PHE WGS data for COMPARE
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB25844 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ngs2021_12_endomix-phe-gradient-Identify the physiological response of poplar to the presence of 8 Phenanthrene gradient concentration.-As part of the ANR EndOMiX project, we carried out an experiment with poplars (Populus canadensis: hybrid Populus deltoides x nigra) grown in soil with a gradient of contamination in Phenanthrene (PHE), we have 8 different concentrations of PHE, and 4 biological replicates (pots with independent plants). We harvested after 4 weeks of growth, the roots and leaves of the poplars from which the RNAs were extracted for sequencing.
2025-06-04 | GSE263776 | GEO
Project description:phe-gradient-ANR EndOMiX project
| PRJNA1099217 | ENA
Project description:N-lactoyl-phenylalanine (Lac-Phe) is a lactate-derived metabolite that suppresses food intake and body weight. Little is known about the mechanisms that mediate Lac-Phe transport across cell membranes. Here we identify SLC17A1 and SLC17A3, two kidney-restricted plasma membrane-localized solute carriers, as physiologic urine Lac-Phe transporters. In cell culture, SLC17A1/3 exhibit high Lac-Phe efflux activity. In humans, levels of Lac-Phe in urine exhibit a strong genetic association with the SLC17A1-4 locus. Urine Lac-Phe levels are also increased following a Wingate sprint test. In mice, genetic ablation of either SLC17A1 or SLC17A3 reduces urine Lac-Phe levels. Despite these differences, both knockout strains have normal blood Lac-Phe and body weights, demonstrating SLC17-dependent de-coupling of urine and plasma Lac-Phe pools. Together, these data establish SLC17A1/3 family members as the physiologic urine transporters for Lac-Phe and uncover a biochemical pathway for the renal excretion of this signaling metabolite. Our data do not exclude the involvement of other transporters in mediating Lac-Phe transport.
2024-10-17 | PXD054202 | Pride
Project description:N-lactoyl-phenylalanine (Lac-Phe) is a lactate-derived metabolite that suppresses food intake and body weight. Little is known about the mechanisms that mediate Lac-Phe transport across cell membranes. Here we identify SLC17A1 and SLC17A3, two kidney-restricted plasma membrane-localized solute carriers, as physiologic urine Lac-Phe transporters. In cell culture, SLC17A1/3 exhibit high Lac-Phe efflux activity. In humans, levels of Lac-Phe in urine exhibit a strong genetic association with the SLC17A1-4 locus. Urine Lac-Phe levels are also increased following a Wingate sprint test. In mice, genetic ablation of either SLC17A1 or SLC17A3 reduces urine Lac-Phe levels. Despite these differences, both knockout strains have normal blood Lac-Phe and body weights, demonstrating SLC17-dependent de-coupling of urine and plasma Lac-Phe pools. Together, these data establish SLC17A1/3 family members as the physiologic urine transporters for Lac-Phe and uncover a biochemical pathway for the renal excretion of this signaling metabolite. Our data do not exclude the involvement of other transporters in mediating Lac-Phe transport.
2025-01-18 | PXD054049 | Pride