SFRS11 Blocking Peptide
- Known as:
- SFRS11 Blocking Peptide
- Catalog number:
- 33r-4478
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- SFRS11 Blocking Peptide
Related genes to: SFRS11 Blocking Peptide
- Gene:
- SRSF11 NIH gene
- Name:
- serine and arginine rich splicing factor 11
- Previous symbol:
- SFRS11
- Synonyms:
- p54, NET2
- Chromosome:
- 1p31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-09
- Date modifiied:
- 2016-06-06
Related products to: SFRS11 Blocking Peptide
Related articles to: SFRS11 Blocking Peptide
- Diffuse large B-cell lymphoma (DLBCL) remains a challenging disease with limited therapeutic options beyond standard immunochemotherapy. ETS transcription factors, including SPIB and SPI1, are implicated in lymphoma pathogenesis and can be targeted by the small molecule TK216, which disrupts ETS-DHX9 interactions. To explore mechanisms of resistance, we generated stable TK216-resistant clones from the ABC-DLBCL line U2932. Resistant clones exhibited a 4-5-fold increase in IC values and lost the ability to undergo G2-M arrest upon treatment. Transcriptomic and mutational analyses revealed three resistance patterns: (i) MDR1/ABCB1 overexpression, leading to multidrug efflux; (ii) Cluster A, enriched for proliferation, Wnt, and transcriptional programs, with mutations in ESR2, USP24, and SFSWAP; and (iii) Cluster B, characterized by actin/microtubule remodeling, altered metabolism, and mutations in SRSF11 and PATJ. Pharmacologic screening revealed an increased sensitivity of resistant cells to BCL2, MCL1, and XPO1 inhibitors, while also showing reduced sensitivity to aurora kinase and microtubule-targeting agents. Venetoclax and selinexor retained activity in resistant models, supporting their potential for rational combinations with TK216. These findings demonstrate that multiple, heterogeneous mechanisms drive resistance to ETS inhibition in DLBCL, highlighting therapeutic strategies to overcome it. - Source: PubMed
Spriano FilippoCascione LucianoTarantelli ChiaraSartori GiulioArribas Alberto JVelasova AdrianaNapoli SaraHavranek OndrejToretsky Jeffrey ABertoni Francesco - Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths worldwide, and its occurrence and development are closely related to complex molecular mechanisms. Alternative splicing of precursor mRNA is a key step in gene expression regulation, and its dysregulation is common in tumors. The serine/arginine-rich splicing factor (SRSF) family, a core protein family in splicing regulation, has been confirmed to play oncogenic roles in various cancers. However, systematic research on the SRSF family in NSCLC remains insufficient. This study aims to systematically analyze the specific expression patterns, clinical prognostic value, collaborative mechanisms and potential biological functions of SRSF individual members in NSCLC by the combination of bioinformatics analysis and experimental verification. - Source: PubMed
Tu ShuqiChen YuhaoZhang YalongChen QiangFan YaguangWang YixuanZhang YangLi SinuoChen JunPan HongliZhou XuexiaLi Xuebing - Serine/arginine-rich splicing factor 11 (SRSF11) is an RNA-binding regulator that modulates alternative splicing and RNA metabolism in a context-dependent manner across selected malignancies. Evidence from colorectal, hepatocellular, gastric, glioma, and a few other cancers indicates that SRSF11 participates in cell-cycle regulation, telomerase recruitment, and epithelial-mesenchymal transition (EMT) through specific signaling axes, including PAK5-SRSF11-HSPA12A in colorectal cancer, METTL3-SRSF11 in gastric and breast cancers, and SRSF11-CDK1/telomerase circuits in hepatocellular carcinoma. These mechanisms highlight SRSF11 as a candidate biomarker for diagnosis and prognosis rather than a universal oncogenic driver. We summarize the current mechanistic, post-translational, and non-coding RNA-mediated regulatory evidence, clarify the limitations of existing data, and propose future multi-omics and functional approaches to validate SRSF11-directed splicing therapy. This review integrates mechanistic insight with clinical evidence while emphasizing cancer-specific rather than generalized conclusions. - Source: PubMed
Publication date: 2026/01/14
Jun YangShanshan LiuJingwen XiaoYu HeJianlong XiaoQingfeng Shi - Deep vein thrombosis (DVT) is a vascular complication with a high incidence after trauma and surgery, and its pathogenesis is closely related to vascular endothelial dysfunction. Recent studies have found that M1 macrophage polarization participates in thrombosis through exosome-mediated miRNA delivery, but the specific mechanism has not yet been clarified. This study focuses on the regulatory role of miR-126-5p in M1 macrophage exosomes and its downstream splicing factor SRSF11 in endothelial senescence and DVT. - Source: PubMed
Publication date: 2025/12/03
Guo PeiyuDu KailiXiao YuZhou ZiranWang BingLou Zhen Kai - Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by deficits in social communication and repetitive behaviours with an aetiology involving genetic and environmental risk factors. Placental alterations, such as epigenetic DNA methylation and structural abnormalities, have been associated with ASD. Circular RNA (circRNA), covalently closed and highly stable molecules, play an epigenetic role by sequestering microRNA (miRNA) and modulating messenger RNA (mRNA) translation, forming posttranscriptional networks essential for gene expression. However, there is a lack of evidence in the literature regarding the involvement of circRNA, the placenta and ASD. To address this gap, the study aimed to map the interactions among circRNA, miRNA and mRNA, investigating their relevance to ASD and placental development using bioinformatics tools, such as circATLAS and miRTargetLink 2.0. The analysis identified 71 circRNA linked to ASD and 30 highly expressed in the placenta, which regulate pathways such as 'immune response,' 'gene transcription,' and 'replication,' and others previously associated with ASD, such as 'Notch and AKT signalling pathway'. Searches in the SFARI database revealed 11 relevant genes in the ASD group, nine in the placenta group and five shared genes (SRSF11, PSMD11, NOTCH1, CREBBP and TBL1X). Further analysis identified the interaction of the circRNA hsa-MAN1A2_0008 with miRNA associated with these genes. These findings suggest that highly expressed circRNA in the placenta regulate critical pathways for placental development and ASD aetiology, underscoring their role in linking placental alterations to ASD. - Source: PubMed
Braz-Barbosa BrayanGottfried CarmemSantos-Terra Júlio