Ask about this productRelated genes to: HS3ST3B1 antibody
- 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 antibody
Related articles to: HS3ST3B1 antibody
- 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. - 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 - Acute myeloid leukemia (AML) shows significant heterogeneity in therapeutic responses. We aimed to develop a gene signature for the stratification of high-risk pediatric AML using publicly available AML datasets, with a focus on literature-based prognostic gene sets. - Source: PubMed
Publication date: 2025/01/24
Song Jong KeonLee Dong HyeokKim HyeryHwang Sang-Hyun