SNRPB

Last update 23 Jan 2025

Basic Info

Synonyms

COD, Sm protein B/B', Sm-B/B'

+ [7]

Introduction

Plays a role in pre-mRNA splicing as a core component of the spliceosomal U1, U2, U4 and U5 small nuclear ribonucleoproteins (snRNPs), the building blocks of the spliceosome (PubMed:11991638, PubMed:18984161, PubMed:19325628, PubMed:25555158, PubMed:26912367, PubMed:28502770, PubMed:28781166, PubMed:28076346). Component of both the pre-catalytic spliceosome B complex and activated spliceosome C complexes (PubMed:11991638, PubMed:28502770, PubMed:28781166, PubMed:28076346). As a component of the minor spliceosome, involved in the splicing of U12-type introns in pre-mRNAs (PubMed:15146077). As part of the U7 snRNP it is involved in histone pre-mRNA 3'-end processing (PubMed:12975319).

100 Clinical Results associated with SNRPB

100 Translational Medicine associated with SNRPB

0 Patents (Medical) associated with SNRPB

327

Literatures (Medical) associated with SNRPB

01 Jan 2025·Annals of the Rheumatic Diseases

Evidence that autoantibody production may be driven by acute Epstein-Barr virus infection in Sjögren's disease

Article

Author: Chu, Elizabeth K ; Fritzler, Marvin J ; Cha, Seunghee ; Yang, Lijun ; Stalvey, Carolyn ; Sebastian, Mathew ; Betancourt, Blas Y ; Hudson, Erin ; Han, Shuhong ; Chan, Edward K L ; Bhattacharyya, Indraneel ; Reeves, Westley H ; Zhuang, Haoyang ; Arja, Rawad Daniel

ObjectivesSjögren’s disease (SD) is an autoimmune disease affecting the exocrine glands that is associated with autoantibodies against Ro60/SS-A, anti-Ro52/TRIM21, La/SS-B and others. We examined the role of acute Epstein-Barr virus (EBV) infection in the pathogenesis of these autoantibodies in a previously healthy patient (patient 1) with primary EBV infection who developed SD with anti-Ro/La and anti-Smith/U1 ribonucleoprotein (Sm/U1RNP) autoantibodies and had lymphoplasmacytic foci on labial salivary gland biopsy.MethodsImmune responses to Epstein-Barr nuclear antigen-1 (EBNA1) and the Ro52/Ro60/La and Sm/U1RNP autoantigens and peptides were examined by immunoassay in patient 1, healthy and disease controls.ResultsAnti-Ro52 and anti-Ro60 autoantibodies were present 7 days after primary infection and underwent IgM to IgG switching, suggesting that EBV infection promoted their production. More than 7 months after primary infection, new and increasing levels of antibodies against EBNA1 and the U1RNP autoantigen appeared concomitantly. These antibodies bound homologous peptide sequences shared by EBNA1, SmB′ and the U1-C (U1RNP) protein, consistent with induction by molecular mimicry. Although Ro60 and EBNA1 crossreact immunologically, we found that anti-Ro60/anti-Ro52 antibody production was stimulated by acute EBV infection long before the onset of anti-EBNA1. Unexpectedly, a subset of healthy control sera had anti-SmB′ peptide antibodies that were not correlated with anti-EBNA1 peptide antibodies. In contrast, anti-SmB′ and EBNA1 peptide antibody levels correlated in anti-Sm/U1RNP+lupus sera.ConclusionsPrimary EBV infection can promote anti-Ro60/anti-Ro52 and anti-U1RNP responses, though by different mechanisms. Some healthy individuals produce anti-SmB′ peptide autoantibodies independently of a response to EBNA1.

