Ask about this productRelated genes to: SLC40A1 antibody
- Gene:
- SLC40A1 NIH gene
- Name:
- solute carrier family 40 member 1
- Previous symbol:
- SLC11A3
- Synonyms:
- MTP1, IREG1, FPN1, HFE4
- Chromosome:
- 2q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-04
- Date modifiied:
- 2019-04-23
Related products to: SLC40A1 antibody
Related articles to: SLC40A1 antibody
- Solute carrier family 40 member 1 (SLC40A1) encodes ferroportin 1 (FPN1), the only known iron efflux transporter in mammalian cells, which is critical for maintaining systemic iron homeostasis and cellular iron balance. SLC40A1 plays a key role in regulating iron homeostasis and is involved in the pathogenesis of inflammatory, fibrotic, neurodegenerative diseases, and cancer, with dysfunction linked to mutations or epigenetic silencing. Its biological functions and regulatory mechanisms are complex and diverse. This article provides an overview of SLC40A1's molecular and biological properties, elucidates its involvement in disease progression, and evaluates its clinical potential. The study seeks to enhance understanding of SLC40A1's mechanisms, laying the groundwork for the development of targeted therapies. - Source: PubMed
Publication date: 2026/05/11
Huang LimianPan LinQin WeilingZhao YihuiHuang YanyunQin Xiao - While iron homeostasis in cancer cells is well-established, its role in mediating crosstalk between tumors and CD8 T cells within the tumor microenvironment (TME) remains largely elusive. In this study, we compare iron levels across primary tissues populated by CD8 T cells. Contrary to the systemic iron deficiency commonly found in cancer patients, the TME exhibits marked iron enrichment compared to lymphatic fluid and peripheral blood, a phenomenon primarily attributed to tumor necrosis. However, this iron-overloaded TME is detrimental to CD8 T cells, triggering their ferroptosis and dysfunction. Mechanistically, tumoral T cell receptor (TCR) hyperactivation and tumor-derived hepcidin cooperatively downregulate the iron exporter SLC40A1 in CD8 T cells, leading to intracellular iron accumulation and ferroptosis. Both genetic restoration of SLC40A1 and iron chelation inhibit CD8 T cell ferroptosis and restore their cytotoxic activity, thereby suppressing tumor growth. Finally, to enhance chimeric antigen receptor T (CAR-T) cell adaptability to the iron-overloaded TME, we engineer SLC40A1-overexpressing CAR-T cells. These engineered cells resist ferroptosis induced by the TME and elicit potent anti-tumor immunity. - Source: PubMed
Publication date: 2026/05/22
Lin ZhenyuChen HuanpengKe YujingXiao HanyueLi ChaoWu ZilongGao HuixinHuang NanqiLu LijuanSun PengBian Yingjie
- Source: PubMed
- Heart failure (HF) is frequently associated with iron deficiency and anemia, negatively impacting patient outcomes. This study aimed to investigate the contribution of genetic variation in iron metabolism-related genes to biochemical and hematological phenotypes in HF. An HF population of 182 patients with functional iron deficiency (ID) and anemia was stratified by sex and heart failure subtype, including HF with reduced ejection fraction (HFrEF) and HF with non-reduced ejection fraction (HFnrEF). Genetic variants in (rs1799945), (rs1439816, rs2304704), and (rs855791) were evaluated. Variants in and were associated with differences in serum iron, ferritin, transferrin saturation, hemoglobin, and RDW. The phenotypic impact of these variants was modulated by sex and heart failure subtype, highlighting the influence of iron availability, inflammatory burden, and erythropoietic demand. In contrast, no significant associations were observed for the variant. In conclusion, genetic variation in key regulators of iron metabolism contributes to the heterogeneity of iron-related biochemical and hematological phenotypes in HF. These findings emphasize the interplay between genetic background, sex, and heart failure physiology and support the relevance of personalized approaches to iron assessment and management in heart failure. - Source: PubMed
Publication date: 2026/04/23
Barbosa MárioAguiar LauraMatias AnaFerreira JoanaCaldeira JoãoMelício AnaFaustino PaulaFalcão Luiz MenezesBicho ManuelInácio Ângela - Mixed histiocytosis (MH), the coexistence of two or more histiocytic disorders in the same patient, is rare and poorly understood. Langerhans cell histiocytosis (LCH) is a clonal myeloid disorder characterized by infiltration of pathological antigen-presenting cells with morphological and phenotypic resemblance to Langerhans cells. Activating mutations of the MAPK/ERK signaling cascade represent the principal driver of LCH pathogenesis and are also central to Erdheim-Chester disease (ECD). - Source: PubMed
Publication date: 2026/05/11
Buianova Anastasiia AGaydina Tatiana AReznik Elena VIarovoi Maksim DKuznetsova Anna ABelova Vera AIgnatyuk Mikhail AShatalov Petr ARepinskaia Zhanna AShinkarina Anna PVolodkin Artem VAtiakshin Dmitrii AKorostin Dmitriy O