Ask about this productRelated genes to: SLC25A42 Blocking Peptide
- Gene:
- SLC25A42 NIH gene
- Name:
- solute carrier family 25 member 42
- Previous symbol:
- -
- Synonyms:
- MGC26694
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2006-09-21
- Date modifiied:
- 2015-12-08
Related products to: SLC25A42 Blocking Peptide
Related articles to: SLC25A42 Blocking Peptide
- Major depressive disorder (MDD) is a heterogeneous condition with substantial variability in antidepressant treatment response. Identifying predictive biomarkers could facilitate personalized treatment strategies and improve clinical outcomes. - Source: PubMed
Publication date: 2026/02/17
Kang JunhoKong NayeongKim ShinLee Hojun - Plasticity of cancer, including epithelial-mesenchymal transition (EMT), cancer stem cell (CSC) self-renewal, and microenvironmental adaptation, drives metastasis, therapy resistance, and poor outcomes in prostate cancer (PCa). Ion channels and extrachromosomal DNA (ecDNA) have emerged as key drivers of such adaptive processes by influencing signaling, metabolism, and immune interactions. - Source: PubMed
Publication date: 2026/02/03
Darbandi SaraUrbanucci AlfonsoHakkola SiniGujral JuanitaDarbandi MahsaEraky AhmedNair SujitChakraborty GoutamTewari AshutoshKyprianou Natasha - The essential cofactor coenzyme A (CoASH) and its thioester derivatives (acyl-CoAs) have pivotal roles in cellular metabolism. However, the mechanism by which different acyl-CoAs are accurately partitioned into different subcellular compartments to support site-specific reactions, and the physiological impact of such compartmentalization, remain poorly understood. Here, we report an optimized liquid chromatography-mass spectrometry-based pan-chain acyl-CoA extraction and profiling method that enables a robust detection of 33 cellular and 23 mitochondrial acyl-CoAs from cultured human cells. We reveal that SLC25A16 and SLC25A42 are critical for mitochondrial import of free CoASH. This CoASH import process supports an enriched mitochondrial CoA pool and CoA-dependent pathways in the matrix, including the high-flux TCA cycle and fatty acid oxidation. Despite a small fraction of the mitochondria-localized CoA synthase COASY, de novo CoA biosynthesis is primarily cytosolic and supports cytosolic lipid anabolism. This mitochondrial acyl-CoA compartmentalization enables a spatial regulation of anabolic and energy-related catabolic processes, which promises to shed light on pathophysiology in the inborn errors of CoA metabolism. - Source: PubMed
Publication date: 2025/09/09
Liu RanZhang ZihanKyaw Aye KGrabińska Kariona AShah HardikShen Hongying - SLC25A42 encodes a mitochondrial carrier that is responsible for the import of CoA into mitochondria. Biallelic pathogenic variants in SLC25A42 have been associated with a recently described mitochondrial disorder characterized by encephalomyopathy with variable severity. To date, 24 affected individuals from 16 different families have been reported. Most are of Arab descent who harbor the founder variant in SLC25A42 (c.871A>G, p.Asn291Asp). In this report, we present 23 additional individuals from 19 unrelated families and their clinical, radiological, and molecular findings. We show again that SLC25A42-related mitochondrial disorder is associated with extremely variable severity. Some individuals with mild presentation may be unrecognized, while others are prone to metabolic decompensations with neuro-regression and irreversible neurological insult, making early diagnosis important. - Source: PubMed
Publication date: 2025/07/09
Alatawi AreejAlshehri OmamahAlessa AminahAl Mutairi FuadAlSaleh NorahEyaid WafaaAlsamri AliFaqeih EissaMushiba AzizaSaleh MohammedAlotaibi MahaTabarki BrahimAljadhai Yaser IKatsonis PanagiotisLichtarge OlivierAlkuraya Fowzan SAlfadhel MajidAlmannai Mohammed - The molecular mechanisms driving hepatocellular carcinoma (HCC) predicting chemotherapy sensitivity remain unclear; therefore, identification of these key biomarkers is essential for early diagnosis and treatment of HCC. We collected and processed Computed Tomography (CT) and clinical data from 116 patients with autoimmune hepatitis (AIH) and HCC who came to our hospital's Liver Cancer Center. We then identified and extracted important characteristic features of significant patient images and correlated them with mitochondria-related genes using machine learning techniques such as multihead attention networks, lasso regression, principal component analysis (PCA), and support vector machines (SVM). These genes were integrated into radiomics signature models to explore their role in disease progression. We further correlated these results with clinical variables to screen for driver genes and evaluate the predict ability of chemotherapy sensitive of key genes in liver cancer (LC) patients. Finally, qPCR was used to validate the expression of this gene in patient samples. Our study utilized attention networks to identify disease regions in medical images with 97% accuracy and an AUC of 94%. We extracted 942 imaging features, identifying five key features through lasso regression that accurately differentiate AIH from HCC. Transcriptome analysis revealed 132 upregulated and 101 downregulated genes in AIH, with 45 significant genes identified by XGBOOST. In HCC analysis, PCA and random forest highlighted 11 key features. Among mitochondrial genes, correlated positively with normal tissue imaging features but negatively with cancerous tissues and was identified as a driver gene. Low expression of was associated with chemotherapy sensitive in HCC patients. In conclusion, machine learning modeling combined with genomic profiling provides a promising approach to identify the driver gene in LC, which may help improve diagnostic accuracy and chemotherapy sensitivity for this disease. - Source: PubMed
Publication date: 2025/06/02
Dou LeiJiang JianhuiYao HongbingZhang BoWang Xueyao