31 Dec 2024·Annals of Medicine

SNRPB and CEP290, predicting the prognosis of diffuse large B cell lymphoma and associated with tumour immune microenvironment

Article

Author: Wang, Ying ; Xie, Wen-Lin ; Tang, Jing ; Bin, Ting ; Lin, Chao ; Xu, Xiao-Jun ; Lu, Bo

BACKGROUNDDiffuse large B-cell lymphoma (DLBCL), the most prevalent type of non-Hodgkin's lymphoma, exhibits significant correlations with efferocytosis-related molecules (ERMs) concerning invasion, metastasis, and clinical outcomes. This study aims to establish an efferocytosis-related gene signature specifically linked to DLBCL.METHODSKey module genes linked to DLBCL were identified via weighted gene co-expression network analysis (WGCNA) in GSE32018. Univariate Cox analysis of GSE31312 revealed ERMs associated with DLBCL survival. Differential expression analysis identified differentially expressed genes (DEGs) between DLBCL subtypes and normal samples. Venn diagram analysis identified common DEGs and key module genes. A DLBCL gene signature was built by using univariate Cox and least absolute shrinkage and selection operator (LASSO) analysis. Gene functional enrichment, immune microenvironment, and immunotherapy analyses compared two risk subgroups. Prognostic gene expression was validated at the single-cell level.RESULTSIn the GSE32018 dataset, 1760 key module genes related to DLBCL were identified. Using GSE31312, 14 ERMs associated with DLBCL prognosis were determined.Then, an ERMs-related prognostic signature, including small nuclear ribonucleoprotein polypeptides B (SNRPB) and centrosomal protein 290 (CEP290), was established. Independent prognostic analysis showed that the RiskScore derived from this signature was a prognostic factor. Significant immune microenvironment differences were observed between two risk subgroups. Additionally, chemotherapeutic drug sensitivity results indicated the signature could predict therapeutic response. Eventually, expression of SNRPB and CEP290 was confirmed in B cells.CONCLUSIONThe prognostic signature comprised of SNRPB and CEP290 based on ERMs-DEGs was established, providing a theoretical basis and reference value for DLBCL research.

01 Dec 2024·International Immunopharmacology

Prognostic significance of immune evasion-related genes in clear cell renal cell carcinoma immunotherapy

Article

Author: Chen, Junlin ; Zhang, Zhiling ; Dong, Pei ; Guo, Shengjie ; Zhong, Weifeng ; Peng, Yulu ; Huang, Tingxuan ; He, Liru ; Liu, Ruiqi ; Han, Hui ; Wei, Wensu ; Liu, Yang ; Zhou, Fangjian ; Ma, Binglei

Clear cell renal cell carcinoma (ccRCC) represents a prevalent malignancy of the urinary system. Despite the integration of immune checkpoint inhibitors (ICIs) into the treatment paradigm for advanced RCC, resistance to immunotherapy has emerged as a pivotal determinant impacting the clinical outlook of ccRCC. Accumulating evidence underscores the pivotal role of immune evasion-related genes and pathways in enabling tumor escape from host immune surveillance, consequently influencing patients' responsiveness to immunotherapy. Nonetheless, the clinical relevance of immune evasion-related genes in ccRCC patients undergoing immunotherapy remains inadequately understood. In this study, we aggregated RNA sequencing and clinical data from ccRCC patients across three cohorts: the Cancer Genome Atlas (TCGA), CheckMate cohorts, and the JAVELIN Renal 101 trial. Leveraging a curated immune evasion-related gene set from Lawson et al., we employed the LASSO algorithm and Cox regression analysis to identify eight genes (LPAR6, RGS5, NFYC, PCDH17, CENPW, CNOT8, FOXO3, SNRPB) significantly associated with immune therapy prognosis (HR, 3.57; 95 % CI, 2.38-5.35; P<0.001). A predictive algorithm developed utilizing these genes exhibited notable accuracy in forecasting patients' progression-free survival in the training set (AUC, 0.835). Furthermore, stratification of patients by risk score revealed discernible differences in immunotherapy response and tumor microenvironment. In summary, we present a prognostic model intricately linked with immune status and treatment response. For ccRCC patients undergoing immunotherapy, this approach holds promise in aiding clinical decision-making by providing more precise and tailored treatment recommendations.

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