Investigation with chitosan-oxalate oxidase-catalase conjugate for degrading oxalate from hyperoxaluric rat chyme.
Ramakrishnan, V; Lathika, K M; D'Souza, S J; Singh, B B; Raghavan, K G.
Indian J Biochem Biophys
; 1997 Aug; 34(4): 373-8
Artículo en Inglés | IMSEAR | ID: sea-26848
Documentos relacionados
Investigation with chitosan-oxalate oxidase-catalase conjugate for degrading oxalate from hyperoxaluric rat chyme.
Generation and characterization of a novel rat model of primary hyperoxaluria type 1 with a nonsense mutation in alanine-glyoxylate aminotransferase gene.
Sel1-like proteins and peptides are the major <i>Oxalobacter formigenes</i>-derived factors stimulating oxalate transport by human intestinal epithelial cells.
Future treatments for hyperoxaluria.
An engineered bacterial therapeutic lowers urinary oxalate in preclinical models and in silico simulations of enteric hyperoxaluria.
Small intestine resection increases oxalate and citrate transporter expression and calcium oxalate crystal formation in rat hyperoxaluric kidneys.
N-acetylcysteine regulates oxalate induced injury of renal tubular epithelial cells through CDKN2B/TGF-ß/SMAD axis.
Absence of the sulfate transporter SAT-1 has no impact on oxalate handling by mouse intestine and does not cause hyperoxaluria or hyperoxalemia.
Reduced active transcellular intestinal oxalate secretion contributes to the pathogenesis of obesity-associated hyperoxaluria.
<i>Oxalobacter formigenes-</i>Derived Bioactive Factors Stimulate Oxalate Transport by Intestinal Epithelial Cells.