SFRS2B Blocking Peptide
- Known as:
- SFRS2B Blocking Peptide
- Catalog number:
- 33r-10221
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- SFRS2B Blocking Peptide
Related genes to: SFRS2B Blocking Peptide
- Gene:
- SRSF8 NIH gene
- Name:
- serine and arginine rich splicing factor 8
- Previous symbol:
- SFRS2B
- Synonyms:
- SRP46
- Chromosome:
- 11q21
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-04
- Date modifiied:
- 2016-06-06
Related products to: SFRS2B Blocking Peptide
Related articles to: SFRS2B Blocking Peptide
- RNA-binding proteins (RBPs) serve essential roles in various cancer types, but their functions in papillary renal cell carcinoma (pRCC) have not been elucidated to date. In our work, differentially expressed RBPs in pRCC were identified after acquisition of RNA-sequencing and clinical data related to pRCC from The Cancer Genome Atlas database(TCGA). Functional enrichment analysis and protein interaction network analysis, along with univariate and multivariate Cox regression analyses, were performed to uncover potential biological effects of the identified RBPs and screen the hub RBPs for pRCC prognosis. We identified 251 up-regulated and 129 down-regulated RBPs, and filtered out seven hub RBPs, namely, SRSF8, CD3EAP, HBS1L, ELAC2, MRPL34, NOP2 and IGF2BP2, for their prognostic relevance. A prognostic risk score model for overall survival of pRCC patients was constructed based on the seven hub RBPs. Further analysis showed that the low-risk group had higher survival rate than the high-risk group in both training and validation cohorts. The predictive accuracy was verified in the Human Protein Atlas database.In addition, we introduced the GSE15641 dataset from the Gene Expression Omnibus (GEO) database for independent external validation, and confirmed the expression levels of HBS1L, MRPL34 and IGF2BP2 through real-time quantitative PCR (RT-qPCR) and Western blotting (WB) using human renal tubular epithelial cell line HK-2 and human papillary renal cell carcinoma cell line Caki-2. In pRCC, CD3EAP was significantly elevated, while ELAC2, IGF2BP2, MRPL34, SRSF8 and HBS1L were significantly reduced. There was no significant difference between tumor and normal tissues in NOP2 expression. Risk score and tumor grade were independent prognostic factors associated with overall survival. In addition, we established a nomogram based on the seven prognostic RBPs to help predict overall survival at 1-3 years. In conclusion, seven differentially expressed hub RBPs were identified as potential prognostic biomarkers for pRCC. Our prognostic model might serve as a support for better treatment decision-making. Our work could provide potential new ideas for diagnosis and research on targeted drugs for pRCC. - Source: PubMed
Publication date: 2026/06/19
Niu TianLi QicongZhang Ao - Recently, an autoantibody signature considered to be predictive of multiple sclerosis (MS) has been reported in an article by Zamecnik et al. published in Nature Medicine, which is characterized by immunoglobulin G (IgG) responses to peptides sharing the amino acid motif P-(SA)-x-(SGA)-R-(SN)-(LRKH). These results are highly important, all the more so as the same motif is present also in two proteins expressed by Epstein-Barr virus (EBV), a pathogen that likely plays a key role in MS pathogenesis. However, clinically relevant autoantibody responses often target conformational epitopes, and peptides often differ from their corresponding proteins in terms of conformation. We were therefore interested in whether these findings can be reproduced at protein level and may thus play a role also in vivo. Here, we report findings from complementary experiments employing a microarray covering nearly 10,000 human full-length proteins and using serum and cerebrospinal fluid samples from patients with a histopathologically confirmed diagnosis of MS. Our data show that prominent IgG responses to full-length proteins bearing the P-(SA)-x-(SGA)-R-(SN)-(LRKH) motif can indeed be found in a substantial proportion of MS patients, although considerable inter-patient variability exists in both the type and number of individual responses. Notably, these IgG responses were more pronounced in patients with histopathologically defined pattern II MS (which is characterized by intralesional IgG and complement deposition) and pattern III MS than in patients with pattern I MS in our study. New motif-bearing candidate antigens identified in this study include RBMY2FP, CHMP2B, SRSF8 (SFRS2B), NUS1 (NgBR, Nogo-B receptor), and RTN2. Further studies investigating the diagnostic, pathophysiological, therapeutic, and prognostic implications of this antibody signature, as well as the potential role of cross-reactivity with EBV-suggested by the presence of the motif of interest in both EBV BRRF2 and EBV envelope glycoprotein M-are warranted and may significantly advance our understanding of MS. - Source: PubMed
Publication date: 2026/04/08
