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A differential expression of uncoupling protein-2 associates with renal damage in stroke-resistant spontaneously hypertensive rat/stroke-prone spontaneously hypertensive rat-derived stroke congenic lines.

08:00 EDT 10th April 2017 | BioPortfolio

Summary of "A differential expression of uncoupling protein-2 associates with renal damage in stroke-resistant spontaneously hypertensive rat/stroke-prone spontaneously hypertensive rat-derived stroke congenic lines."

Uncoupling protein-2 (UCP2), a mitochondrial anion transporter involved in mitochondrial uncoupling, limiting reactive oxygen species formation, is significantly downregulated in kidneys of high-salt-fed stroke-prone spontaneously hypertensive rat (SHRSP), where it associates with increased renal damage occurrence.

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This article was published in the following journal.

Name: Journal of hypertension
ISSN: 1473-5598
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Correction: Adipocyte arrestin domain-containing 3 protein (Arrdc3) regulates uncoupling protein 1 (Ucp1) expression in white adipose independently of canonical changes in β-adrenergic receptor signaling.

[This corrects the article DOI: 10.1371/journal.pone.0173823.].

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Medical and Biotech [MESH] Definitions

A mitochondrial uncoupling protein that is expressed in many tissues and exhibits the greatest expression in SKELETAL MUSCLE. It regulates mitochondrial ATP production and the generation of REACTIVE OXYGEN SPECIES.

A mitochondrial uncoupling protein that is expressed in BROWN ADIPOSE TISSUE. It is critical for NONSHIVERING THERMOGENESIS to prevent heat loss in NEONATES.

A mitochondrial uncoupling protein that is expressed in heart and skeletal muscle tissues. It functions to regulate tissue respiration, energy balance, and THERMOGENESIS. Mutations in the UCP3 gene are associated with OBESITY.

A nuclear and cytoplasmic protein that associates with KINETOCHORES and contains a C-terminal TUDOR DOMAIN. It plays a critical role in the cellular response to DNA DAMAGE and localizes to DOUBLE-STRAND DNA BREAKS. It may also function in M PHASE CELL CYCLE CHECKPOINTS and as an enhancer of TUMOR SUPPRESSOR PROTEIN P53-mediated transcriptional activation.

Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE. The most severe form is KIDNEY FAILURE. Renal function may deteriorate slowly (RENAL INSUFFICIENCY, CHRONIC) or precipitously (RENAL INSUFFICIENCY, ACUTE).

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