Ask about this productRelated genes to: SLC25A16 Blocking Peptide
- Gene:
- SLC25A16 NIH gene
- Name:
- solute carrier family 25 member 16
- Previous symbol:
- -
- Synonyms:
- GDA, D10S105E, HGT.1, ML7
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-30
- Date modifiied:
- 2016-10-05
Related products to: SLC25A16 Blocking Peptide
Related articles to: SLC25A16 Blocking Peptide
- As a degenerative disease, the pathophysiology of intervertebral disc herniation (IDH) closely related to mitochondrial dysfunction. However, the specific molecular mechanisms involved have yet to be precisely established. - Source: PubMed
Publication date: 2026/02/14
Wang YihaoBie YongchenZhang YunHuang YingWu KailiMa XuexiaoLi Yan - 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 - Biopsychosocial factors, including family history, influence the development of breast cancer. Malignancies in women with a family history of breast cancer may be detectable based on DNA methylation and microRNA. : The present study extended an integrative analysis of DNA methylation and microRNA to identify genes associated with biopsychosocial factors. : We identified 3060 healthy women from the Taiwan Biobank and included 32 blood plasma samples for analysis of biopsychosocial factors and epigenetic changes. GEO databases and bioinformatics approaches were used for the identification and validation of potential genes. : Our integrative analysis revealed GNPDA1 and SLC25A16 as potential genes. Age, a family history of cancer, and alcohol consumption were associated with GNPDA1 and SLC25A16 based on the current data set and the GEO data set. GNPDA1 and SLC25A16 exhibited significant expression in breast cancer tissues based on UALCAN analysis, where they were overexpressed and underexpressed, respectively. Through a MethSurv analysis, GNPDA1 hypomethylation and SLC25A16 hypermethylation were associated with poor prognoses in terms of overall survival in breast cancer. Moreover, through a MetaCore functional enrichment analysis, GNPDA1 and SLC25A16 were associated with the BRCA1, BRCA2, and pro-oncogenic actions of the androgen receptor in breast cancer. Further, GNPDA1 and SLC25A16 were enriched in known targets of approved cancer drugs as potential genes associated with breast cancer. : These two genes might serve as biomarkers for the early detection of breast cancer, especially for women with a family history of breast cancer. - Source: PubMed
Publication date: 2025/03/30
Khairi SabiahWang Chih-YangAnuraga GanggaPrayugo Fidelia BereniceAnsar MuhamadLesmana Mohammad Hendra SetiaIrham Lalu MuhammadShen Chen-YangChung Min-Huey - Diabetic nephropathy (DN) is a common microvascular complication of diabetes. Mitochondrial dysfunction in the kidney caused by diabetes has previously been linked to the pathogenesis of DN. By mass spectrometry, we identified characteristic proteins of DN from the renal mitochondria in mouse model. To identify the core proteins among them, Mendelian randomization (MR) analysis, microarray data validation, and drug-target interaction analysis were employed. MR analysis found that 189 candidate targets had a causal link with DN risk factors (estimated glomerular filtration rate (eGFR), urinary albumin excretion, and serum creatinine). After systematic analysis, we validated that SLC25A16, CTNND1, C2CD2L, ALDH3A2, NEU1, APEH, CORO1A, NUDT19, and NDUFA4L2 are the core proteins with promising druggability in DN. This study suggests the feasibility of using MR analysis for DN drug target screening, and provides potential insights into mitochondrial dysfunction research, which may contribute to further DN pathogenesis exploration. - Source: PubMed
Publication date: 2025/03/24
Liu YangWu RongZhou ZhelunZhou JunanZhang JiaaiWang Xiaoyi - Alternative splicing (AS), a crucial mechanism in post-transcriptional regulation, has been implicated in diverse cancer processes. Several splicing variants of solute carrier (SLC) transporters reportedly play pivotal roles in tumorigenesis and tumor development. However, an in-depth analysis of AS landscapes of SLCs in colon adenocarcinoma (COAD) is lacking. Herein, we analyzed data from The Cancer Genome Atlas and identified 1215 AS events across 243 SLC genes, including 109 differentially expressed AS (DEAS) events involving 62 SLC genes in COAD. Differentially spliced SLCs were enriched in biological processes, including transmembrane transporter activity, transporter activity, ferroptosis, and choline metabolism. In patients with COAD, tumor tissues exhibited higher expression of longer mitochondrial carrier SLC25A16 isoforms than adjacent normal tissues, consistent with bioinformatics analysis. Protein-coding sequences and transmembrane helices of survival-related DEAS were predicted, revealing that shifts in splicing sites altered the number and structure of their transmembrane proteins. We developed a prognostic risk model based on the screened 6-SLC-AS (SLC7A6_RI_37208 (SLC7A6-RI), SLC11A2_AP_21724, SLC2A8_ES_87631, SLC35B1_AA_42317, SLC39A11_AD_43204, and SLC7A8_AP_26712). Knockdown of the intronic region of SLC7A6-RI isoform enhanced colon cancer cell proliferation. In vivo, knockdown of the intronic region of SLC7A6-RI isoform enhanced tumor growth in colon cancer. Mechanistically, si-SLC7A6-RI isoform exerted oncogenic effects by activating the PI3K-Akt-mTOR signaling pathway and promoting cell proliferation, evidenced by increased expression of key regulators Phosphorylated Mammalian Target of Rapamycin (p-mTOR) and a cell proliferation marker Proliferating Cell Nuclear Antigen (PCNA) using western blotting. Our study elucidated SLC-AS in COAD, highlighting its potential as a prognostic and therapeutic target and emphasizing the suppressive influence of SLC7A6-RI in colon cancer progression. - Source: PubMed
Publication date: 2024/10/15
Sun ChaoZeng BoningZhou JilongLi NanLi MingweiZhu ChaoweiXie ShouxiaWang YifeiWang ShaoxiangWang Xiao