Ask about this productRelated genes to: SECISBP2 antibody
- Gene:
- SECISBP2 NIH gene
- Name:
- SECIS binding protein 2
- Previous symbol:
- -
- Synonyms:
- SBP2
- Chromosome:
- 9q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-10
- Date modifiied:
- 2018-07-27
Related products to: SECISBP2 antibody
Related articles to: SECISBP2 antibody
- Myxofibrosarcoma (MFS) is a rare soft-tissue sarcoma with limited systemic therapy options, necessitating preclinical platforms that better simulate clinical drug responses. We investigated how 2D monolayers versus 3D spheroids shape the baseline transcriptome and doxorubicin (DOX)-responsive programs across six patient-derived MFS cell lines. RNA sequencing revealed that 3D culture induces a distinct transcriptomic state characterized by the enrichment of microenvironment-associated stress programs, such as hypoxia, inflammatory/NF-κB signaling, and glycolysis, alongside the suppression of proliferation-related pathways. Although the global DOX-induced transcriptional response was highly environment-dependent, we identified a robust core of six regulators-MCRIP1, FGF12, HGF, EMSY, FZD2, and SECISBP2-whose transcriptional changes consistently correlated with cell survival rates across both 2D and 3D geometries. These genes are involved in transcriptional plasticity, redox homeostasis, and bypass survival signaling, providing a mechanistic basis for DOX resistance that transcends culture conditions. Our findings demonstrate that while culture geometry is a critical determinant of the MFS transcriptome, a robust set of environment-agnostic regulators dictates DOX efficacy. Integrating 3D systems with these specific transcriptomic readouts enhances the interpretability of drug screenings and supports the prioritization of rational therapeutic combinations for this rare sarcoma. - Source: PubMed
Publication date: 2026/04/21
Yoshimatsu YukiShiota YomogiKondo Tadashi - Infected wounds heal considerably slowly among patients with diabetes because of biofilm barriers and immune dysregulation. Therefore, treatment strategies must simultaneously eliminate infection and accelerate healing. In this study, we present a dual-mechanism nanoplatform composed of indocyanine green (ICG)-loaded lentinan (LNT)‑functionalized selenium nanoparticles (ICG@LNT‑SeNPs). This platform disrupts the pathological cycle by integrating near‑infrared‑triggered photothermal eradication of methicillin-resistant Staphylococcus aureus (MRSA) biofilms with selenium‑driven immunometabolic reprogramming of macrophages. The selenium (Se) component facilitates metabolic adaptation and functional remodeling of pro‑inflammatory macrophages by activating the NRF2/HIF‑1α axis, inducing transition into an M2 phenotype, which is characterized by elevated expression of repair‑associated factors (e.g., Il10 and Arg1). ICG@LNT‑SeNPs also enhance the defensive properties of cellular antioxidants by upregulating the expression of Secisbp2 (a key regulator of selenoprotein biosynthesis), Gpx4, and Txnrd2. This combined antibacterial‑metabolic‑immune mechanism causes vascular endothelial cells and fibroblasts to migrate, enhancing subsequent collagen deposition and angiogenesis and, thus, accelerating wound closure. This mechanism demonstrated more mature tissue reconstruction in diabetic mice with MRSA-infected wounds. Overall, the proposed SeNPs-based therapeutic strategy promotes infected diabetic wounds healing through macrophage immunometabolic reprogramming. The findings may help identify new targets and provide insights for developing promising management approaches for chronic wounds. - Source: PubMed
Publication date: 2026/04/17
Chen YangxiaZhong LiZhang ZehangLiu WeiLi ShuoshanXie ZhenmouLi KaixinLi SiqiCai GuiyueLiang XiaoshuangXu LigengZheng JudunChen TianfengChen Rongyi - Host gene expression profiling holds great potential in improving the differential diagnostics of bacterial and viral infections. We investigated its discriminative value in children with suspected serious infections. - Source: PubMed
Publication date: 2026/04/09
Piri RuutValta MillaLempainen JohannaIvaska LauriEzer SiniKere JuhaKatayama ShintaroPeltola Ville - To present the first Korean case of thyroid hormone metabolism defect (THMD) caused by compound heterozygous mutations and to expand our current understanding of its clinical spectrum. - Source: PubMed
Publication date: 2025/11/28
Yang JinaAhn Jung MinJeong Hwal Rim - Selenoproteins contain the selenocysteine (Sec, U), which is essential for redox regulation due to its reactive selenol group. The current set of 25 human selenoproteins was defined by the presence of SECIS elements in the 3' UTR coupled with in-frame UGA codons through a stop codon readthrough mechanism. However, the discovery of novel selenoproteins and SECIS elements remains limited by the constraints of SECIS prediction methods. In this study, we focus on SECISBP2, the core SECIS-binding protein, to analyze its binding RNAs using RNA immunoprecipitation sequencing (RIP-Seq) technology. We constructed the 3S-DB, a database of 1,333 SECISBP2-bound RNAs with potential SECIS functions for UGA recoding, including most known selenoprotein transcripts. Importantly, we validate that the 3' UTRs of PDF and ATP5MJ exhibit SECIS activity using luciferase assays and by fusing them to known selenoprotein RNAs. In summary, our results provide a valuable resource of mRNAs with potential for UGA recoding and previously unrecognized SECIS elements, with the potential to expand the known selenoproteome and advance our understanding of their roles in redox biology and beyond. Furthermore, this work offers new insights into non-canonical stop codon readthrough and the broader mechanisms governing translational regulation of the genetic code. - Source: PubMed
Publication date: 2025/10/25
Si ChenfangZhang LuGao JingNiu KongyanLi YunxiaLiu NanShan BingZhang Yaoyang