Ask about this productRelated genes to: HS3ST3B1 Blocking Peptide
- Gene:
- HS3ST3B1 NIH gene
- Name:
- heparan sulfate-glucosamine 3-sulfotransferase 3B1
- Previous symbol:
- -
- Synonyms:
- 3OST3B1, 30ST3B1
- Chromosome:
- 17p12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-05
- Date modifiied:
- 2015-12-04
Related products to: HS3ST3B1 Blocking Peptide
Related articles to: HS3ST3B1 Blocking Peptide
- Long-term survival of lung transplant recipients remains limited by chronic lung allograft dysfunction (CLAD). CLAD is only diagnosed following a persistent and substantial decline in lung function, after which irreversible damage to the lungs has occurred, limiting opportunities to effectively intervene at an early stage. There is a critical need for earlier detection prior to its clinical manifestation. The immunological drivers of CLAD remain unclear, limiting the development of predictive biomarkers and new therapies. - Source: PubMed
Publication date: 2026/06/23
Iacono GiuliaBegka ChristinaCardwell BaileyDaunt CarmelChatzis RoxannePattaroni CelineButler AlanaMacowan MatthewLevvey BronwynSnell Gregory IWestall Glen PMarsland Benjamin J - BACKGROUND: Acute myeloid leukemia (AML), a biologically heterogeneous malignancy, requires improved prognostic models, particularly for patients with intermediate-risk profiles and lacking definitive genetic markers. Therefore, this study aims to identify biologically coherent and clinically informative gene signatures using a novel prognostic modeling approach integrating gene expression profiles with protein–protein interaction networks. METHODS: We applied network propagation using Personalized PageRank with seed genes from a literature-based six-gene signature (LBS6) and two recurrent AML mutations (IDH1 and IDH2). Network-informed modules were derived and optimized using LASSO–Cox regression models trained on the TCGA–LAML cohort (n = 132, adult AML) and externally validated in the BeatAML 1.0 (n = 308, adult AML) and TARGET–AML (n = 1,889, pediatric AML) cohorts. Cox proportional hazards models were used to evaluate associations with overall survival. Functional enrichment analyses were conducted using KEGG and Gene Ontology databases. RESULTS: From LBS6 propagation, a ten-gene signature (LBS6-Derived Network Gene Signature [LBSnet]: PTP4A3, HS3ST3B1, ECHS1, PLA2G4A, ETFB, NDST3, CSK, ARL6IP5, PLD1, and NDUFS8) was derived, stratifying patients in the TCGA–LAML based on overall survival (HR = 3.84, p < 0.0001) and was validated in the BeatAML 1.0 (HR = 1.94, p < 0.0001) and TARGET–AML (HR = 1.57, p < 0.0001) cohorts. Joint network propagation using IDH1 and IDH2 seed genes produced a five-gene signature metabolic and chromatin-modifying functions (G6PD, ENO1, SDHA, H3-3 A, IL4I1), demonstrating prognostic significance in the TCGA–LAML cohort (HR = 2.91, p < 0.0001), BeatAML 1.0 (HR = 1.33, p = 0.07), and TARGET–AML (HR = 1.34, p < 0.001). These network-derived risk scores remained independent predictors of overall survival in multivariate Cox models adjusted for age and key genetic covariates, including FLT3-ITD, NPM1, and CEBPA mutations. Functional enrichment analyses revealed significant involvement in fatty-acid oxidation, mitochondrial respiration, and platelet activation pathways. CONCLUSION: This study presents a novel network-based framework for prognostic modeling in AML, generating biologically interpretable gene signatures with validated predictive power across adult and pediatric cohorts. Integrating transcriptomic data with molecular interaction networks provides a scalable strategy for biomarker discovery, enhancing risk stratification and offering insight into potential metabolic vulnerabilities in AML. - Source: PubMed
Publication date: 2025/12/03
Song Jong KeonKim HyeryHwang Sang-Hyun - The RNA-binding protein polypyrimidine tract-binding protein 1 (PTBP1), also known as heterogeneous nuclear ribonucleoprotein I (hnRNP I), mediates gene expression through splicing regulation. Its role in virus infection is undefined. - Source: PubMed
Publication date: 2025/11/20
Sun WeikangZhang MengyuWang RuilinYang JieRasool Ameena TurLuo RenjieLiu XiangdongCao PengLi Erguang - Chordoma is a special malignant tumor that lacks effective therapeutic targets, which can lead to incomplete treatment and metastasis. Inflammation plays an important role in chordoma progression and malignant phenotype. Inflammatory factors such as NF-kappaB and STAT3 are continuously activated in many tumors and contribute to the malignant phenotype of tumors and are potential therapeutic targets. This study suggest TNF-alpha and NF-kappaB signaling pathways were consistently activated in chordomas. Long-term TNF-alpha treatment induces chordoma resistance to EGFR family inhibitors. The underlying mechanism is realized by the key molecules HS3ST3A and HS3ST3B1. These two enzymes are potential targets for chordoma treatment, as well as for combination drugs treatment. It should be emphasized that the above analysis lacks experimental verification. - Source: PubMed
Publication date: 2025/09/09
Tang HaoShuaiZhu QingRunFan JinHongLi XinAoYan ZhenYeWang FengWang HaiFengWang DaChuan - This study explores the mechanism of miR-19b-3p in bladder cancer (BCa) cell proliferation and apoptosis to provide the latest theoretical basis for miR-19b-3p to become a novel biomarker and therapeutic target for BCa. miR-19b-3p, lncRNA SNHG20, and HS3ST3B1 expressions in BCa tissues or cells were detected via RT-qPCR or Western blot. Cell proliferation was evaluated via CCK-8 and colony formation assays. Cell apoptosis was assessed via flow cytometry, and apoptosis related factors Bax and Bcl-2 were detected via Western blot. Dual luciferase and RIP assays confirmed the binding of miR-19b-3p and lncRNA SNHG20. The binding between lncRNA SNHG20, TARDBP, and HS3ST3B1 was analyzed by RIP, RNA pull down, and co-immunoprecipitation. The RNA stability of lncRNA SNHG20 and HS3ST3B1 was tested after actinomycin D treatment. A nude mouse xenograft tumor model was established to validate the effect of miR-19b-3p on BCa in vivo. miR-19b-3p was weakly expressed in BCa, while lncRNA SNHG20 and HS3ST3B1 were highly expressed. Overexpression of miR-19b-3p repressed BCa cell proliferation but facilitated apoptosis. Mechanistically, miR-19b-3p decreased lncRNA SNHG20 expression by binding to lncRNA SNHG20 and reducing its stability, thus repressing the interaction between lncRNA SNHG20-TARDBP-HS3ST3B1. Further in vivo experiments also revealed that miR-19b-3p restrained the in vivo tumorigenicity of BCa cells and promoted apoptosis by suppressing the lncRNA SNHG20/HS3ST3B1 axis. In conclusion, overexpression of miR-19b-3p represses BCa cell proliferation and promotes apoptosis by suppressing the lncRNA SNHG20/HS3ST3B1 axis. - Source: PubMed
Publication date: 2025/09/06
Dai HongshuangZhang YunzhuYu SiwenFeng YueQiao Zhongjie