Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Disruption of aldose reductase gene (Akr1b1) causes defect in urinary concentrating ability and divalent cation homeostasis.

Biochemical and biophysical research communications - 22 Oct 2000

Aida K, Ikegishi Y, Chen J, Tawata M, Ito S, Maeda S, Onaya T

Abstract excerpt

Aldose reductase (AKR1B1) is the first enzyme in the polyol pathway through which glucose is converted to sorbitol, and has been implicated in the etiology of diabetic complications. However, its physiological role is still not well understood. In the kidney, AKR1B1 is quite abundant in the colle...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aldehyde Reductase
Share to Cations
Share to Chlorides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Creatinine

Share to Deamino Arginine Vasopressin

Share to Magnesium

Share to Phosphates

Share to Potassium

Source

Identifiers

PMID: 11032718
DOI: 10.1006/bbrc.2000.3648

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-11032718-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Disruption of aldose reductase gene (Akr1b1) causes defect in urinary concentrating ability and divalent cation homeostasis.PMID 11032718Read ↗

Aldo-keto reductase 1B: Much learned, much more to doSemantic proximity Read ↗

Kidney collecting duct acid-base “regulon”Semantic proximity Read ↗

AKR1D1 knockout mice develop a sex-dependent metabolic phenotype.Semantic proximity Read ↗

Aquaporin 11 insufficiency modulates kidney susceptibility to oxidative stress.Semantic proximity Read ↗

Retinol dehydrogenase 12 (RDH12) knock out may cause hyperuricemia phenotype in mice.Semantic proximity Read ↗

Mild nephrogenic diabetes insipidus caused by Foxa1 deficiency.Semantic proximity Read ↗

Biochemistry and physiology of hexose-6-phosphate knockout mice.Semantic proximity Read ↗

Atp6v0a4 knockout mouse is a model of distal renal tubular acidosis with hearing loss, with additional extrarenal phenotype.Semantic proximity Read ↗

Localization of the GLUT8 glucose transporter in murine kidney and regulation in vivo in nondiabetic and diabetic conditionsSemantic proximity Read ↗

Rab-GAP TBC1D4 (AS160) is dispensable for the renal control of sodium and water homeostasis but regulates GLUT4 in mouse kidney.Semantic proximity Read ↗

Urinary Sodium Wasting and Disrupted Collecting Duct Function in Mice with dRTA-Causing <i>SLC4A1</i> MutationsSemantic proximity Read ↗

Structure, function, and trafficking of SLC4 and SLC26 anion transporters.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.