SLC13A3 Antibody - N-terminal region (ARP41628_P050)
- Known as:
- SLC13A3 Antibody - N-terminal region (ARP41628_P050)
- Catalog number:
- arp41628_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SLC13A3 Antibody - N-terminal region (ARP41628_P050)
Related genes to: SLC13A3 Antibody - N-terminal region (ARP41628_P050)
- Gene:
- SLC13A3 NIH gene
- Name:
- solute carrier family 13 member 3
- Previous symbol:
- -
- Synonyms:
- NADC3, SDCT2
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-13
- Date modifiied:
- 2016-02-17
Related products to: SLC13A3 Antibody - N-terminal region (ARP41628_P050)
Related articles to: SLC13A3 Antibody - N-terminal region (ARP41628_P050)
- Perivascular spaces (PVS) support brain homeostasis through metabolite delivery and waste clearance, yet the genetic determinants of PVS morphology during childhood remain unknown. Here, we leveraged cross-sectional Adolescent Brain Cognitive Development Study data (N = 6,600; ages 9-10), including genomics and 3T structural MRI. - Source: PubMed
Publication date: 2026/05/21
Morrel JessicaAhmadi HedyehTorgerson CarinnaCuster RachelLan HaoyuGauderman W JamesChoupan JeiranHerting Megan M - Obesity is a well-established risk factor for increased severity and mortality in acute pancreatitis. However, the mechanisms by which obesity alters pancreatic immune regulation and favors the progression of acute pancreatitis are not elucidated yet. Here, we identify a neutrophil-driven immune-metabolic pathway that controls ferroptosis during pancreatic inflammation. We show that infiltrating myeloid cells represent the principal source of the immunometabolite itaconate during acute pancreatitis. Through paracrine transfer via the SLC13A3 transporter, myeloid-derived itaconate protects pancreatic acinar cells from ferroptosis by sustaining NRF2-dependent antioxidant responses. Obesity disrupts this protective axis by suppressing ACOD1 expression in infiltrating neutrophils. Proteomic profiling of pancreatic neutrophils from obese mice confirmed reduced ACOD1 abundance and decreased expression of enzymes linked to the tricarboxylic acid cycle and pyruvate metabolism. This metabolic reprogramming limits itaconate production and weakens NRF2-driven redox defenses, leading to downregulation of the xCT-GPX4 ferroptosis-protective pathway and increased lipid peroxidation in the pancreas of obese mice with pancreatitis. Pharmacological restoration of itaconate signaling with the cell-permeable derivative 4-octyl itaconate reactivates NRF2 signaling, the xCT-GPX4 antioxidant axis, and the trans-sulfuration pathway, mitigating pancreatic injury. Together, these findings identify neutrophil-derived itaconate as a key modulator of ferroptosis susceptibility and reveal immune cell metabolism as a critical determinant of obesity-associated severity in acute pancreatitis. - Source: PubMed
Publication date: 2026/05/21
Jiménez-Cañete NéstorAliena-Valero AliciaBressan Caroline APérez SalvadorTorres-Cuevas IsabelBenkenstein LauraPinto SandraCuadrado AntonioSastre JuanRius-Pérez Sergio - Hyperlipidemia refers to the abnormal elevation in the levels of one or more plasma lipids and lipoproteins. - Source: PubMed
Publication date: 2026/04/09
Alwahsh MohammadAlejel RahafHamadneh LamaHasan AyaAl-Hiari YusufAl-Qirim TariqHergenröder Roland - Cells can produce various metabolites, and both immune cells and the immune microenvironment are profoundly influenced by these metabolites. By reshaping the metabolic state of immune cells via metabolites, the host immune response can be effectively regulated, further impacting their behavior in inflammation. Itaconate, as a bypass metabolite of the tricarboxylic acid (TCA) cycle, has long been regarded as a small molecule involved in energy metabolism. However, recent studies reveal its production depends on immune response gene 1 (IRG1), which encodes aconitate decarboxylase. Under the stimulation of inflammation, the expression of IRG1 is significantly upregulated, leading to the rapid accumulation of itaconate within immune cells (especially macrophages), thus making it a key link between metabolism and immune response. Evidence indicates that macrophages are the cell type extensively synthesizing itaconate during M1 polarization driven by potent inflammatory signals (e.g., LPS stimulation). Concurrently, itaconate participates in regulating immune tolerance to cancer therapy via the transmembrane transporter SLC13A3. Under different pathological contexts the IRG1- itaconate axis exhibits distinct dynamic regulatory characteristics: During acute inflammation, itaconate limits excessive release of pro-inflammatory factors and reduces tissue damage by inhibiting succinate dehydrogenase (SDH), activating the Keap1-Nrf2 antioxidant pathway, blocking the ATF3/IκBζ-dependent pro-inflammatory program, and regulating the TET2-mediated epigenetic network. In chronic inflammation or certain tumor microenvironments, however, it may indirectly promote immunosuppression by inhibiting antigen presentation and weakening T cell cytotoxic effects. This bidirectional and environment-dependent nature makes it a key entry point for understanding the maintenance of immune homeostasis, inflammatory regulation and disease progression. This review systematically examines the production mechanisms, biochemical properties, central signaling pathways, and cross-cell effects of Itaconate as an immunomodulatory metabolite. It emphasizes its dual role in regulating inflammatory responses through multiple signaling axes and its contrasting behaviors in different disease contexts. By elucidating its molecular mechanisms, this study aims to provide novel theoretical foundations and potential therapeutic strategies for precision interventions in inflammatory diseases, while outlining future research directions and the clinical translation potential of itaconate-based approaches. - Source: PubMed
Publication date: 2026/02/10
Liu YangZhang PengyuKong WeijieLi JinghuiYang HaoqiangBai HengqiFan GexuCao XinfangLi Yanjun - Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), is a prevalent chronic liver disorder with complex pathogenesis and limited therapeutic options. Here, we identify the solute carrier SLC13A3 as a critical regulator of MASLD progression. In a mouse model fed a high-fat, high-cholesterol, and high-fructose (HFHCHF) diet, hepatic SLC13A3 expression was significantly upregulated and positively correlated with disease severity. Liver-specific overexpression of Slc13a3 exacerbated hepatic steatosis, lipid accumulation, and metabolic dysfunction, whereas Slc13a3 knockdown attenuated these pathological phenotypes. Targeted metabolomic analysis revealed that SLC13A3 modulates hepatic NAD levels, thereby influencing the expression of key lipid metabolism genes, including SREBF1, CD36, PPARγ, and SCD1. These findings highlight a previously unrecognized role of SLC13A3 in MASLD pathogenesis and suggest its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/02/14
Du JiangxiaShen MinhuiMu YuanPeng ShuoranXu ZhifeiYang XiaochunYang BoLuo PeihuaYan HaoHe Qiaojun