b cells nf κb (Cusabio)
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Structured Review
Cusabio
b cells nf κb
B Cells Nf κb, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/b cells nf κb/product/Cusabio
Average 93 stars, based on 10 article reviews
B Cells Nf κb, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/b cells nf κb/product/Cusabio
Average 93 stars, based on 10 article reviews
b cells nf κb - by Bioz Stars,
2026-02
93/100 stars
Images
1) Product Images from "Diagnostic oral microbiota signatures for gastric cancer and associations with carcinogenic signaling pathways"
Article Title: Diagnostic oral microbiota signatures for gastric cancer and associations with carcinogenic signaling pathways
Journal: Journal of Oral Microbiology
doi: 10.1080/20002297.2026.2613531
Figure Legend Snippet: Expression of apoptosis-related genes in GC and HCs. (A) Heatmap of the Spearman’s rank correlation analysis between 8 genera and 30 significant pathways in GC. (B) Heatmap of the Spearman’s rank correlation analysis between 8 genera and 63 significant orthologs in GC. (C) Correlation analysis between 3 genera (columns) and 4 functional profiles (Ko04215-apoptosis, K07190-phosphorylase kinase alpha/beta subunit, K12767-serine/threonine-protein kinase, K08291-G protein-coupled receptor kinase) in GC and HCs. Full pathway and ortholog names are provided in Table S8. (D–I) Plasma level of (D) IL-6, (E) STAT3, (F) TGF- β , (G) NF-kB, (H) p -Smad2, and (I) p -Smad3 from 16 samples selected based on age and sex variance in each group. (J) Correlation analysis between 3 genera (columns) and 6 target molecules (rows) in GC and HCs. * p < 0.05, ** p < 0.01, and *** p < 0.001. PKA; phosphorylase kinase alpha/beta subunit, AKT; protein kinase B, GRK; G protein-coupled receptor kinases, IL-6; Interleukin-6, STAT3; Signal transducer and activator of transcription 3, TGF-β1; Transforming growth factor beta 1, NF-κB; Nuclear factor kappa-light-chain-enhancer of activated B cells. All p -values were adjusted for multiple comparisons using the Benjamini–Hochberg FDR correction.
Techniques Used: Expressing, Functional Assay, Clinical Proteomics
![Proposed mechanism of gastric carcinogenesis illustrating the directionality of molecular differences observed in this study. The schematic framework is adapted from previously reported carcinogenic signalling pathways in gastric cancer, including the TGF-β/Smad2/3 pathway [ , ], the PI3K/AKT/NF-κB pathway , and the IL-6–mediated JAK/STAT3 pathway [ , ]. Molecules analysed in this study are highlighted, with red and blue arrows indicating relatively higher and lower levels, respectively, in patients with GC compared with HCs, based on group-wise comparisons of PICRUSt-inferred orthologs and plasma cytokine measurements. The figure is intended to contextualise these observational findings within established literature-based signalling frameworks and does not represent direct experimental validation of mechanistic pathways. TGF-β; transforming growth factor beta, TFGBR; TGF- β receptor, PI3K; phosphoinositide 3-kinases, AKT; protein kinase B, GPCR; G protein-coupled receptor, GRK; G protein-coupled receptor kinases, NF-κB; nuclear factor kappa-light-chain-enhancer of activated B cells, IL-6; interleukin 6, STAT3; signal transducer and activator of transcription 3, JAK; Janus kinase, PTEN; phosphatase and tensin homologue.](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_4691/pmc12794691/pmc12794691__ZJOM_A_2613531_F0006_C.jpg "... including the TGF-β/Smad2/3 pathway [ , ], the PI3K/AKT/NF-κB pathway , and the IL-6–mediated JAK/STAT3 pathway [ ...")
Figure Legend Snippet: Proposed mechanism of gastric carcinogenesis illustrating the directionality of molecular differences observed in this study. The schematic framework is adapted from previously reported carcinogenic signalling pathways in gastric cancer, including the TGF-β/Smad2/3 pathway [ , ], the PI3K/AKT/NF-κB pathway , and the IL-6–mediated JAK/STAT3 pathway [ , ]. Molecules analysed in this study are highlighted, with red and blue arrows indicating relatively higher and lower levels, respectively, in patients with GC compared with HCs, based on group-wise comparisons of PICRUSt-inferred orthologs and plasma cytokine measurements. The figure is intended to contextualise these observational findings within established literature-based signalling frameworks and does not represent direct experimental validation of mechanistic pathways. TGF-β; transforming growth factor beta, TFGBR; TGF- β receptor, PI3K; phosphoinositide 3-kinases, AKT; protein kinase B, GPCR; G protein-coupled receptor, GRK; G protein-coupled receptor kinases, NF-κB; nuclear factor kappa-light-chain-enhancer of activated B cells, IL-6; interleukin 6, STAT3; signal transducer and activator of transcription 3, JAK; Janus kinase, PTEN; phosphatase and tensin homologue.
Techniques Used: Clinical Proteomics, Biomarker Discovery