Ask about this productRelated genes to: SNRPA1 Blocking Peptide
- Gene:
- SNRPA1 NIH gene
- Name:
- small nuclear ribonucleoprotein polypeptide A'
- Previous symbol:
- -
- Synonyms:
- Lea1, U2A'
- Chromosome:
- 15q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-11-28
- Date modifiied:
- 2018-02-02
Related products to: SNRPA1 Blocking Peptide
Related articles to: SNRPA1 Blocking Peptide
- Ovarian cancer (OC) remains the most lethal gynecological malignancy, with profound tumor microenvironment (TME) heterogeneity contributing to the suboptimal clinical response to immune checkpoint inhibitors (ICIs). Therefore, delineating the metabolic heterogeneity of T cells within the TME is imperative for identifying precise prognostic biomarkers and refining individualized immunotherapeutic strategies. - Source: PubMed
Publication date: 2026/04/24
Tian HuadongLiu XiaotongWang GuojiaoWang ZimoLuo Yuexi - Programmed cell death (PCD) encompasses multiple regulated processes whose dysregulation shapes cancer fitness, yet current computational studies largely use known PCD genes for prognosis rather than discovering regulators. We developed xNNPCD, an interpretable neural-network framework that links CRISPR-Cas9 perturbation signatures from CMap to gene dependency profiles from DepMap. The model constrains hidden neurons to five PCD pathways and iteratively refines a prior gene-pathway mask matrix derived from GO, KEGG, and Reactome using pathway-neuron ablation. This converts binary gene-pathway relationships into continuous-valued associations and improves dependency prediction over random forests, standard fully connected multi-layer perceptron, and its own non-iterative variant. The learned matrix recovers annotated death regulators and nominates candidate regulators, including , and ; combined with dependency scores, it further separates pathway coupling from regulatory direction. Transferring the refined relationship matrix and learned weights to compound-induced perturbation data enables drug screening, identifying BRD-K19103580 and decitabine as targeted therapeutic agents for apoptosis and ferroptosis, respectively. The pathway-resolved drug profiles can facilitate the rational design of combination therapies targeting complementary PCD pathways to overcome single-pathway resistance. Overall, xNNPCD offers a generalizable, interpretable approach for mapping the regulatory landscape and elucidating the molecular processes of PCD in cancer. - Source: PubMed
Publication date: 2026/05/13
Yin QingyangChen Liang - Acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is a major challenge in the treatment of lung adenocarcinoma (LUAD). Our previous study demonstrated that EGFR signaling activates calcium/calmodulin-dependent protein kinase 2 (CAMK2). However, the relationship between this mechanism and TKI resistance has not been fully elucidated. - Source: PubMed
Publication date: 2026/05/18
Li LingmeiRen DanyangWang YutianZhang JiaojiaoYan ChenhuiQu TongyuanHe RuiminZhang WenshuaiLi WanghaoFeng NingruiWang YaleiGuo YuhongQi LishaCao LuGuo QianruZhao QiangYe ZhaoxiangCao Wenfeng - Hexavalent chromium [Cr(VI)] is a common occupational and environmental toxicant and an established carcinogen causing lung cancer in humans. The mechanism through which Cr(VI) exposure causes lung cancer remains to be clearly defined. No effective strategies are currently available to prevent lung cancer resulting from chronic Cr(VI) exposure. Kava is traditionally consumed by South Pacific Islanders to reduce anxiety. Epidemiology and experimental studies suggest that kava has anticancer potential and may be used as a preventive agent to reduce the risk of various cancers including lung cancer. The purpose of this study is to determine the effect of AB-Free Kava and its active component dihydromethysticin (DHM) on chronic Cr(VI) exposure-induced cell malignant transformation and the underlying mechanism. The study was performed by pretreating immortalized but nontumorigenic human bronchial epithelial cells (BEAS-2B) with AB-Free Kava (25 μg/mL) or DHM (10 μM) followed by exposing cells to 0.25 μM Cr(VI) (KCrO) for 20 weeks to determine the impact of AB-Free Kava or DHM on chronic Cr(VI) exposure-induced cell transformation, cancer stem cell (CSC)-like properties, and tumorigenesis. The extent of cell transformation was evaluated by soft agar colony formation assays, Western blot analysis of cancer stemness marker expression levels, and nude mouse xenograft tumorigenesis assays. It was found that AB-Free Kava or DHM pretreatment significantly reduces Cr(VI)-induced cell transformation, CSC-like properties, and tumorigenesis. Mechanistically, it was determined that AB-Free Kava or DHM impairs Cr(VI)-induced cell transformation by down-regulating RNA splicing factor small nuclear ribonucleoprotein polypeptide A' (SNRPA1) expression to reduce the protooncogene, cancer stemness marker, and driver c-MYC expression. It was further determined that DHM and SNRPA1 regulate c-MYC expression through affecting c-MYC protein stability. It was concluded that AB-Free Kava or DHM inhibits Cr(VI)-induced cell transformation, CSC-like properties, and tumorigenesis by down-regulating RNA splicing factor SNRPA1 expression to increase the protooncogene c-MYC protein degradation. - Source: PubMed
Publication date: 2026/05/14
Li EmilyBian TengfeiFinkelberrg MatthewLiu ZulongBi ZhuoyueCarlson DavidXing ChengguoYang ChengfengWang Zhishan - The Solute carrier family 25 member 3 (SLC25A3), a mitochondrial solute carrier protein, has been implicated in tumor progression. Nonetheless, the connection between SLC25A3 and hepatocellular carcinoma (HCC) remains ambiguous. - Source: PubMed
Publication date: 2026/01/24
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