Ask about this productRelated genes to: SLC1A1 Blocking Peptide
- Gene:
- SLC1A1 NIH gene
- Name:
- solute carrier family 1 member 1
- Previous symbol:
- -
- Synonyms:
- EAAC1, EAAT3
- Chromosome:
- 9p24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-15
- Date modifiied:
- 2016-10-05
Related products to: SLC1A1 Blocking Peptide
Related articles to: SLC1A1 Blocking Peptide
- This study was conducted to delineate layer-specific transcriptomic alterations in the keratoconus (KC) epithelium and stroma and to identify potential biomarkers using machine learning (ML)-based analysis. - Source: PubMed
Publication date: 2026/05/08
Du KaiyuePeng RongmeiXiao GegeQu YiHan LiangHong Jing - Renal cell carcinomas (RCCs) depend on the trimeric sodium-coupled aspartate and glutamate transporter, SLC1A1/EAAT3; however, pharmacologically targeting SLC1A1 is challenging. Here we determined a cryo-EM structure of human SLC1A1 bound to compound 3e, a recently described SLC1A1-selective bicyclic imidazo[1,2 α]pyridine-3-amine (BIA) inhibitor with an unclear mechanism of action. 3e binds a membrane-embedded allosteric pocket accessible only in the apo state, when SLC1A1 is unbound to substrate and sodium, and likely prevents sodium and substrate binding. Moreover, by forming a wedge between the trimerization domain and the substrate-binding transport domain, alongside a cholesterol moiety from the lipid bilayer, 3e blocks SLC1A1's elevator-like movements that support the transport cycle. Mutations in this binding pocket abolish the 3e interaction and counteract 3e's cytotoxicity in RCC cells, confirming on-target activity and explaining SLC1A1 selectivity. The subsequent design of two new SLC1A1-selective BIA derivatives, PBJ1 and PBJ2, was directed by the SLC1A1-3e structures; both inhibited SLC1A1-dependent aspartate, glutamate, and cysteine metabolism and showed enhanced cytotoxicity. - Source: PubMed
Publication date: 2026/04/22
Koochaki PoonehQiu BiaoCoker Jesse AEarsley AlexanderWang Nancy SRomigh ToddGoins Christopher MSalem CarleighMi DehuiDays EmilyBauer Joshua AStauffer Shaun RBoudker OlgaChakraborty Abhishek A - Multiple myeloma (MM) is a glutamine (Gln)-auxotroph and Gln-addicted cancer, with Gln synthetase (GS)-deficient MM cells avidly taking up extracellular Gln to sustain their metabolism. Thus, MM cells create a peculiar metabolic niche in the patients' bone marrow (BM), where low levels of Gln contribute to the osteolytic bone lesions by inhibiting the osteoblastic differentiation of mesenchymal stromal cells (MSCs). The effects of the altered MM metabolic niche on other BM cell populations remain to be clarified. We demonstrate here that MM cells secrete high amounts of glutamate through the exchange transporter /xCT. In turn, BM MSCs, but neither MM cells nor osteoblasts (OBs), actively take up extracellular glutamate through the transporter EAAT3 (), whose expression decreases during osteogenesis. GS-positive MSCs secrete Gln, a process boosted by extracellular glutamate in undifferentiated MSCs, but not in differentiated OBs. Coculture of MSCs with MM cells promotes the expression of the bidirectional transporter SNAT5 (), suggesting its involvement in Gln efflux. Consistently, MSCs, derived from either patients with MM or healthy donors, sustain MM growth in a low-Gln environment, an effect suppressed by the inhibition or silencing of glutamate uptake or Gln synthesis. In conclusion, a metabolic cycle occurs in MM BM microenvironment, where Gln-auxotroph MM cells extrude glutamate that is converted into Gln by MSC, sustaining in turn MM anabolism through Gln secretion. The inhibition of this metabolic trade-off impairs MM cell growth, thus highlighting novel potential, niche-oriented therapeutic targets. - Source: PubMed
Publication date: 2026/01/14
Taurino GiuseppeGriffini ErikaToscani DeniseMaccari ChiaraTardito SaverioBianchi Massimiliano GCasati LaviniaDander EricaD'Amico GiovannaAndreoli RobertaGiuliani NicolaBussolati OvidioChiu Martina - Postoperative cognitive dysfunction is a type of cognitive impairment that occurs after surgery. Here, this experiment investigated the role of PLCG1 in sevoflurane-induced model and the molecular mechanisms underlying its regulation of ferroptosis. Single-cell RNA sequencing data and bioinformatic analyses were performed using GEO datasets (GSE196239). Mice were exposed to 2.3% sevoflurane for 2 h daily for 3 consecutive days. PLCG1 expression was up-regulation in patients exposed to sevoflurane. Specifically, blood samples from these patients exhibited elevated levels of PLCG1 mRNA. Consistently, in a mouse model of sevoflurane exposure, both mRNA and protein levels of PLCG1 were significantlyincreased in brain tissue. Single-cell RNA sequencing analysis revealed that PLCG1 was predominantly expressed in astrocytes (marked by AQP4, GFAP, LUZP2, and SLC25A28) and neurons (marked by B3GAT2, ENO2, GNG2, and SLC1A1) in sevoflurane-exposed patients. In contrast, PLCG1 expression was undetectable in B cells (CD74, CD79B, CD80, CD86), T cells (CD4, CD8B, CD69, CD247), or macrophages (CD36, CD68, CD83, CD163). In conclusion, PLCG1 drives neuronal ferroptosis in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. In conclusion, PLCG1 drives neuronal in the context of sevoflurane exposure by enhancing mitochondrial oxidative stress and facilitating LAMP2A Ubiquitination, thereby impairing the LAMP2A/HSPA8 pathway. These findings position PLCG1 as a promising biomarker and potential therapeutic target for monitoring and mitigating sevoflurane-induced neurotoxicity. - Source: PubMed
Publication date: 2026/02/27
Chen JianCai YangWang JingruYue KunSun Yingying - Recurrent implantation failure (RIF) is a significant clinical challenge in assisted reproduction, yet its underlying molecular mechanisms remain poorly understood. This study aimed to characterize and integrate the metabolomic, proteomic, and transcriptomic profiles of the RIF endometrium to identify novel pathophysiological networks and potential diagnostic biomarkers. - Source: PubMed
Publication date: 2026/02/16
Huang XiaoqinDai JinjieZhang HongChen HuijiaHan Ting-LiZou HengZhang Shen