SLC13A3 Pre-design Chimera RNAi
- Known as:
- SLC13A3 Pre-design Chimera RNAi
- Catalog number:
- H00064849-R02
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- SLC13A3 Pre-design Chimera RNAi
Related genes to: SLC13A3 Pre-design Chimera RNAi
- 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 Pre-design Chimera RNAi
Related articles to: SLC13A3 Pre-design Chimera RNAi
- Allergic asthma is characterized by chronic airway inflammation that fails to resolve efficiently. Defective efferocytosis and metabolic reprogramming of macrophages are crucial factors in allergic diseases. While PKM2 is known to participate in phagocytosis and metabolism, its specific role in modulating asthma remains unclear. - Source: PubMed
Publication date: 2026/07/15
Chen LingliLiu YileChen YatingZhang YueYu LeiZhu YantongPeng WangWu MaolanZheng Xiangrong - The sodium-coupled citrate transporter NaCT (SLC13A5) imports extracellular citrate into cells. In the CNS, SLC13A5 is described to be expressed predominantly in neurons. Cytosolic citrate levels rely on citrate generated in mitochondria and imported from other CNS cells, regulating intermediary metabolism and supplying acetyl-CoA for lipid synthesis and histone acetylation. Despite evidence for NaCT's role in neurometabolic homeostasis, its transcriptional behavior across Alzheimer's disease (AD) progression and across astrocyte subtypes remains uncharacterized at single-cell resolution. We analyzed single-nucleus RNA sequencing data from 1,378,211 nuclei across 84 donors in the Seattle Alzheimer's Disease Brain Cell Atlas (SEA-AD) Middle Temporal Gyrus dataset to profile SLC13A5 and seven citrate metabolism genes across a continuous AD pseudoprogression score. SLC13A5 expression was restricted to astrocytes (∼20% prevalence) and concentrated in the Astro 2 supertype (24.0%), a homeostatic subtype characterized by low C3 (1.6%) and CD44 (5.5%), which expanded with pseudoprogression (Spearman rho = +0.345, FDR < 0.001). The A1-reactive Astro 3 supertype, where SLC13A5 prevalence was 0.87%, declined concordantly (rho = -0.393). Opposing compositional and transcriptional forces produced apparent stability in overall SLC13A5 prevalence. SLC13A3 and ACO1 showed progressive donor-level declines correlating with Braak stage and Thal phase (rho range: -0.307 to -0.349, FDR < 0.01). APOE4 carriers exhibited lower SLC13A5 prevalence specifically within Astro 2 nuclei (median 17.6% vs. 25.9%; Wilcoxon p = 0.025), though this association did not survive multivariate regression. No difference in Astro 2 SLC13A5 expression was detected between cognitively resilient and expected-AD donors with equivalent high Braak burden (p = 0.888). Contrary to the prevailing description of NaCT as a neuronal transporter, SLC13A5 expression in the SEA-AD MTG dataset is restricted to astrocytes, concentrated in the homeostatic Astro 2 subtype, and maintained as this subtype expands with advancing AD pathology. Supertype-resolved SLC13A5 and SLC13A3 expression provide more informative readouts of astrocytic metabolic state than bulk measurements. - Source: PubMed
Publication date: 2026/06/08
Fernanda Schuck Patríciada Costa Ferreira GustavoRezende Freitas Hércules - 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