Ask about this productRelated genes to: SLFN12 antibody
- Gene:
- SLFN12 NIH gene
- Name:
- schlafen family member 12
- Previous symbol:
- -
- Synonyms:
- FLJ10260
- Chromosome:
- 17q12
- Locus Type:
- gene with protein product
- Date approved:
- 2006-04-05
- Date modifiied:
- 2019-03-19
Related products to: SLFN12 antibody
Related articles to: SLFN12 antibody
- PDE3A is a key member of the cyclic nucleotide phosphodiesterase family. By modulating intracellular cAMP and cGMP levels, it participates in diverse physiological processes such as platelet activation, cardiac function, oocyte maturation, and vascular smooth muscle cell proliferation. Recent studies have revealed that PDE3A also plays critical roles in multiple malignant tumors. This study aims to investigate the regulation of PDE3A expression, its role in cancer, and its potential as a therapeutic target, with a particular focus on its impact on tumor cell proliferation, metastasis, and resistance to chemotherapy. - Source: PubMed
Publication date: 2026/02/05
Pu ShengyuZhang QiheMiao MiChen BohongXu JiaruiLei JingyiTang XiaojiangHao Na - We examined the role of SLFN12, a member of the Schlafen (SLFN) family of interferon-regulated genes and proteins in leukemogenesis, and its potential as a therapeutic target in acute myeloid leukemia (AML). We explored the effects of velcrins, a class of small molecules able to modulate SLFN12 biological activity, on AML cells. Velcrin treatment of AML cells stabilized SLFN12 and promoted SLFN12 complex formation with phosphodiesterase 3A or phosphodiesterase 3B. Such effects were associated with growth-inhibitory and proapoptotic responses, as well as potent suppressive effects on leukemic cell growth. In addition, velcrin treatment suppressed clonogenic capacity of primitive leukemic progenitors and significantly extended survival in a mouse AML xenograft model. Taken together, these findings establish an important role of SLFN12 in leukemogenesis and raise the potential for the use of velcrins as a therapeutic strategy for AML. - Source: PubMed
Guillen Magaña Jamie NZannikou MarkellaBaran AnetaSmall SaraSchieber MichaelSchipma Matthew JBartom Elizabeth TKocherginsky MashaSaleiro DianaBeauchamp Elspeth MEckerdt FrankPlatanias Leonidas C - Sepsis-induced immunosuppression involves complex molecular mechanisms, including dysregulated long noncoding RNAs (lncRNAs), which remain poorly understood. - Source: PubMed
Publication date: 2025/04/07
Zhang WenjiaLi YanLi GangZhang AijiaSun Wende - Gliomas are the most prevalent form of primary brain tumours. Recently, targeting the PD-1 pathway with immunotherapies has shown promise as a novel glioma treatment. However, not all patients experience long-lasting benefits, underscoring the necessity to discover reliable biomarkers for predicting treatment outcomes. This study applied a range of advanced artificial intelligence methods to identify a new biomarker linked to the effectiveness of anti-PD-1 immunotherapy in glioma patients. Through an extensive analysis of single-cell RNA sequencing and bulk transcriptomic data from over 3000 patients, the gene SLFN12 emerged as a significant and independent predictor of immunotherapy response. Our results indicate that elevated SLFN12 expression is associated with worse overall survival across various glioma cohorts. Notably, we found that patients with high SLFN12 levels are less likely to respond favourably to anti-PD-1 treatment, positioning SLFN12 as a clinically valuable biomarker for personalised treatment decisions. Functional studies revealed that SLFN12 is involved in key immune-related pathways, shedding light on its potential role in altering the tumour microenvironment and impacting immunotherapy outcomes. Additional laboratory experiments confirmed the role of SLFN12 in promoting glioma cell proliferation, migration and macrophage recruitment. In summary, this study identifies SLFN12 as a novel biomarker for predicting immunotherapy response in glioma patients, offering new insights for precision immunotherapy approaches. - Source: PubMed
Chen ZiguiLiu ChaoZheng WeiFang YuhuaZhang HeLuo JiaweiLi JialeQiu YingqiPeng JunXia YingMiao ChangfengLuo Qisheng - Cellular senescence (CS) is a hallmark of Alzheimer's disease (AD). However, the mechanisms through which CS contributes to AD pathogenesis remain poorly understood. We found that CS level in AD was higher compared with the healthy control group. Transcriptome-based differential expression analysis identified 113 CS-related genes in blood and 410 in brain tissue as potential candidate genes involved in AD. To further explore the causal role of these genes, an integrative mendelian randomization analysis was conducted, combining AD genome-wide association study summary statistics with expression quantitative trait loci (eQTL) and DNA methylation quantitative trait loci (mQTL) data from blood samples, which identified five putative AD-causal genes (CENPW, EXOSC9, HSPB11, SLC44A2, and SLFN12) and 18 corresponding DNA methylation probes. Additionally, integrative analysis between eQTLs and mQTLs from blood uncovered two genes and 12 corresponding regulatory elements involved in AD. Furthermore, two genes (CDKN2B and ITGAV) were prioritized as putative causal genes in brain tissue and were validated through in vitro experiments. The multi-omics integration study revealed the potential role and underlying biological mechanisms of CS driven by genetic predisposition in AD. This study contributed to fundamental understanding of CS in AD pathogenesis and facilitated the identification of potential therapeutic targets for AD prevention and treatment. - Source: PubMed
Xu YudiLiu ShutongZhou ZhaokaiQin HongzhuoZhang YuyuanZhang GeMa HongxuanHan XinweiLiu HuiminLiu Zaoqu