Ask about this productRelated genes to: SLC25A14 Blocking Peptide
- Gene:
- SLC25A14 NIH gene
- Name:
- solute carrier family 25 member 14
- Previous symbol:
- -
- Synonyms:
- BMCP1, UCP5
- Chromosome:
- Xq26.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-09
- Date modifiied:
- 2016-10-05
Related products to: SLC25A14 Blocking Peptide
Related articles to: SLC25A14 Blocking Peptide
- In long-lived neurons, precise control of mitochondrial gene expression is critical for maintaining bioenergetic capacity and preventing dysfunction linked to neurodegeneration. This control is executed by nuclear-encoded mitochondrial central dogma (NEM-CD) genes, yet their tissue-specific regulation, particularly in large mammalian brains, remains poorly defined. We conducted a comparative transcriptomic analysis of 214 NEM-CD genes across four buffalo tissues (brain/cerebellum, heart, kidney, and ovary) to elucidate organ-specific regulatory strategies. RNA sequencing and differential expression analysis revealed a definitive quantitative hierarchy (kidney > heart > brain > ovary), with tissue identity explaining 46.36% of intra-species transcriptomic variance (PC1). While the heart and kidney upregulated structural oxidative phosphorylation (OXPHOS) and translational machinery to meet high-throughput demands, the brain uniquely enriched genes governing transcriptional elongation (e.g., TEFM), RNA surveillance (e.g., PNPT1), and DNA repair (OGG1, POLG). Crucially, these findings were anchored by targeted LC-MS/MS proteomic screening, identifying brain-exclusive mitochondrial specialists such as SFXN3 and SLC25A14 (UCP5). Intra-species analysis revealed that the buffalo neuronal program participates in a robust body-wide regulatory plan (systemic coherence; median ρ = 0.8027), a synchronized architecture also observed in humans (median ρ = 0.9264). Subsequent cross-species compression identified a core set of highly conserved mitochondrial regulatory genes (e.g., ANGEL2, AARS2, RECQL4, MTFMT) that maintain strict evolutionary stability between humans and buffalo. Collectively, this study identifies a conserved "Precision-over-Throughput" neuroprotective strategy in mammalian brains, prioritizing transcriptional fidelity and genome maintenance over biogenic volume. This shared regulatory framework provides a stable comparative foundation for understanding mitochondrial dysregulation in both humans and large farm animals, offering a high-fidelity roadmap for neurodegenerative research. - Source: PubMed
Publication date: 2026/08/17
Sadeesh E MLahamge Madhuri SAmpadi A NKumari SwetaMohiddin Roshan - 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 - Attention-deficit hyperactivity disorder (ADHD) is the most prevalent neurodevelopmental disorder worldwide. To improve treatment strategies against ADHD a better understanding of underlying pathophysiology is required. Spontaneously hypertensive rats (SHR) from the strain SHR/NCrl are a suitable rodent model of ADHD. Here we compared the gene expression in the brains of SHR/NCrl strain to that of other genetically related hypertensive and normotensive rat strains that do not show an ADHD phenotype. In addition, the impact of physical activity on genes that display such differences was also addressed because high physical activity is one non-pharmacological option to cure ADHD symptoms. RNA was isolated from the medulla oblongata, the olfactory bulb, and the cortex. Gene expression was analyzed by qRT-PCR. The cortical expression of GLUT1 was also analyzed by Western Blot. Physical activity was improved by free access to running wheels for six months. Female rats were used in this study and sacrificed at the age of 7.5 months. The results show that gene expression in SHR/NCrl differs from other SHR strains in the olfactory bulb, medulla oblongata, and the cortex. Main differences were obtained for , coding for the protein UCP5, , coding for the protein glucose transporter (GLUT) 1 in the cortex and and for in the medulla oblongata. The expressions of and in the medulla oblongata were normalized in physical active rats. Our study further underlines the usefulness of the SHR/NCrl strain as an ADHD animal model when combined with proper controls. Furthermore, this study identifies genes that are specifically down-regulated in the medulla oblongata of SHR/NCrl and that are affected by activity status. - Source: PubMed
Publication date: 2025/08/18
Sato TsunehisaSchreckenberg RolfSchlüter Klaus-Dieter - Progress in research on expression profiles in osteoarthritis (OA) has been limited to individual tissues within the joint, such as the synovium, cartilage, or meniscus. This study aimed to comprehensively analyze the common gene expression characteristics of various structures in OA and construct a diagnostic model. - Source: PubMed
Publication date: 2024/07/31
Gao QichangMa YimingShao TuoTao XiaoxuanYang XianshengLi SongGu JiaaoYu Zhange - Head and neck paragangliomas (HNPGLs) are rare neoplasms with a high degree of heritability. Paragangliomas present as polygenic diseases caused by combined alterations in multiple genes; however, many driver changes remain unknown. - Source: PubMed
Savvateeva MariaKudryavtseva AnnaLukyanova ElenaKobelyatskaya AnastasiyaPavlov VladislavFedorova MariaPudova ElenaGuvatova ZulfiyaKalinin DmitryGolovyuk AlexanderBulavkina ElizavetaKatunina IrinaKrasnov GeorgeSnezhkina Anastasiya