Slc7a5 siRNA_Lentivectors
- Known as:
- Slc7a5 siRNA_Lentivectors
- Catalog number:
- i065309c
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Slc7a5 siRNA_Lentivectors
Related genes to: Slc7a5 siRNA_Lentivectors
- Gene:
- SLC7A5 NIH gene
- Name:
- solute carrier family 7 member 5
- Previous symbol:
- -
- Synonyms:
- LAT1, E16, D16S469E, MPE16, CD98
- Chromosome:
- 16q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-28
- Date modifiied:
- 2016-10-05
Related products to: Slc7a5 siRNA_Lentivectors
Related articles to: Slc7a5 siRNA_Lentivectors
- Tumor recurrence remains a major challenge in the management of pituitary neuroendocrine tumors (PitNETs). This study aimed to investigate recurrence-associated metabolic alterations in PitNETs using an integrated metabolomic approach. - Source: PubMed
Publication date: 2026/05/29
Pei Zhi-JieLi Gao-WeiYu Jiang-HaoYang Hong-RuiFang YiZhou Liang-Xue - The heat shock protein beta-1 (HSPB1/HSP27) is highly expressed and phosphorylated in cancer tissues. However, the precise role of HSPB1 in cancer remains unclear. In this study, we report the unexpected findings elucidating the essential role of HSPB1 in adapting amino acid deficiency by upregulating amino acid transporter SLC7A5 function. HSPB1 regulates estrogen receptor-positive (ER+) breast cancer cell proliferation in a SLC7A5-dependent manner. In response to cellular stress, which is specified as amino acid-deficient conditions, HSPB1 was phosphorylated at Ser 78 residue by stress MAPK p38. SLC7A5 is associated with phosphorylated HSPB1 for its functional activation, leading to upregulated amino acid incorporation. In addition, HSPB1 and SLC7A5 overexpression increased acetylated α-tubulin levels. SLC7A5 overexpression did not change acetyl-CoA level, but SLC7A5 knockdown decreased ATAT1 and induced HDAC6 upregulation. Furthermore, HSPB1 and SLC7A5 induced paclitaxel and tamoxifen resistance. Therefore, the HSPB1-SLC7A5 axis contributes to the acquisition of tolerance to both tamoxifen and paclitaxel in breast cancer cells, uncovering a novel therapeutic target against drug resistance in breast cancer. - Source: PubMed
Publication date: 2026/05/27
Suzuki YukakoKitayama NarumiKudo RyuheiSilwal KarishmaMatsuda ShioriOhishi MakiUeno AyanoAshitani SanaeIgarashi KaoriMasuda TakeshiIshikawa TakamasaSoga TomoyoshiSaito Yasuhiro - In this issue of Cell, Mao et al. reveal that B cells play an unexpected, immune-independent role in exercise physiology by facilitating multi-organ communication. Secreting TGF-β1, they transcriptionally reprogram hepatic glutamine metabolism via GLS2 and SLC7A5, preserving skeletal muscle glutamate levels, which sustain mitochondrial function, Ca⁺ signaling, and ATP production, enhancing exercise capacity. - Source: PubMed
Moreno-Fernandez Maria EDivanovic Senad - Targeted delivery systems offer a promising approach for selectively modulating cellular processes; yet the intracellular consequences of targeted nutrient delivery to trophoblast cells remain poorly defined. Here, we investigated a previously validated placenta-targeting peptide conjugated to liposomes encapsulating stable isotope-labelled L-arginine and L-lysine to examine cellular uptake and downstream molecular responses in a trophoblast-like cell model. Peptide-dependent uptake of fluorescently labelled liposomes was confirmed in BeWo cells, demonstrating selective internalisation compared with non-targeted controls. Encapsulation of isotope-labelled amino acids enabled direct quantification of intracellular delivery and incorporation into the cellular proteome using stable isotope labelling by amino acids in cell culture (SILAC). Quantitative proteomic analysis revealed coordinated changes in proteins associated with translation, metabolism, and nitric oxide synthase regulation following targeted liposomal uptake. Notably, V-type proton ATPase subunit G1 (ATP6V1G1) and large neutral amino acid transporter small subunit 1 (SLC7A5) showed increased incorporation of labelled amino acids and were independently validated by Western blotting. Together, these findings establish a proof-of-concept platform for targeted intracellular amino acid delivery to trophoblast-like cells and define the resulting proteomic responses. This work provides mechanistic insight into intracellular amino acid utilisation and a framework for future studies in placental cell biology. - Source: PubMed
Publication date: 2026/04/23
Mazey EmilyFlannery SarahFischer RomanKandzija NevaZhang WeiYamada YumaTokeshi ManabuJohnson ErrinAkbar NaveedBancroft JamesHannan Fadil MVatish Manu - Acute mountain sickness (AMS) arises from hypobaric hypoxia at high altitude and still lacks effective pharmacological treatments. Although hypoxic preconditioning via gradual ascent prevents AMS, the underlying molecular adaptations have not yielded therapeutics. Here, inspired by metabolic reprogramming during stepwise altitude adaptation, we screened for anti-hypoxia compounds and identified H0802 (N-(pyridin-2-yl) pyridine-2-carbothioamide) as the most promising candidate. H0802 markedly enhances hypoxic tolerance in mice, prolongs survival under acute hypoxia, improves survival during simulated high-altitude exposure, and attenuates hypoxia-induced lung injury, accompanied by combined anti-inflammatory and antioxidant effects. Transcriptomic profiling shows that H0802 elicits a gene expression signature resembling hypoxia, including key hypoxia-related genes (, , , , , and ) involved in glucose and oxygen metabolism. Mechanistically, H0802 stabilizes endogenous hypoxia-inducible factor (HIF) proteins under normoxia by preventing ubiquitin-dependent degradation, thereby activating hypoxia-responsive genes. In vivo, H0802 pretreatment lowers circulating glucose and hepatic glycogen while increasing brain glucose uptake, suggesting a metabolic shift that preserves cerebral energy during acute hypoxic stress; it also modulates whole-body oxygen consumption. H0802 represents a candidate for anti-AMS therapy, and phenotypic optimization of H0802 provides a potential route for drug discovery. - Source: PubMed
Publication date: 2026/04/22
Yin LehuaLiu ZhehanLi YiranLi LeiLi XihengYang XingxingZhang JinyanHuang ShaoyiSun HaoYan XuHe WeihuiZhang ShaoyuGao JianqinChen JiaLiu YaohuiHan QiuyingZhou TaoHe XinhuaChen Yuan