Ask about this productRelated genes to: UCP4 antibody
- Gene:
- SLC25A27 NIH gene
- Name:
- solute carrier family 25 member 27
- Previous symbol:
- -
- Synonyms:
- UCP4, FLJ33552
- Chromosome:
- 6p12.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-08
- Date modifiied:
- 2015-12-08
Related products to: UCP4 antibody
Related articles to: UCP4 antibody
- Lenvatinib is the first-line drug used in the systemic treatment of advanced hepatocellular carcinoma (HCC), although its therapeutic efficacy is limited by emerging resistance mechanisms. Our study aims to investigate the molecular pathways underlying lenvatinib resistance in HCC to inform circumvention strategies for therapeutic resistance. Our findings demonstrated that solute carrier family 25 member 27 (SLC25A27) is upregulated in lenvatinib-resistant (Lenva-R) HCC cells by RNA sequencing (RNA-seq). Similarly, SLC25A27 expression is higher in Lenva-R than lenvatinib-sensitive (Lenva-S) HCC cells and tissues via Quantitative real-time PCR (qRT-PCR), western blot, and immunohistochemistry (IHC) in vitro and vivo. Cell Counting Kit-8 (CCK-8) assay was performed to determine cell viability. Colony formation assay was performed to determine cell proliferation capacity. DCFH-DA staining was used to detect the levels of intracellular reactive oxygen species (ROS). Observation of mitochondrial morphology by using transmission electron microscopy (TEM). The corresponding assay kits were used to analyze the levels of malondialdehyde (MDA), glutathione (GSH)/ oxidized glutathione disulfide (GSSG) ratio, and mitochondrial membrane potential (MMP). Gain- and loss-of-function experiments demonstrated that SLC25A27 promotes survival, proliferation and lenvatinib resistance in vitro. Mechanistic studies showed that SLC25A27 inhibits ferroptosis pathway via activating solute carrier family 7 member A11 (SLC7A11)/glutathione peroxidase 4 (GPX4). Dual-luciferase reporter experiments confirmed signal transducer and activator of transcription 3 (STAT3) significantly enhances SLC25A27 transcription. Moreover, artesunate promotes ferroptosis by inhibiting the STAT3/SLC25A27/ SLC7A11/GPX4 axis in vivo and in vitro. Overall, our study confirmed the combination of artesunate and lenvatinib significantly enhances the anti-HCC effect of lenvatinib, which promising therapeutic strategy to circumvent resistance in HCC. - Source: PubMed
Publication date: 2026/03/31
Bi RanranMa LuyuanGu RuolanDong ShilongLi XinyangLiu WenpengZhang PengfeiGao FengShen ChuanZhao Caiyan - Patients with epilepsy commonly experience patterns of seizures that change with sleep/wake behavior or diurnal rhythms. The cellular and molecular mechanisms that underlie these patterns in seizure activity are not well understood but may involve non-neuronal cells, such as astrocytes. Our previous studies show the critical importance of one specific astrocyte factor, the brain-type fatty acid binding protein Fabp7, in the regulation of time-of-day-dependent electroshock seizure threshold and neural activity-dependent gene expression in mice. Here, we examined whether Fabp7 influences differential seizure activity-dependent protein expression, by comparing knockout (KO) to wild-type (WT) mice under control conditions and after reaching the maximal electroshock seizure threshold (MEST). - Source: PubMed
Publication date: 2025/09/03
Berg Adam PTariq Shahroz HFlores Carlos CLefton MicahOwada YujiDavis Christopher JFerraro Thomas NJacobs Jon MGritsenko Marina ALee YoolSchroeder Wheaton LGerstner Jason R - Low-grade gliomas (LGG) are a heterogeneous category of brain tumors characterized by a variable clinical course, frequently associated with unfavorable prognosis and therapeutic challenges. Understanding the molecular mechanisms underlying LGG progression is crucial for improving prognosis and therapeutic strategies. This study integrates single-cell RNA sequencing and bioinformatics to explore the role of METCGs (mitochondrial electron transport chain genes) in LGG and construct a predictive model for prognosis, and through in vitro experiments, the feasibility of this model was validated. - Source: PubMed
Publication date: 2025/10/08
Li YangLiu QingSu JunJiang LiangqiLi ZhenPeng Hao - The alternative splicing and N6-methyladenosine (mA) modifications occurring during porcine reproductive and respiratory syndrome virus (PRRSV) infections remain poorly understood. Transcriptome and MeRIP-seq analyses were performed to identify the gene expression changes, splicing and m6A modifications in the lungs of PRRSV-infected pigs. In total, 1624 differentially expressed genes (DEGs) were observed between PRRSV-infected and uninfected pigs. We observed significant alterations in alternative splicing (54,367 events) and m6A modifications (2265 DASEs) in numerous genes, including LMO7, SLC25A27, ZNF185, and ECM1, during PRRSV infection. LMO7 and ZNF185 exhibited alternative splicing variants and reduced mRNA expression levels following PRRSV infection. Notably, LMO7 inhibited c-JUN, SMAD3, and FAK expression, whereas ZNF185 affected the expression of FAK, CDH1, and GSK3β downstream. Additionally, ECM1 influenced FAK expression by targeting ITGB3 and AKT2, suggesting its involvement in extracellular matrix accumulation through the ITGB3-AKT2/FAK pathway. These changes may facilitate viral invasion and replication by modulating the expression of genes and proteins participating in crucial cellular processes associated with immunity and the extracellular matrix. We highlight the importance of these genes and their associated pathways in PRRSV infections and suggest that targeting these may be a promising therapeutic approach for treating viral infections. - Source: PubMed
Publication date: 2023/09/09
Lin ChenghongZeng MuSong JiaLi HuaFeng ZhengLi KuiPei Yangli - Although uncoupling protein 4 (UCP4) is the most abundant protein reported in the brain, the biological function of UCP4 in cerebellum and pathological outcome of UCP4 deficiency in cerebellum remain obscure. To evaluate the role of Ucp4 in the cerebellar Purkinje cells (PCs), we generated the conditional knockdown of Ucp4 in PCs (Pcp2;Ucp4 mice) by breeding Ucp4 mice with Pcp2 mice. Series results by Western blot, immunofluorescent staining, and triple RNAscope in situ hybridization confirmed the specific ablation of Ucp4 in PCs in Pcp2;Ucp4 mice, but did not affect the expression of Ucp2, the analog of Ucp4. Combined behavioral tests showed that Pcp2;Ucp4 mice displayed a characteristic bradykinesia in the spontaneous movements. The electromyogram recordings detection excluded the possibility of hypotonia in Pcp2;Ucp4 mice. And the electrical patch clamp recordings showed the altered properties of PCs in Pcp2;Ucp4 mice. Moreover, transmission electron microscope (TEM) results showed the increased mitochondrial circularity in PCs; ROS probe imaging showed the increased ROS generation in molecular layer; and finally, microplate reader assay showed the significant changes of mitochondrial functions, including ROS, ATP, and MMP in the isolated cerebellum tissue. The results suggested that the specific knockdown of mitochondrial protein Ucp4 could damage PCs possibly by attacking their mitochondrial function. The present study is the first to report a close relationship between UCP4 deletion with PCs impairment, and suggests the importance of UCP4 in the substantial support of mitochondrial function homeostasis in bradykinesia. UCP4 might be a therapeutic target for the cerebellar-related movement disorder. - Source: PubMed
Publication date: 2023/09/09
Wang Ya-YunLiu HuiLi Shu-JiaoFeng BanHuang Yun-QiangLiu Shui-BingYang Yan-Ling