Ask about this productRelated genes to: SNRPA antibody
- Gene:
- SNRPA NIH gene
- Name:
- small nuclear ribonucleoprotein polypeptide A
- Previous symbol:
- -
- Synonyms:
- U1A, U1-A, Mud1
- Chromosome:
- 19q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2014-11-19
Related products to: SNRPA antibody
Related articles to: SNRPA antibody
- Small Nuclear Ribonucleoprotein Polypeptide A (SNRPA), an RNA-binding protein associated with HCC survival, emerges as a key regulator requiring mechanistic study. - Source: PubMed
Publication date: 2026/05/01
Chang QingyaoWang YidiXu Jun - Type 2 inflammatory diseases (T2IDs) often coexist, but their shared genetic basis remains unclear. This study explores common genetic basis between asthma and other T2IDs and identifies pleiotropic loci and mechanisms. - Source: PubMed
Publication date: 2026/05/17
Chen Xing-RuLiu Chun-Tao - Lactate in the tumor microenvironment (TME) is typically generated by cells exhibiting high glycolytic flux, exemplified by tumor cells. However, in glycolysis-low malignancies such as prostate cancer, stroma-derived lactate may drive noncanonical signaling and functions that remain unclear. Here, we identified APCDD1 cancer-associated fibroblasts (CAFs) as a distinct stromal population that secretes lactate into the TME in response to androgen deprivation therapy (ADT). Lactate uptake by prostate cancer cells induces androgen receptor variant 7 expression, thereby conferring resistance to ADT. Mechanistically, lactate-induced lactylation of the spliceosome component SNRPA at Lys (K123) enhances its recognition of cis-acting elements, increases chromatin binding, and promotes androgen receptor splicing. Targeting lactate transport with monocarboxylate transporter inhibitors effectively restores ADT sensitivity. These findings reveal a metabolic-epigenetic axis linking lactate in the microenvironment to alternative splicing regulation and suggest a promising therapeutic strategy to overcome ADT resistance. - Source: PubMed
Publication date: 2026/01/16
Zhao DiweiMo ZijunZhang TianyouCai XinyangYang ZhenyuChen DongZhao JunliangLi YuanweiZhou FangjianLi ZhenLi YonghongWang Jun - The steady-state abundance of mRNA is governed by the interplay between transcription and degradation, yet the contribution of RNA stability to cancer biology remains incompletely understood. Here, we systematically investigate RNA decay dynamics across 22 cancer types using RNA-seq data from the Cancer Cell Line Encyclopedia. By inferring transcriptome-wide RNA stability profiles, we identify distinct molecular subtypes defined by post-transcriptional regulation. Integrative analyses reveal that RNA-binding proteins (RBPs) and microRNAs (miRNAs), including SNRPA and RBMX, act as key modulators of RNA stability and are essential for cancer cell proliferation and survival. Somatic mutations, particularly those affecting miRNA binding sites, were found to significantly perturb RNA decay, implicating dysregulation of pathways such as nonsense-mediated decay. Furthermore, machine learning models demonstrate that RNA stability profiles predict sensitivity to 24 anticancer drugs, nominating specific RBPs as candidate biomarkers for therapeutic response. Collectively, our findings establish RNA stability as a pivotal layer of gene regulation in cancer, with broad implications for molecular stratification and precision oncology. - Source: PubMed
Publication date: 2025/12/08
Tong YangWang YutingLiu GeruiWei YihuYang XiaoxiaoYuan JiapeiYang YangZhang Qiang - Identifying novel molecular targets for castration-resistant prostate cancer (CRPC) is crucial. This study examines the expression and functional role of small nuclear ribonucleoprotein polypeptide A (SNRPA), a core component of the U1 snRNP complex, in CRPC. Bioinformatics analyses indicate a positive correlation between SNRPA overexpression and the aggressiveness of prostate cancer, with high levels linked to poor outcomes. Single-cell RNA data further shows increased SNRPA expression in prostate cancer cells. Expression of SNRPA is also elevated in both locally-treated CRPC tissues and various CRPC cells. Knockdown via shRNA or knockout using CRISPR/Cas9 significantly reduced cellular proliferation, migration, and invasion in CRPC cells, while inducing apoptosis. SNRPA depletion decreased complex I activity, ATP production, and mitochondrial membrane potential, increased reactive oxygen species levels, and downregulated NDUFB8/NDUFS9 expression. In contrast, SNRPA overexpression enhanced the aggressive phenotype of CRPC cells, boosting mitochondrial complex I activity and ATP generation, while upregulating NDUFB8/NDUFS9. In vivo studies using xenograft models further validated the therapeutic potential of targeting SNRPA. SNRPA knockdown significantly inhibited CRPC xenograft growth, reduced ATP levels, and altered redox balance, as evidenced by decreased glutathione/glutathione disulfide ratio and increased lipid peroxidation. These effects were accompanied by decreased proliferation, increased apoptosis and downregulated NDUFB8/NDUFS9. Our findings collectively suggest that SNRPA plays a crucial role in driving CRPC progression and represents a promising therapeutic target. - Source: PubMed
Publication date: 2025/12/07
Liu Xiao-LongJin LuYang Yong-QiangLu Mei-HuaXue Bo-Xin