Ask about this productRelated genes to: SFXN3 antibody
- Gene:
- SFXN3 NIH gene
- Name:
- sideroflexin 3
- Previous symbol:
- -
- Synonyms:
- SFX3, SLC56A3
- Chromosome:
- 10q24.31
- Locus Type:
- gene with protein product
- Date approved:
- 2004-11-24
- Date modifiied:
- 2017-11-24
Related products to: SFXN3 antibody
Related articles to: SFXN3 antibody
- One of the most diverse types of blood cancer is acute myeloid leukemia, or AML, and there remains an urgent need to identify novel molecular targets for its diagnosis and treatment. The present investigation identified Sideroflexin 3 (SFXN3) as a possible prognostic biomarker in AML by integrating transcriptome and survival data from the TCGA and GTEx databases. Clinical correlation analysis revealed a strong association between increased SFXN3 expression and both advanced age and poor overall survival. Stratified survival analyses confirmed the predictive value of the model across multiple clinical subgroups. It has been demonstrated through the implementation of functional assays that SFXN3 exerts a pivotal role in the promotion of AML cell proliferation and the suppression of apoptosis. This function is primarily attributed to the activation of the Wnt/β-Catenin signaling pathway. Mechanistically, the transcription factor REST was identified as a direct upstream regulator of SFXN3, capable of binding to its promoter region and transcriptionally activating it. The present study has identified the REST-SFXN3-Wnt/β-Catenin axis as a critical regulator of AML cell growth and survival. Furthermore, pharmacological experiments revealed that SFXN3 knockdown significantly enhanced AML cell sensitivity to decitabine, suggesting that co-targeting SFXN3 could improve chemotherapeutic efficacy and help overcome drug resistance. This research provides a comprehensive clarification of the role of SFXN3 in AML, its biological function, and its upstream regulation. Furthermore, the present study unveils a novel signaling pathway involving REST-SFXN3-Wnt/β-Catenin, which may serve as a therapeutic target. These results provide a valuable insight into the underlying causes of AML and offer a potential framework for precision therapy approaches. - Source: PubMed
Publication date: 2026/02/19
Wang XiaolingHuang YoucaiSun MingweiCai ShuyiHu XiaoyuZheng YiFang ShuminLi SumeiTu YanyangTang Huanwen - Mitochondria contribute to compartmentalized metabolism in eukaryotic cells, supporting key enzymatic reactions for cell function and energy homeostasis. However, this compartmentalization necessitates regulated metabolite transport across mitochondrial membranes. Although many transport proteins have been identified, several mitochondrial amino acid transporters remain largely uncharacterized. Using CRISPR-Cas9-mediated candidate transporter knockouts coupled with assessment of metabolite transport via a mitochondrial swelling assay, we identify SFXN1, previously characterized for its role in mitochondrial serine transport, as a protein that mediates mitochondrial transport of a range of other polar neutral amino acids including proline, glycine, threonine, taurine, hypotaurine, β-alanine, and γ-aminobutyric acid (GABA). Furthermore, the SFXN1 paralogues SFXN2 and SFXN3 partially complement loss of SFXN1 to enable glycine transport, while SFXN2 and SFXN5 partially complement loss of SFXN1 to enable GABA transport. Altogether, these data suggest that sideroflexins facilitate the transport of polar neutral amino acids across the inner mitochondrial membrane. - Source: PubMed
Publication date: 2025/07/02
Block SamuelChi FangtaoRosen Paul CPineda S SebastianDarnell Alicia MAbbott Keene LPena Izabella AHeiman MyriamYilmaz Ömer HKory NoraVander Heiden Matthew G - The human sideroflexin (SFXN) gene family, also classified as solute carrier family 56 (SLC56), encodes a group of five mitochondrial transmembrane proteins (SFXN1-SFXN5) involved in key aspects of mitochondrial metabolism, cellular homeostasis, and development. SFXNs are highly conserved across eukaryotic species, with evolutionary the origin traced back to the earliest metazoans. Functionally, each of the five family members exhibits distinct functional specialization. Particularly, SFXN1 and SFXN3 facilitate mitochondrial serine transport, supporting one-carbon metabolism. SFXN2 and SFXN4 are implicated in mitochondrial iron regulation, heme biosynthesis, and iron-sulfur cluster assembly. SFXN5, predominantly expressed in the brain, is proposed to regulate citrate metabolism and immune cell functions. Mutations or dysregulation of SFXN genes have been linked to certain human diseases, including congenital sideroblastic anemia, oxidative phosphorylation disorders, neurodegenerative conditions, and cancers. Structurally, SFXNs share conserved transmembrane domains and key motifs critical for substrate transport, mitochondrial iron homeostasis, and overall mitochondrial function. The evolutionary trajectory of the SFXN family-from amino acid transport to functionally specialized roles in higher organisms-highlights their biological and clinical significance. Comparative studies across model organisms reveal both conserved and divergent functions, emphasizing their importance in health and disease. A comprehensive understanding of the SFXN family not only advances fundamental mitochondrial research but also opens avenues for novel therapeutic interventions. - Source: PubMed
Publication date: 2025/06/20
Katsafadou Angeliki INebert Daniel WKrupenko Sergey AThompson David CVasiliou Vasilis - Cervical cancer (CC) ranks among the most prevalent malignant gynecological neoplasms. Given the significant challenges in treating and detecting CC at an early stage, this study aims to identify key biomarkers associated with the prognosis and progression of this malignancy. Mendelian randomization (MR), expression quantitative trait locus (eQTL) data, survival assessments, and differential expression analyses were used to identify potential biomarkers. Based on the expression profiles of the identified genes, a risk signature was developed. The correlation between gene expression levels and the clinical characteristics of CC patients was also examined. Additionally, qRT-PCR, Transwell migration, and wound healing assays were conducted to validate the reliability of PFKFB4 expression, as well as cellular migration and invasion capabilities. The genes PFKFB4, SFXN3, and ITGB2 were identified as critical targets for CC. MR analysis revealed that ITGB2 and PFKFB4 exhibited a negative correlation with CC development, whereas SFXN3 demonstrated a positive association with the disease. Mechanistic investigations highlighted a strong link between these genes and the immune microenvironment. The developed risk signature displayed significant correlations with the prognosis, metastatic stages, and histological classifications of CC patients. Furthermore, the expression level of PFKFB4 was significantly associated with the T and M stages in CC patients. Notably, PFKFB4 was significantly overexpressed in cervical cancer cells and tissue samples, and its silencing markedly inhibited cell migration and invasion. In summary, this study elucidates the molecular mechanisms underlying CC progression and identifies potential candidate biomarkers that could inform treatment strategies for this malignancy. - Source: PubMed
Publication date: 2025/05/26
Pang GuoshaRuan XiqinYao WenboCao Minghua - Preeclampsia (PE), a hypertensive pregnancy disorder, remains a leading cause of maternal and perinatal morbidity and mortality. Mitochondria-related placental metabolic dysfunction is implicated in PE, but its mechanistic role is unclear. This study aimed to identify mitochondria-related genes (MRGs) and their possible regulatory mechanisms in PE. - Source: PubMed
Publication date: 2025/04/05
Ye XunjiaYu JieyingZhuo YouyuanYong AnluWei JiachunLi RuimanWan ShuoWang GuangYang Xuesong