Ask about this productRelated genes to: SLC25A21 antibody
- Gene:
- SLC25A21 NIH gene
- Name:
- solute carrier family 25 member 21
- Previous symbol:
- -
- Synonyms:
- ODC1, ODC
- Chromosome:
- 14q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-18
- Date modifiied:
- 2016-02-18
Related products to: SLC25A21 antibody
Related articles to: SLC25A21 antibody
- Craniosynostosis is defined by premature cranial suture fusion and is biologically heterogeneous. To map mitochondrial-associated signals in craniosynostosis and rank follow-up candidates, we integrated two public microarray datasets (GSE27976, GSE50796), corrected batch effects, and analyzed 14,186 shared genes using limma. This identified 798 nominal DEGs (388 upregulated and 410 downregulated), of which 19 remained significant after Benjamini-Hochberg correction. Intersecting the nominal DEG list with the MitoCarta 3.0 inventory yielded 24 mitochondrial DEGs (MitoDEGs). Complementary feature selection reduced these 24 MitoDEGs to an eight-gene panel (TMEM11, SLC25A21, GPT2, CYP27A1, MRPS30, ACAA2, GSR, and LIG3); a multigene score reached an apparent AUC of 0.806 in the integrated dataset. Correlation-based co-expression analyses linked the panel to mitochondrial translation, electron transport, amino-acid metabolism, redox control, and cell-matrix signaling. Among craniosynostosis cases, consensus clustering on the eight genes separated two molecular subtypes with distinct GSVA pathway profiles. For experimental support in a genetically defined mouse model, we profiled bilateral coronal suture complexes from Fgfr2C361Y/+ knock-in (KI) pups and WT littermates. Jess capillary immunoassay showed higher CYP27A1 abundance in KI sutures (P = 0.0276), whereas ACAA2, LIG3, MRPS30, and TMEM11 were not significant. Data-independent acquisition (DIA) proteomics identified 523 differentially abundant proteins (516 increased, 7 decreased in KI), followed by stricter-threshold reporting, sensitivity analysis, and threshold-free rank-based enrichment. MitoCarta proteins and mitochondrial pathways remained supported under these more conservative analyses. These results support mitochondria-associated transcriptomic and proteomic changes in craniosynostosis and prioritize a limited set of mitochondrial candidates for future mechanistic work. - Source: PubMed
Publication date: 2026/06/08
Zeng HanWang YuDong MiaoYue YingyingJin Xiaolei - Mitochondrial 2-oxodicarboxylate carrier (SLC25A21) plays a crucial role in maintaining mitochondrial function and regulating apoptosis. Whether SLC25A21 influences cell death solely through apoptosis remains unclear. Here, we reported that mitochondrial protein Methylcrotonoyl-CoA carboxylase beta chain (MCCC2) co-localized with mitochondrial inner membrane protein SLC25A21 and promoted its lysosomal degradation in colorectal cancer (CRC) cells. The ectopic overexpression of SLC25A21 significantly inhibited the malignant behaviors of CRC cells. Overexpression of SLC25A21 induced cell death and cell cycle arrest at the G2/M phase, and triggered hallmark ferroptotic alterations, including lipid peroxidation (LPO) and reactive oxygen species (ROS) accumulation, increased Malondialdehyde (MDA) contents, GSSG/GSH and NADP + /NADPH ratios, and abnormal mitochondrial morphologies. Mechanistically, SLC25A21 formed a complex with Glutathione Peroxidase 4 (GPX4) and activated the MEK-ERK and p38 MAPK signaling pathways, together reducing the GPX4 pool in mitochondria. Treatment of CRC cells with a GPX4 agonist inhibited SLC25A21-induced ferroptosis, thereby reducing the production of LPO and ROS, and restoring partially malignant behaviors of the cells. In vivo, SLC25A21 inhibited tumor growth by activating ferroptosis. Relatively high expression of SLC25A21 was associated with unfavorable outcomes in multiple patient cohorts, suggesting a complex role for SLC25A21 in CRC progression. Together, we identified SLC25A21-GPX4 interaction as an important regulatory axis in mitochondrial redox maintenance. - Source: PubMed
Publication date: 2026/04/21
Liu WanjunXie WenqingHuang MinghanOu ZhimeiWu MeihuaLv LiLi CaibinLuo QianxinWang QianWu KetongChen Daici - Intracranial aneurysm (IA) is a cerebrovascular disease that lacks effective methods for early diagnosis and risk prediction. Considering the pivotal roles of senescence and inflammation in many diseases, this study aimed to identify related biomarkers for IA and explore their underlying mechanisms. - Source: PubMed
Li XiaoyanLi YingyingZhang LeMao JieLi Bin - Hyperlipidemia complications caused by obesity are a hot issue threatening human health worldwide, and there is an urgent need to explore low-toxicity health foods for intervention. polysaccharides (SFPS) display cholesterol-lowering properties, but the underlying mechanism has not been elucidated. This study investigates the mechanisms by exploring changes in gut microbiota composition, gene expression, and metabolites in mice fed a high-fat diet after intervention with fucoidan (SFF) and SFPS through 16S rRNA sequencing, transcriptomics, and non-targeted metabolomics. The experimental findings indicated that SFPS markedly enhanced the abundance of Akkermansia while concurrently reducing the levels of Actinobacteria, Erysipelotrichaceae, Bifidobacteriaceae, and Peptostreptococcaceae. This was achieved by upregulating the expression of Mt1, Prlr, and slc25a21 and downregulating SREBP-1, thereby inhibiting the cholesterol metabolism pathway. These changes resulted in increased hepatic production and fecal excretion of bile acids and reduced hepatic cholesterol. Our results shed light on the mechanisms behind the cholesterol- and lipid-lowering effects of SFPS, suggesting its potential as a therapeutic agent for hypercholesterolemia. - Source: PubMed
Publication date: 2025/11/11
Su NingHan ShiweiLi ZhengyangLing XiaoyuKong LingqingSong Dafeng - Thrombocytopenia is a common adverse side effects of Linezolid (LZD) but the underlying mechanism remains unclear. This study aimed to analyze the mechanism of LZD induced thrombocytopenia for LZD induced thrombocytopenia. - Source: PubMed
Publication date: 2025/09/22
Yang YaWang NingXiong LirongFu PeishuTian YanpingLuo ShenglinSun FengjunXia Peiyuan