Ask about this productRelated genes to: SLC1A5 antibody
- Gene:
- SLC1A5 NIH gene
- Name:
- solute carrier family 1 member 5
- Previous symbol:
- RDRC, M7V1
- Synonyms:
- AAAT, ASCT2
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-09-27
- Date modifiied:
- 2016-02-17
Related products to: SLC1A5 antibody
Related articles to: SLC1A5 antibody
- Extracellular vesicles (EVs) are versatile therapeutic candidates due to biological roles in intercellular communication and amenability to bioengineering. Compared with lipid nanoparticles (LNPs), native or surface-modified EVs may have favorable immunogenicity and biodistribution profiles. However, when administered intravenously (IV), EVs are rapidly cleared and accumulate mostly in the liver and spleen. With the goal of modifying EV biodistribution, we engineered EVs to display the human endogenous retrovirus (HERV) envelope glycoprotein Syncytin-1, an SLC1A5-binding fusogenic viral protein essential for syncytiotrophoblast formation in pregnancy. Here, we comprehensively characterize engineered Syncytin-1+ EVs, examine their interactions with cells , and assay biodistribution, immunogenicity, and pharmacokinetics and in non-human primates. IV-administered Syncytin-1+ EVs are well tolerated, persist in the blood stream, and have altered organ biodistribution compared with unmodified EVs, suggesting therapeutic potential of Syncytin-1+ EVs at specific sites. - Source: PubMed
Publication date: 2026/05/05
Troyer ZachSoumakis MirandaShirk Erin NGololobova OlesiaMarquez SarahFabiano MartinaPachane BiancaRyu TaekyungNa Chan-HyunCastell NatalieBaumann IsabellaQueen SuzanneMankowski Joseph LWitwer Kenneth W - Cancer progression is influenced by the dynamic interplay between tumor cells and the surrounding stromal microenvironment. Therapy-induced senescence (TIS) of stromal fibroblasts represents a common outcome of anticancer treatments, contributing to tumor progression through the senescence-associated secretory phenotype (SASP). While SASP cytokines promote cancer malignancy, the contribution of secreted metabolites from senescent cells remains poorly understood. Here, we investigate the role of senescent stromal metabolism in regulating prostate and ovarian cancer cell invasion. Conditioned media (CM) from TIS-induced human prostate (HPFs) and ovarian fibroblasts (HOFs) promote enhanced invasion of cancer cells. Invasion is partially preserved after exposure to boiled CM, suggesting a role for heat-stable metabolic factors. Metabolomic profiling of senescent fibroblasts-derived CM reveals a significant increase in Glutamine (Gln) levels, identifying senescent stromal fibroblasts as a previously unrecognized source of extracellular Gln in the tumor microenvironment (TME). Exposure of cancer cells to senescent CM increases Gln uptake, together with upregulation of the transporter SLC1A5 and increased intracellular Gln. This metabolic adaptation is associated with increased malignant phenotype including epithelial-to-mesenchymal transition (EMT) and stemness features. Extracellular Gln depletion, pharmacological inhibition of glutaminase-1 (GLS1) in cancer cells, or Gln synthetase (GS) silencing in fibroblasts markedly impair senescent fibroblasts CM-induced invasion, EMT markers expression, and stemness features in cancer cells. Stromal-derived Gln is associated with increased cancer cell invasion through activation of a redox-dependent NRF2/ETS1 signaling axis. Analysis of patient-derived transcriptomic datasets further suggests chemotherapy-associated upregulation of Gln metabolism and expression. These findings identify senescent stromal-derived Gln as a key metabolic driver of prostate and ovarian cancer aggressiveness and reveal a TIS-associated metabolic vulnerability that could be explored in future preclinical studies. - Source: PubMed
Publication date: 2026/04/24
Lori GiuliaMancini CaterinaPaffetti CaterinaDesideri DayanaPranzini EricaSanti AliceLeri ManuelaBiagioni AlessioBenelli MatteoSpatafora PietroManicone Fedele MariaSorbi FlaviaLeo AngelaFambrini MassimilianoSerni SergioMagherini FrancescaTaddei Maria Letizia - - Source: PubMed
Publication date: 2026/04/30
Chen HongyuLi Chengchen - Diabetic retinopathy (DR) represents a key microvascular disorder resulting from prolonged diabetes mellitus. Hyperglycemia, a common driver of diabetes-related vision loss, can pathologically activate lipogenesis (DNL); however, the underlying mechanisms remain incompletely understood. This work sought to profile signature genes correlated with DNL and DR, and offer novel insights into the disease's underlying pathogenesis. - Source: PubMed
Publication date: 2026/04/07
Jin ZhenghongDong YichenXue RongFan XialianWan Guangming - - Source: PubMed
Publication date: 2026/04/20
Yao XinqiWu JieSong YuShen Hao