Ask about this productRelated genes to: SLC41A3 antibody
- Gene:
- SLC41A3 NIH gene
- Name:
- solute carrier family 41 member 3
- Previous symbol:
- -
- Synonyms:
- FLJ20473
- Chromosome:
- 3q21.2-q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-26
- Date modifiied:
- 2018-02-13
Related products to: SLC41A3 antibody
Related articles to: SLC41A3 antibody
- Hepatocellular carcinoma (HCC) represents a highly aggressive cancer associated with substantial patient mortality. Members of the solute carrier (SLC) protein family have been implicated in facilitating tumor development and progression. However, the specific functions and relevance of SLC41A3 in the context of HCC pathogenesis are not well defined. - Source: PubMed
Publication date: 2026/06/03
Gong BiyanCao DunfuHu ShidongZhou XiangyiZhang LeidaDai FengshengPeng Jianheng - Oncogenic driver mutations were once considered mutually exclusive in non-small cell lung cancer (NSCLC), and the optimal management for these patients with co-mutations of driver genes remains controversial. We report a 66-year-old never-smoking female patient with exon 19 deletion (19del) metastatic NSCLC. Progression occurred after around seven months of first-line treatment with osimertinib. After the progression, the molecular testing revealed fusion in a liver metastasis, two novel fusions ( and ), and an fusion with a mutation allele frequency of 0.19% in circulating tumor DNA (ctDNA), including the known 19del. Pralsetinib was added to osimertinib, resulting in a response lasting 4 months. Molecular detection of both liver and ctDNA revealed the presence of fusions, while 19del still existed, but fusions disappeared. After one month with alectinib only, osimertinib was added due to the progression, resulting in another response of more than two months. Upon progression with quadruple alterations ( 19del, C797S, amplification, and fusions), cabozantinib-gefitinib combination was initiated, leading to rapid deterioration. Interestingly, an 3 fusion was detected at baseline before EGFR-TKI initiation and persisted throughout the patient's treatment course. The patient died about 18 months after the initial diagnosis of metastatic NSCLC. This case demonstrates that iterative molecular profiling in metastatic NSCLC identifies actionable alterations to optimize clinical management. At the same time, comprehensive genomic testing remains essential for therapeutic decision-making, with ctDNA analysis complementing tissue-based approaches. Notably, the fusion may represent a novel resistance mechanism contributing to the limited efficacy of EGFR-TKI. - Source: PubMed
Publication date: 2026/03/12
Wang XiuwenQiu LiwenLiang JizhenLiu FeiMa XiaoxueYang Pan - Pulmonary arterial hypertension (PAH) involves ionic homeostasis and vascular remodeling. While cytosolic magnesium ([Mg]ᵢ) depletion is a hallmark of PAH, the role of mitochondrial Mg (Mg) remains elusive. mitochondrial RNA splicing 2 (Mrs2), the primary Mg influx transporter, is hypothesized to drive PAH by orchestrating mitochondrial ionic imbalance and dysfunction. - Source: PubMed
Publication date: 2026/03/16
Chen Ruo-NanWeng Xue-QinYan YanChen Qin-YeLin Yi-ChenLiu LanZhuang Xiao-LingGui Long-XinSham James S KLin Mo-JunLin Da-Cen - Magnesium ion (Mg), particularly its free intracellular form, is indispensable for regulating diverse cellular functions. This critical role implies the existence of dedicated transporters and channels in the plasma membrane that coordinate Mg uptake, intracellular storage, and efflux to maintain homeostasis. Although numerous molecular entities responsible for such Mg transport have been reported over the past decades, there is still limited knowledge of their precise functions and disease implications. This review focuses on the solute carrier family 41 (SLC41), which consists of three isoforms (A1, A2, and A3) that share homology with the prokaryotic magnesium transporter E (MgtE) Mg transporter family. Accumulating evidence has established SLC41A1 as the Na/Mg exchanger-a predominant Mg-efflux system. By contrast, the subcellular site of SLC41A2-mediated Mg flux remains undefined, with potential roles at either the plasma membrane or organellar membranes, and SLC41A3 facilitates Na-dependent Mg efflux from mitochondria. Additionally, several studies have reported the association between SLC41s and diseases, including Parkinson's disease, hepatocellular carcinoma, and nephronophthisis-related ciliopathies. By synthesizing current knowledge, this review aims to enhance the understanding of SLC41 transporters in health and disease and to explore their potential as therapeutic targets for clinical intervention. - Source: PubMed
Publication date: 2026/02/09
Cao YuRao CaijunDu Zhipeng - This study aimed to identify a novel prognostic signature derived from an EGFR Tyrosine kinase inhibitors (TKI-resistant) macrophage subpopulation and to evaluate its clinical and therapeutic relevance in HCC. We utilized single-cell RNA sequencing data from HCC patients. An EGFR-TKI resistance score was calculated across all cell types. Macrophages, which exhibited the highest resistance score, were sub-clustered to identify the most resistant subpopulation. Marker genes from this sub-cluster were intersected with differentially expressed genes (DEGs) from the TCGA-LIHC cohort. A robust prognostic model was constructed. The model's performance was rigorously validated, and the signature was further characterized through multi-omics analysis and its correlation with immune checkpoint blockade (ICB) response and drug sensitivity. scRNA-seq analysis unequivocally identified macrophages as possessing the highest EGFR-TKI resistance score. We identified seven key prognostic genes: SLC41A3, DCAF13, PPM1G, NDC80, FAM83D, FUCA2, and UQCRH. A risk model built on these seven genes effectively stratified patients into high- and low-risk groups with significantly different overall survival (OS) in the TCGA cohort, a finding successfully validated in the independent GSE76427 cohort. A clinical nomogram integrating the risk score demonstrated excellent predictive accuracy, with AUC values for 1-, 3-, and 5-year OS of 0.816, 0.781, and 0.799, respectively. The low-risk group was associated with a favorable immune-infiltrated phenotype and was predicted to be more sensitive to immunotherapy. Conversely, the high-risk group exhibited distinct genomic features and was predicted to be more sensitive to specific targeted agents, including Navitoclax and Sorafenib. We identified and validated a novel 7-gene prognostic signature derived from a subpopulation of EGFR-TKI-resistant macrophages. This signature accurately predicts patient survival, offers insights into the molecular mechanisms of therapy resistance in HCC, and provides a promising tool for improved patient stratification and the development of personalized treatment strategies. - Source: PubMed
Li XiaominLi ZhilongZhai JinfangZou Binbin