Jarius SRuprecht KMetz IKönig F BHaas JBrück WPaul FWildemann B - Alternative splicing is an important mechanism of transcriptomic and proteomic diversity and is progressively involved in cardiovascular disease (CVD) pathogenesis. Serum response factor (SRF), a critical transcription factor in cardiac development and function, may itself undergo splicing regulation, potentially altering its function in disease states. The objective of this study is to identify SRF-associated alternative splicing events in cardiac pathological conditions and examine regulatory interactions with splicing factors using RNA-seq data. Three human heart RNA-seq databases (PRJNA198165, PRJNA477855, PRJNA678360) were used, comprising various cardiac conditions like non-ischemic cardiomyopathy (NICM), ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), and heart failure with reduced ejection fraction (HFrEF), with and without left ventricular assist device (LVAD) support. Splicing events were identified using the rMATS tool, and correlation analyses were performed between SRF and predicted splicing factors. Functional enrichment of SRF-correlated genes was assessed via Gene Ontology (GO) and KEGG pathways. The skipped exon (SE) events were the predominant splicing type across all datasets. SRF chr6, including (Exon 2, 43,173,847-43,174,113), (Exon 4, 43,176,548-43,176,667), and (Exon 5, 43,178,294-43,178,485), were most frequently involved in SE and mutually exclusive exon (MXE) events across multiple heart failure subtypes. Correlation analysis revealed strong positive associations between SRF and several splicing factors (HNRNPL, HNRNPD, SRSF5, and SRSF8). GO and KEGG analyses revealed enrichment of muscle development, sarcomere structure, lipid metabolism, and immune signaling pathways. Our study shows that SRF is subject to extensive alternative splicing in heart failure, particularly at Exon 2 and Exon 5, suggesting isoform-specific roles in cardiac remodeling. The strong co-expression with specific splicing factors delineates a regulatory axis that may explain the pathological transcriptome in cardiomyopathy. These findings provide a foundation for exploring splicing-based biomarkers and therapeutic targets in cardiac pathology for SRF. - Source: PubMed
Publication date: 2025/08/11
Abdi Sayed Aliul HasanAzhar GoharZhang XiaominSharma ShakshiHafeez MohibWei Jeanne Y - The CLK1 kinase phosphorylates SR proteins to modulate their splicing regulatory activity. Skipping of alternative exon 4 on the pre-mRNA produces a CLK1 variant lacking the catalytic site. Here, we aimed to understand how various SR proteins integrate into the regulatory program that controls exon 4 splicing. Previously, we observed that the depletion of SRSF10 promoted the inclusion of exon 4. Using the expression of tagged proteins and CRISPR/Cas9-mediated knockouts in HCT116 cells, we now identify TRA2β, TRA2α, SRSF4, SRSF5, SRSF7, SRSF8, and SRSF9 as activators of exon 4 inclusion. In contrast, SRSF3, SRSF10, and SRSF12 elicit exon 4 skipping. Using CRISPR/dCas13Rx and RNA immunoprecipitation assays, we map an enhancer in exon 4 interacting with TRA2β. Notably, CLK1 kinase inhibitors antagonized the repressor activity of HA-SRSF10, HA-SRSF12, and HA-SRSF3. Our results suggest that exon 4 inclusion is determined primarily by a balance between the activities of TRA2 proteins and CLK-phosphorylated SRSF3. CLK-phosphorylated SRSF10 and SRSF12 would interact with TRA2 proteins to prevent their enhancer activity, allowing SRSF3 to enforce exon 4 skipping more efficiently. Our study provides insight into the complex regulatory network controlling the alternative splicing of , which uses CLK1-mediated phosphorylation of SR proteins to regulate the inclusion of catalytic exon 4 in transcripts. - Source: PubMed
Publication date: 2024/11/18
Shkreta LulzimDelannoy AurélieToutant JohanneChabot Benoit - Recent evidence suggests that splicing factors (SFs) and alternative splicing (AS) play important roles in cancer progression. We constructed four SF-risk-models using 12 survival-related SFs. In Luminal-A, Luminal-B, Her-2, and Basal-Like BRCA, SF-risk-models for three genes (, , and ), four genes (, , , and ), three genes (, , and ), and three genes (, , and ) were constructed. These models have a promising prognosis-predicting power. The co-expression and protein-protein interaction analysis suggest that the 12 SFs are highly functional-connected. Pathway analysis and gene set enrichment analysis suggests that the functional role of the selected 12 SFs is highly context-dependent among different BRCA subtypes. We further constructed four AS-risk-models with good prognosis predicting ability in four BRCA subtypes by integrating the four SF-risk-models and 21 survival-related AS-events. This study proposed that SFs and ASs were potential multidimensional biomarkers for the diagnosis, prognosis, and treatment of BRCA. - Source: PubMed
Publication date: 2021/09/24
Zhang HeHan BaoaiHan XingxingZhu YuyingLiu HuiWang ZhiyongCui YanfenTian RanGao ZicongTian RuinanRen SixinZuo XiaoyanTian JianfeiZhang FeiNiu Ruifang