Similar Datasets
Project description:Interventions: Patients with spleen deficiency and qi stagnation syndrome SDQSS:NA;Patients with DHS with damp-heat accumulation syndrome:NA;Patients with SPOS with stasis and internal resistance syndrome:NA;Patients with SKYDS of Spleen and Kidney Yang Deficiency Syndrome:NA;Patients with liver-kidney yin deficiency syndrome LKYDS:NA;QBDS patients with deficiency of both qi and blood syndrome:NA
Primary outcome(s): Serum metabolites;Fecal microbiome;lipidomics
Study Design: Diagnostic test for accuracy
| 105810 | ecrin-mdr-crc
Project description:ABSTRACT:The SODIUM POTASSIUM ROOT DEFECTIVE 1 (NaKR1) encodes a soluble metal binding protein that is specifically expressed in companion cells of the phloem. The nakr1-1 mutant phenotype includes high Na+, K+, Rb+ and starch accumulation in leaves, short roots, late flowering and decreased long-distance transport of sucrose. Using traditional and DNA microarray-based mapping, a 7 bp deletion was found in an exon of NaKR1 that caused a premature stop. The mutant phenotypes were complemented by the native gene and by GFP and GUS fusions driven by the native promoter. NAKR1-GFP was mobile in the phloem, it moved into sieve elements and into a novel symplasmic domain of the root meristem. Grafting experiments revealed that the high Na+ accumulation was due primarily to loss of NaKR1 function in the leaves. This supports a role for the phloem in recirculating Na+ to the roots to limit Na+ accumulation in leaves. The onset of root phenotypes coincided with NaKR1 expression after germination. Short root length was primarily due to a decrease in cell division rate in the root meristem indicating a role for NaKR1 expression in the phloem in root meristem maintenance.
2010-12-23 | GSE24385 | GEO
Project description:We applied RNAseq analysis on microdissected outer medullary collecting duct renal segments from mice fed a normal (0.3% Na+) or high Na+ (3%) diet for 3 days. Among 11688 genes sequenced, 293 have an expression significantly modified (p<0.05), 78 with a -1<log2FC>1. In addition to expected results like the decreased expression of genes participating at the Na+ reabsorption (Scnn1a, SGK1), we observed the stimulation of ATP12a gene that participate at a recently described Na+ secretion pathway.
2024-01-01 | GSE244598 | GEO
Project description:Ubiquitylation plays an important role in the control of Na+ homeostasis by the kidney. It is well established that the epithelial Na+ channel ENaC is regulated by the ubiquitin-protein ligase NEDD4-2, limiting ENaC cell surface expression and activity. Ubiquitylation can be reversed by the action of deubiquitylating enzymes (DUBs). One such DUB, USP2-45, was identified previously as an aldosterone-induced protein in the kidney, and is also a circadian output gene. In heterologous expression systems USP2-45 binds to ENaC, deubiquitylates it and enhances channel density and activity at the cell surface. Because the role of USP2-45 in renal Na+ transport had not been studied in vivo, we investigated here the effect of Usp2 gene inactivation in this process. We demonstrate first that the USP2-45 protein has a rhythmic expression with a peak at ZT12. Usp2-KO mice did not show any differences to wild-type littermates with respect to the diurnal control of Na+ or K+ urinary excretion and plasma levels neither on standard diet, nor after acute and chronic changes to low and high Na+ diets, respectively. Moreover, they had similar aldosterone levels either at low or high Na+ diet. Blood pressure measurements using telemetry did not reveal variations as compared to control mice. Usp2-KO did neither display alternations in ENaC or Na+,Cl--cotransporter (NCC) expression, nor were there any changes in regulatory protein levels, as evidenced by immunoblotting and transcriptome analysis. We conclude that USP2-45 is not crucial for the regulation of Na+ balance or maintenance of blood pressure in vivo.
2013-01-16 | GSE43517 | GEO