SFRS6 Blocking Peptide
- Known as:
- SFRS6 Blocking Peptide
- Catalog number:
- 33r-4356
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- SFRS6 Blocking Peptide
Related genes to: SFRS6 Blocking Peptide
- Gene:
- SRSF6 NIH gene
- Name:
- serine and arginine rich splicing factor 6
- Previous symbol:
- SFRS6
- Synonyms:
- SRP55, B52
- Chromosome:
- 20q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-17
- Date modifiied:
- 2016-10-05
Related products to: SFRS6 Blocking Peptide
Related articles to: SFRS6 Blocking Peptide
- The human serine-arginine rich splicing factor 6 (SRSF6) is part of the SR-protein family consisting of 12 members and is involved in (alternative-) splicing regulation. It is composed of an N-terminal RRM domain, followed by a pseudo-RRM and a C-terminal serine/arginine-rich disordered domain. Despite extensive studies on the functions of SRSF6, its determinants for specific RNA-recognition have remained unresolved due to a lack of high-resolution structures based on unambiguous boundaries of individual domains and the involved disordered regions. We here provide the first near-complete NMR backbone and sidechain assignments of human SRFS6 RRM1 and backbone assignments of the pseudo-RRM2 (ΨRRM2), as well as the tandem RRM. The derivable carbon secondary chemical shifts were used to define secondary structure elements as well as exact domain boundaries, showcasing a canonical βαββαβ-fold for either RRM. Consequently, we defined the inter-domain linker with a length of 37 residues. Furthermore, N-relaxation data measured for the single and tandem RRMs indicate that the two RRMs tumble as one entity. However, the minor chemical shift differences between the respective constructs suggest a merely transient interaction with no defined interface between the two RRMs. Lastly, we show that AlphaFold3 models are majorly supported by our solution NMR data, but there are subtle inconsistencies with regard to the formation of the β-strand. In sum, our initial work underlines the role of NMR for visualizing crucial functional details of biology and sets the critical basis for future high-resolution structures of and residue-resolved determinants of specific RNA-recognition by the splicing regulator SRSF6. - Source: PubMed
Publication date: 2026/05/05
von Ehr JulianSchlundt Andreas - Late-onset Alzheimer´s disease (LOAD) is a heterogeneous disorder influenced by complex genetic factors. We previously described (; 27–35 CAG repeats) in the huntingtin () gene as potential modifiers in around 6% of AD population. The caudate nucleus, the most affected region in Huntington’s disease, is highly sensitive to these CAG repeats. We hypothesized that induce gene expression deregulation, including altered microRNA (miRNA) profiles, leading to altered disease progression. - Source: PubMed
Publication date: 2026/04/20
Castilla-Silgado JuanPerez-Oliveira SergioPinto-Hernandez PaolaFernandez-Sanjurjo ManuelCorte-Torres Maria DanielaFernandez-Alvarez OlayaIglesias-Gutierrez EduardoMenendez-Gonzalez ManuelAlvarez VictoriaTomas-Zapico Cristina - There is a need for novel therapies for diabetic retinopathy (DR) because existing therapies treat only certain features of DR and do not work optimally for all patients. While proteomic studies provide insight into disease pathobiology, they are often limited to small sample sizes due to high costs, limiting their generalizability and reproducibility. Moreover, they often yield lists of tens to hundreds of proteins with differential expression, making it difficult to prioritize the most biologically relevant biomarkers beyond using arbitrary fold-change and false-detection rate cutoffs. Here, we applied a two-stage multimodal AI approach: first, we integrated EHR and proteomics data to rationally prioritize candidate protein biomarkers and, next, validated these biomarkers in an independent cohort. These protein biomarkers of DR are rooted in the EHR data and thereby more likely to be biological drivers of disease. - Source: PubMed
Publication date: 2026/02/24
Lin Jonathan BMataraso Samson JChadha MadhumeetaVelez GabrielMruthyunjaya PrithviAghaeepour NimaMahajan Vinit B - 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 - Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. tRNA-derived fragments (tRFs) have been shown to play various roles in HCC tumorigenesis. In the current study, we identified that tRF-Glu-i-0545 (tRF-E), which is derived from an internal region of tRNA-Glu, is a tumor suppressor in HCC. tRF-E was significantly downregulated in HCC samples, and low tRF-E levels were associated with poor prognosis of HCC patients from multiple cohorts. tRF-E sensitized HCC cells to ferroptosis in vitro and in vivo. Mechanistically, tRF-E interrupted binding of VDAC2 to the E3 ligase Nedd4 to block ubiquitination and promote VDAC2 stabilization, which enhanced iron-dependent lipid peroxidation and ultimately triggered ferroptosis. The RNA binding protein SRSF6 cleaved tRNAGluTTC to generate tRF-E, and hypoxia inhibited tRF-E biogenesis by suppressing SRSF6. Specifically, hypoxia-induced alternative splicing of SRSF6 mRNA produced a long transcript containing a poison cassette exon, which led to nonsense-mediated mRNA decay. In conclusion, this study identifies a tumor suppressive tRF that enhances ferroptosis sensitivity in HCC and illustrates the potential of tRFs in cancer treatment. - Source: PubMed
Publication date: 2026/03/26
Han LinyuHuo YanfeiYang YantingZhang LongLi CanHan PengXiaoGong ChenglongZhang NashaYang Ming