monoclonal apoptotic cleavage product of human U1-70K protein antibody
- Known as:
- mab apoptotic cleavage reagent H. sapiens U1-70K protein (anti-)
- Catalog number:
- MQR 2.201
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- ModiQuest
- Gene target:
- monoclonal apoptotic cleavage product human U1-70K protein antibody
Related products to: monoclonal apoptotic cleavage product of human U1-70K protein antibody
Related articles to: monoclonal apoptotic cleavage product of human U1-70K protein antibody
- Lung cancer (LC) is the most common malignancy and the leading cause of cancer death. LC-derived exosomes have been found to play a critical role in tumor initiation, progression, metastasis and drug resistance. Therefore, the objective of this study is to identify prognostic markers based on lung cancer-derived exosomes in patients with different subtypes of lung cancer, including small cell lung cancer (SCLC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large cell carcinoma (LCC). Additionally, we aim to develop corresponding prognostic models to predict the outcomes of these patients. In this study, the mRNAs information about LC-derived exosomes was collected from Vesiclependia database, and the mRNAs data of LCC, LUAD, LUSC and LCC tumors and paracancerous tissues was obtained from the GEO database and UCSC database. The prognostic models based on exosomes-related differential expression genes (ExoDEGs) by univariate Cox, LASSO, and multivariate Cox regression analyses. The independent prognostic value of the risk model was systematically analyzed. A LUAD prognostic risk model of 12 ExoDEGs (CDH17, DAAM2, FKBP3, FLNC, GSTM2, PGAM4, HPCAL1, FERMT2, LYPD1, SNRNP70, KIR3DL2 and GPX3) and a LUSC prognostic risk model of 7 ExoDEGs (FGA, ERH, HID1, CSNK2A1, SLC7A5, ACOT7 and FUNDC1) were constructed. Kaplan-Meier curve, ROC curve and stratification survival analysis confirmed that the LUAD and LUSC risk models both possessed reliable predictive value for the prognosis of LUAD and LUSC patients. The expression level of ExoDEGs for building the LUAD and LUSC risk models is significantly correlated with immunosuppressive activity of patients, and the immunosuppressive activity is lower in the high-risk groups. We established a LUAD prognostic model with 12 ExoDEGs and a LUSC prognostic model with 7 ExoDEGs, which can be used as independent prognostic indicators for patients LUAD and LUSC. The identified ExoDEGs have the potential to be as prognostic markers and may also serve as novel candidate targets for the treatment of LUAD and LUSC. - Source: PubMed
Publication date: 2025/04/03
Zhang YongxiangChen FengCao YuqiZhang HaoZhao LinglingXu Yijun - Hepatitis C is a contagious disease caused by infection with the hepatitis C virus (HCV) through blood and mother-to-child routes. This study intends to characterize the serum molecular features of hepatitis C using proteomics and transcriptomics. - Source: PubMed
Publication date: 2025/03/13
Wang JianqiongXia AndongTang MinYang ShengjunShen YandiDao JinhuaTao RuiYue Wei - Osteosarcoma (OS) is the most common malignant bone tumor, characterized by a high propensity for metastasis. Recent studies have highlighted the role of alternative splicing in cancer metastasis, although the precise mechanisms underlying aberrant splicing in OS invasion and metastasis remain unclear. Here, we analyzed consistently differentially expressed genes and differentially alternative splicing events between primary and metastatic OS to identify potential genes associated with OS progression. U1 small nuclear ribonucleoprotein 70K (SNRNP70) emerged as both differentially expressed and spliced, with elevated SNRNP70 levels correlating with poor prognosis in pateints with OS. Functional experiments demonstrated that SNRNP70 overexpression enhanced the proliferation and metastasis of OS cells in vitro, while its depletion reduced these capabilities in vivo. Mechanistically, SNRNP70 directly interacted with CD55, modulating its alternative splicing and promoting tumor progression in OS. Additionally, metastatic OS samples exhibited increased infiltration of resting immune cells, and single-cell RNA sequencing revealed communication between SNRNP70-expressing osteoblastic cells and macrophages via the ADGRE5/CD55 signaling pathway. Overall, our results showed that SNRNP70 knockdown inhibited OS progression, which was associated with the splicing of CD55, indicating SNRNP70 as a promising target for OS treatment. - Source: PubMed
Publication date: 2024/12/20
Li WenyueWang LinzhuTian WenJi WeihangBing DanyangWang YanXu BingqianFeng JiayueZhang PengLiang HaihaiGu YunyanYang Baofeng - Osteoarthritis affects millions worldwide, yet effective treatments remain elusive due to poorly understood molecular mechanisms. While genome-wide association studies (GWAS) have identified over 100 OA-associated loci, identifying the genes impacted at each locus remains challenging. Several studies have mapped expression quantitative trait loci (eQTL) in chondrocytes and colocalized them with OA GWAS variants to identify putative OA risk genes; however, the degree to which genetic variants influence OA risk via alternative splicing has not been explored. We investigated the role of alternative splicing in OA pathogenesis using RNA-seq data from 101 human chondrocyte samples treated with PBS (control) or fibronectin fragment (FN-f), an OA trigger. We identified 590 differentially spliced genes between conditions, with FN-f inducing splicing events similar to those in primary OA tissue. We used CRISPR/Cas9 to mimic an SNRNP70 splicing event observed in OA and FN-f-treated chondrocytes and found that it induced an OA-like expression pattern. Integration with genotyping data revealed 7,188 splicing quantitative trait loci (sQTL) affecting 3,056 genes. While many sQTLs were shared, we identified 738 and 343 condition-specific sQTLs for control and FN-f, respectively. We identified 15 RNA binding proteins whose binding sites were enriched at sQTL splice junctions and found that expression of those RNA binding proteins correlated with exon inclusion. Colocalization with OA GWAS identified 6 putative risk genes, including a novel candidate, PBRM1. Our study highlights the significant impact of alternative splicing in OA and provides potential therapeutic targets for future research. - Source: PubMed
Publication date: 2024/11/12
Byun SeyounCoryell PhilipKramer NicoleD'Costa SusanThulson ElizaShine JacquelineParkus SylvieChubinskaya SusanLoeser Richard FDiekman Brian OPhanstiel Douglas H - SAP18 protein was originally discovered in association with the SIN3 transcriptional repressor complex. Subsequent biochemical fractionation studies identified SAP18 as a component of another distinct trimeric complex termed as the apoptosis- and splicing-associated protein (ASAP) complex. The existence of SAP18 in distinct complexes highlights its dual role in transcriptional and splicing regulation. In our study, we aim to define the in vivo interactome of SAP18 using proximity-dependent biotin identification (BioID). Mass spectrometry analysis of streptavidin-purified biotinylated proteins revealed new SIN3-associated interactors, including RBBP4 and SAP30BP. Notably, we identified 72 spliceosomal proteins as highly enriched interactors. Additionally, a complementary immunoprecipitation assay validated novel interactions of SAP18 with the prespliceosomal components SNRNP70, SNRPA, SF3B1, U2AF1, and the SR protein SRSF1. Mutational analysis using a C-terminal SAP18 double point mutant, which is known to be deficient in ASAP-interaction, demonstrated a debilitated interaction with the prespliceosomal proteins. Altogether, our results present a refined understanding of the SAP18 interactome, uncovering its association with the prespliceosome in conjugation with ASAP components. - Source: PubMed
Publication date: 2024/11/01
Kumari SwetaAdhikary AnkitaSingh Kusum Kumari