Ask about this productRelated genes to: SLC25A25 antibody
- Gene:
- SLC25A25 NIH gene
- Name:
- solute carrier family 25 member 25
- Previous symbol:
- -
- Synonyms:
- KIAA1896, PCSCL, MCSC
- Chromosome:
- 9q34.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-05
- Date modifiied:
- 2016-10-05
Related products to: SLC25A25 antibody
Related articles to: SLC25A25 antibody
- The progression of acute coronary syndrome (ACS) is primarily determined by the transition from stable to vulnerable atherosclerotic plaque. The primary objective of this study was to investigate the mechanism of SLC25A25 antisense RNA 1 (SLC25A25-AS1) in ACS. The level of SLC25A25-AS1 was determined using reverse transcription quantitative real-time PCR (RT-qPCR) in serum samples from healthy controls (n = 81) and ACS patients (n = 162). The clinical relevance of SLC25A25-AS1 in ACS was evaluated through correlation, receiver operating characteristic (ROC), and logistic regression analyses. SLC25A25-AS1 was significantly downregulated in ACS patients. Overexpression of SLC25A25-AS1 protected oxidized low-density lipoprotein (ox-LDL) treated human coronary artery smooth muscle cells (HCASMCs) from damage in an atherosclerosis model. Specifically, these protective effects were against abnormal cell proliferation, inflammatory responses, cell migration, and maintenance of the contractile phenotype in HCASMCs. Both bioinformatics analyses and experimental validation confirmed the existence of the SLC25A25-AS1/ microRNA‑34a‑5p (miR-34a-5p)/Forkhead box P1 (FOXP1) regulatory axis. Collectively, SLC25A25-AS1 modulated ox-LDL-induced atherosclerotic responses in HCASMCs through the miR-34a-5p/FOXP1 pathway. These findings suggested that SLC25A25-AS1 may play a protective role in ACS by alleviating ox-LDL-induced HCASMC dysfunction and inflammation via the miR-34a-5p/FOXP1 axis. - Source: PubMed
Publication date: 2026/07/29
Wang QiupingChen DongshengLi Ting - Lactation traits are important indicators for evaluating the production performance of dairy cows and the economic efficiency of dairy production. Identifying potential regulatory genes is essential for elucidating the molecular mechanisms underlying lactation and facilitating molecular breeding. This study aimed to identify candidate genes and regulatory pathways potentially associated with lactation traits in dairy cows by integrating transcriptome expression profiles of primary bovine mammary epithelial cells (BMECs) from eight Holstein cows with lactation phenotypic data. A gene co-expression network was constructed using weighted gene co-expression network analysis (WGCNA). Co-expression modules associated with lactation traits were identified, and candidate genes were further screened by integrating gene significance, module membership, functional enrichment analysis, random forest analysis, gene-phenotype association analysis, single-gene gene set enrichment analysis (GSEA), ROC curve analysis, and tissue expression profiling. Four co-expression modules, namely MEdarkturquoise, MEsteelblue, MEbrown, and MEskyblue3, were significantly associated with lactation traits ( < 0.05). Genes in these modules were mainly enriched in biological processes and pathways related to ribosome biogenesis, protein translation, the cell cycle, oxidative phosphorylation, and the PI3K-Akt signaling pathway, which may be involved in lactation regulation. Through multi-strategy cross-screening, four candidate genes were ultimately identified. 2 was associated with daily milk yield (DYM), A with total milk solids (TMS), and 25 and 2 with milk fat percentage (MFP) and fat-to-protein percentage ratio (FPP). Reverse transcription quantitative real-time PCR (RT-qPCR) validation showed that 2 and were relatively highly expressed in mammary tissue, suggesting that they may be involved in lactation-related biological processes in dairy cows. These findings provide potential candidate regulators and theoretical support for further studies on the molecular mechanisms of lactation traits; however, their functional roles require further validation through in vitro and in vivo experiments. - Source: PubMed
Publication date: 2026/07/16
