BTG3 antibody
- Known as:
- BTG3 (anti-)
- Catalog number:
- orb101585
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- BTG3 antibody
Related genes to: BTG3 antibody
- Gene:
- BTG3 NIH gene
- Name:
- BTG anti-proliferation factor 3
- Previous symbol:
- -
- Synonyms:
- ANA, tob55, APRO4, ANA/BTG3
- Chromosome:
- 21q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-29
- Date modifiied:
- 2017-03-10
Related products to: BTG3 antibody
Related articles to: BTG3 antibody
- Intervertebral disc degeneration (IDD) is a prevalent disease with an increasing incidence, and aging is a key risk factor for its progression. Therefore, this study aimed to explore the role of aging-related genes in IDD through bioinformatics analysis. Differentially expressed aging-related genes were obtained from the CellAge, GSE150408 and GSE124272 datasets, followed by biomarker screening via machine learning. Finally, the identified biomarkers were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), Western Blot (WB), and immunohistochemistry (IHC) assays. A total of 33 aging-related differentially expressed genes (DEGs) were screened in IDD, and machine learning combined with ROC curve analysis identified PPM1D, PIK3C2A, and BTG3 as aging-related biomarkers for IDD; Gene Set Enrichment Analysis (GSEA) revealed that these three biomarkers were enriched in gene functions including cellular senescence, multicellular organismal aging, negative regulation of cellular senescence, and Ribosome. In addition, the multifactorial regulatory network showed that transcription factor E2F1 and hsa-miR-147 co-regulated both PPM1D and BTG3. In experiments validating biomarker expression levels, BTG3 and PIK3C2A exhibited consistent expression trends across IHC, RT-qPCR, WB assays and the two datasets. BTG3 and PIK3C2A may play more critical roles in the progression of IDD, thereby providing novel insights for the development of new therapeutic strategies for IDD patients. - Source: PubMed
Publication date: 2026/04/09
Zhang FanYuan LeiDing HengLou ZhenkaiLi Xingguo - B-cell translocation gene 3 (), a tumor suppressor, is reduced in expression in several malignancies, including ovarian cancer, colorectal cancer, and gastric cancer, but its role in oral squamous cell carcinoma (OSCC) is unknown. This study aimed to investigate the expression of in OSCC, as well as explore its impact on the biological behavior of OSCC and the potential regulatory mechanisms. expression levels in OSCC and normal tissues were examined using the GEO database and the Kaplan-Meier Plotter database was used for survival analysis. Western blotting and quantitative real-time PCR were used to assess expression levels in OSCC tissues and neighboring normal tissues, as well as in oral epithelial cells (HOEC) and OSCC cell lines (CAL27 and SCC15). We found the expression level of was lower in OSCC tissues than in surrounding normal tissues, with higher expression indicating a better prognosis. In vitro assay demonstrated that overexpression of inhibited OSCC cell proliferation, migration, and invasion, resulting in cell cycle arrest at the G1 phase, as well as negatively regulating the PI3K/AKT signaling pathway and inhibiting EMT progression; knockdown had the opposite effect. represents a potential therapeutic target in OSCC treatment. - Source: PubMed
Publication date: 2026/03/17
Zhang SuChen XiLiang ZhuangWang WeiHu Tenglong - - Source: PubMed
Publication date: 2026/02/12
Beyrend-Frizon Guillaume - In the context of liver resection and transplantation, hepatic ischemia-reperfusion injury (hepatic IRI) remains a significant clinical challenge, profoundly impacting both postoperative short- and long-term recovery. A novel cell death pathway, PANoptosis, is implicated in infections, malignancies and sterile inflammation. While the specific role of PANoptosis in the development of hepatic IRI remains unclear, this study aims to provide new insights and perspectives into the underlying mechanisms, thereby addressing this knowledge gap. - Source: PubMed
Publication date: 2025/12/30
Tulahong AlimuXu XinluAbulaiti AimitajiTuergan TalaitiQiao PingpingZhu DalongLiu ChangRuze RexiatiAji TuerganailiShao Yingmei - MicroRNAs (miRNAs) are critical regulators of gene expression in cancer biology and cardiovascular disease. miR-106b-5p, a member of the miR-106b-25 cluster, has been widely studied for its oncogenic activity in various malignancies. However, its role as a direct molecular driver of anthracycline-induced cardiotoxicity has only recently been uncovered. This finding highlights new therapeutic possibilities at the intersection of oncology and cardiovascular medicine. This review outlines the dual role of miR-106b-5p as a key modulator in both tumor progression and chemotherapy-induced cardiac dysfunction. miR-106b-5p is upregulated in numerous cancers-including breast, prostate, lung, gastric, colorectal, hepatocellular, and esophageal-and promotes tumorigenesis via suppression of tumor suppressors such as PTEN, BTG3, p21, and SMAD7, leading to activation of oncogenic pathways like PI3K/AKT and TGF-β. Importantly, we present the first evidence that miR-106b-5p is significantly upregulated in the myocardium in response to doxorubicin treatment, where it drives left ventricular dysfunction by targeting PR55α, a key regulator of PP2A activity. This pathway results in cytoplasmic HDAC4 accumulation, aberrant activation of the YY1 transcription factor, and upregulation of sST2, a biomarker linked to adverse cardiac remodeling and poor prognosis. In response, we developed AM106, a novel locked nucleic acid antagomir that silences miR-106 b-5p. Preclinical studies demonstrate that AM106 restores PR55α/PP2A activity, reduces sST2 expression, and prevents structural and functional cardiac damage without compromising anti-tumor efficacy. In parallel, artificial intelligence (AI) tools could be leveraged in the future-based on established AI applications in miRNA cancer research-to accelerate the identification of miR-106b-5p-related biomarkers and guide personalized therapy selection. Our findings position miR-106b-5p as a previously unrecognized molecular bridge between cancer and doxorubicin-induced cardiotoxicity. The development of the AM106 antagomir represents a promising approach with potential clinical applicability in cardio-oncology, offering dual benefits: tumor control and cardioprotection. Coupling this innovation with AI-driven analysis of patient data may enable precision risk stratification, early intervention, and improved outcomes. miR-106b-5p thus emerges as a central therapeutic target and biomarker candidate for transforming the clinical management of cancer patients at risk for heart failure. - Source: PubMed
Publication date: 2025/10/14
Asensio Lopez Maria Del CarmenRuiz Ballester MiriamBastida Nicolas Francisco JoseSoler Pardo FernandoAlonso-Romero Jose LuisCaro-Martinez CesarPascual Figal DomingoLax Antonio