Ask about this productRelated genes to: Slc25a27 Blocking Peptide
- 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: Slc25a27 Blocking Peptide
Related articles to: Slc25a27 Blocking Peptide
- Circular RNAs (circRNAs) exhibit significant sex- and development stage-specific expression patterns in the gonads of various fish species, yet their functions and regulatory mechanisms in male reproductive development remain largely unexplored in crucian carp (). In this study, we characterized the expression features and biological functions of circSPEF2, a circular RNA derived from the reproduction-related gene . Our results showed that circSPEF2 expression was markedly elevated in mature testes and progressively upregulated during gonadal maturation. Functional studies suggested that circSPEF2 likely does not act through a ceRNA-dependent mechanism. Transcriptome sequencing following circSPEF2 overexpression identified 45 upregulated and 70 downregulated differentially expressed genes, with GO and KEGG enrichment analyses revealing significant alterations in multiple gonadal development-related genes and signaling pathways. Subsequent siRNA-mediated knockdown of circSPEF2, combined with qRT-PCR validation, confirmed that circSPEF2 positively regulates the expression of genes associated with cell maturation and differentiation, including , , and , while concurrently suppressing that of proliferation- and apoptosis-related genes such as , , and . Furthermore, RNA pull-down combined with mass spectrometry identified three candidate circSPEF2-binding proteins, namely, hnRNP A/B, SRSF2, and CFAP263. Collectively, these findings indicate that circSPEF2 plays an important role in male gonadal development in fish and provide new insights into the post-transcriptional regulatory mechanisms underlying vertebrate male reproduction. - Source: PubMed
Publication date: 2026/04/23
Gou FangGao YanmeiWang RuiZhong DongmeiYang RongLiu Shaojun - The development of new analytical tools has revealed the heterogeneity of neutrophils in healthy and diseased subjects. Knowledge of this heterogeneity has led to the identification, in healthy individuals, of a minor subset of blood neutrophils that express anti-protease genes characteristic of in vivo long-lived neutrophils, similar to those we previously described in vitro, which are expanded in autoimmune diseases. We can reprogram normal human blood neutrophils in vitro using GM-CSF, TNF, and IL-4, resulting in long-lived (LL) cells with enhanced glycolysis and oxygen consumption. We further report that these LL neutrophils express numerous genes associated with metabolism and mitochondria, including PLPP3 and SLC25A27. In addition, we confirmed that LL neutrophils express anti-peptidase genes, the most expressed being the PI3 gene, and secrete the peptidase inhibitor elafin and the secretory leukocyte protease inhibitor. Extracellular flux analysis revealed that PI3-expressing LL neutrophils exhibit enhanced glycolysis and respiration in response to pro-inflammatory cytokines, whereas non-reprogrammed neutrophils remain unresponsive. PI3-expressing LL neutrophils have a mitochondrial respiration partly driven by pyruvate oxidation, as demonstrated by the use of an inhibitor of mitochondrial pyruvate carrier. In contrast, oxygen consumption in control neutrophils was driven by fatty acid oxidation, as shown by the effect of inhibiting carnitine palmitoyltransferase 1. Thus, the reprogramming of neutrophils with GM-CSF, TNF, and IL-4 into cells capable of producing peptidase inhibitors is associated with an original metabolic phenotype characterized by active mitochondrial pathways. - Source: PubMed
Publication date: 2026/05/05
Breton YannGignac JulesLam Tân KhoaFortin Christopher MMortazavi HelyaAllaeys IsabelleBourgoin Sylvain GPoubelle Patrice EPelletier Martin - 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