Mu TongQiao ZhixuanHu HonghongMa YunJiang ZiyanHuang YuxinSun Zhihong - The brain is uniquely vulnerable to mitochondrial dysfunction, a primary hallmark of neurodegenerative diseases. While mitochondria are universally recognized as cellular powerhouses, their organ-specific functional architectures remain poorly defined. In this study, we present a high-resolution transcriptomic analysis compared across cerebellar tissue (used as the neural reference) and peripheral tissues (heart, kidney, and ovary) to map the coordination of transport, signaling, and detoxification. Using ovarian tissue as a stable physiological baseline, our findings demonstrate that neural mitochondria are fundamentally architected for metabolic surveillance and repair rather than sheer bioenergetic throughput. To safely meet the extreme metabolic demands of synaptic transmission, the brain exhibits reduced transcriptional emphasis on bulk bioenergetic exchange pathways relative to signaling and repair modules in favor of three highly specialized functional pillars: tightly regulated transport (e.g., SFXN4, SLC25A14, and SLC25A22, SLC25A25), highly responsive metabolic signaling (anchored by EFHD1 and retrograde communication), and targeted detoxification and protein repair (e.g., MSRA and MSRB2). Furthermore, phylogenetic conservation analysis comparing the bovine lineage to the human transcriptomic reference data across 90 million years of mammalian evolution confirms that these neural-specific adaptations exhibit highly conserved expression hierarchies. This evolutionary rigidity proves that this specific neurochemical architecture is a deeply conserved, essential requirement for protecting the central nervous system. Consequently, defining this baseline establishes a critical molecular framework for identifying precise therapeutic targets to combat oxidative stress, excitotoxicity, and age-related neurodegeneration. - Source: PubMed
Publication date: 2026/07/17
Sadeesh E MLahamge Madhuri SAmpadi A NMohiddin Roshan - Seasonal crude protein (CP) and phosphorus (P) deficiency in northern Australian pastures reduces feed intake and growth of grazing ruminants, but the hepatic mitochondrial mechanisms underlying this response remain unclear. We characterized the hepatic mitochondrial transcriptome of sheep exposed to CP-P deficiency or matched-intake feed restriction. Merino wethers were assigned for 63 d to one of three treatments ( = 8/group): High CP-P, Low CP-P, or Restricted, in which High CP-P feed was offered at the same energy intake as the Low CP-P group. Liver RNA was sequenced, and transcripts encoding mitochondrial proteins were identified using MitoCarta 3.0. Differentially expressed genes (DEGs) were defined as adjusted < 0.05 and |log2FC| ≥ 0.585. Of 804 mitochondrial genes detected, 83 were differentially expressed in at least one pairwise comparison. The greatest transcriptional response occurred in contrasts against High CP-P (Low CP-P vs. High CP-P: 38 DEGs in 8 enriched pathways; Restricted vs. High CP-P: 37 DEGs in 10 enriched pathways). In both low-intake treatments, , , , and were upregulated, suggesting altered folate-mediated one-carbon metabolism. Restricted sheep also showed higher expression of several transporters (, , , , and ), indicative of enhanced mitochondrial nucleotide and metabolite exchange under CP-P adequate energy restriction. In contrast, Low CP-P sheep showed higher expression of and relative to either High CP-P or Restricted sheep, a nutrient-deficiency specific transporter response. expression was also higher in Restricted sheep than in both other groups. These findings suggest that reduced metabolizable energy intake was associated with the bulk of the hepatic mitochondrial transcriptional response, particularly in folate-mediated one-carbon metabolism, whereas CP-P deficiency was associated with a smaller but distinct transporter signature. The liver mitochondrial transcriptome may provide mechanistic insight into nutritional adaptation under CP and P deficiency in grazing sheep. - Source: PubMed
Publication date: 2026/05/31
Fernandez Elmer EInnes David JBottje Walter GFortes Marina R SPoppi Dennis PQuigley Simon PBond Jude JHudson Nicholas J - Physical inactivity contributes to the development of chronic diseases. Activation of orphan nuclear receptors estrogen-related receptors (ERRα/β/γ) has emerged as a molecular strategy to mimic exercise-induced benefits. - Source: PubMed
Publication date: 2026/04/06
de Souza-Lima JosivaldoAstrosa-Martin Benjamín DanielGalaz-Rodríguez Camilo ArturoSilva-Bernal Jorge ErnestoOrellana-Pizarro Luis IgnacioMena-Díaz Carlos Alberto