
- Gene target:
- Easy blot Mini SKit HGH
Related genes to: Easy blot Mini SKit HGH
- 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
Related articles to: Easy blot Mini SKit HGH
- To explore the application value of three novel serum markers, collagen X-type α1 chain (COL10A1), gastrokine 2 (GKN2), and lipase F (LIPF), in the diagnosis of gastric cancer. - Source: PubMed
Wang FasheLi BaiLi ShangyinTang YanTao Tan - Gastric adenocarcinoma (GAC) is characterized by molecular heterogeneity that limits early detection and targeted treatment. We applied weighted gene coexpression network analysis (WGCNA) to paired RNA-seq data from 119 GAC and peritumoral tissue (PTT) samples and identified six coexpression modules with distinct biological identities. Four modules were positively correlated with GAC and two were negatively correlated. Among the 30 hub genes evaluated, several outperformed established clinical biomarkers in accuracy. Specifically, SPARC (AUC = 0.89), COL3A1 (0.87), and COL1A2 (0.85) exceeded MUC5AC (0.76), VEGFA (0.68), and ERBB2 (0.64). Validation in the TCGA-STAD cohort confirmed concordant expression trends for MEblack (5/5 genes) and MEmagenta (4/5), with an overall fold-change correlation of ρ = 0.58 (p = 6.96 × 10⁻⁴). Immune deconvolution delineated two opposing microenvironmental axes, with an adaptive-immune-epithelial program (MEblack) associated with B-cell abundance, and a fibroblast-collagen program (MEmagenta) associated with cancer-associated fibroblast enrichment. DepMap CRISPR screening identified ribosomal hub genes as cell-intrinsic dependencies in gastric cancer cell lines. Among all hub genes, SPARC, COL3A1, COL1A2, GKN1, and GKN2 emerged as the potential biomarker candidates, with SPARC additionally showing a validated unfavorable prognostic association in STAD. - Source: PubMed
Publication date: 2026/08/10
Mourão Ronald Matheus da SilvaMoreira Fabiano CordeiroSilva Jéssica Manoelli Costa daCosta Daniel de Souza Avelar daSilva Valéria Cristiane Santos daVidal Amanda FerreiraMagalhães Leandro Lopes deAnaissi Ana Karyssa MendesDemachki SamiaBarra Williams FernandesAssumpção Paulo Pimentel de - Lung cancer is the second most commonly diagnosed malignancy worldwide and remains the leading cause of cancer-related death. Non-small cell lung cancer (NSCLC) accounts for approximately 80-85% of lung cancers. Given the low rate of early detection and substantial interpatient heterogeneity, management of NSCLC, particularly locally advanced disease, remains challenging. This study aimed to characterize clinical heterogeneity and progression-associated molecular features of locally advanced NSCLC and to identify candidate biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/06/24
Tian YuanhuiDeng YanLiao XiaoliYuan ShutaoLi Ke - Acute upper gastrointestinal bleeding (UGIB) is a critical emergency commonly encountered in gastroenterology. Its pathogenesis is complex and involves diverse etiologies. Emerging evidence indicates that pyroptosis, dysregulated immune-inflammatory responses, and gut microbiome imbalance are pivotal mechanisms driving gastric mucosal injury and hemorrhage. This review systematically synthesizes the risk factors, pathophysiological mechanisms, risk prediction models, and therapeutic strategies for UGIB, with particular emphasis on the intricate interplay among pyroptosis, immunity, and the microbiome and on their value as potential therapeutic targets. We first summarize the common etiologies and risk factors of UGIB, including pharmacological agents, infections, advanced age, comorbidities, and genetic predispositions. We then delineate the pathogenic role of pyroptosis in gastric mucosal injury, with particular focus on activation of the GKN2-NLRP3 axis. Next, we discuss the utility of systemic inflammatory markers such as the neutrophil-to-lymphocyte ratio (NLR) and C-reactive protein (CRP) in UGIB risk stratification, together with the mechanisms by which gut microbiome dysbiosis compromises mucosal barrier integrity and amplifies inflammatory responses through microbial metabolites and pathogen translocation. The core section provides an in-depth analysis of the reciprocal, self-amplifying network linking pyroptosis, immune activation, and microbiome perturbation, thereby elucidating the basis for the frequent co-occurrence of systemic inflammation and microbial dysbiosis in UGIB. Finally, we critically evaluate established risk-scoring systems (Glasgow-Blatchford Score, Rockall score, and AIMS65) and emerging biomarkers. Overall, this review assesses emerging therapeutic strategies, including pyroptosis inhibitors and microbiome-modulating interventions, and provides a theoretical framework for personalized management of UGIB. - Source: PubMed
Publication date: 2026/06/01
Mei LijunZhang PiaoXiang TaoSun Chengcheng - 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