Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin.

Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Research Abstract Details 

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Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Abstract Text:

Defects in renal proximal tubule transport manifest in a number of human diseases. Although variable in clinical presentation, disorders such as Hartnup disease, Dent's disease, and Fanconi syndrome are characterized by wasting of solutes commonly recovered by the proximal tubule. One common feature of these disorders is aminoaciduria. There are distinct classes of amino acid transporters located in the apical and basal membranes of the proximal tubules that reabsorb >95% of filtered amino acids, yet few details are known about their regulation. We present our physiological characterization of a mouse line with targeted deletion of the gene collectrin that is highly expressed in the kidney. Collectrin-deficient mice display a reduced urinary concentrating capacity due to enhanced solute clearance resulting from profound aminoaciduria. The aminoaciduria is generalized, characterized by loss of nearly every amino acid, and results in marked crystalluria. Furthermore, in the kidney, collectrin-deficient mice have decreased plasma membrane populations of amino acid transporter subtypes B(0)AT1, rBAT, and b(0,+)AT, as well as altered cellular distribution of EAAC1. Our data suggest that collectrin is a novel mediator of renal amino acid transport and may provide further insight into the pathogenesis of a number of human disease correlates.

Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Publishing Authors By Initials

For similar male urogenital diseases: urologic diseases: kidney diseases: renal tubular transport, inborn errors: renal aminoacidurias research abstracts see: male urogenital diseases: urologic diseases: kidney diseases: renal tubular transport, inborn errors: renal aminoacidurias research

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Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Renal physiology

VOLUME: 292

Page Numbers: F533-44

Journal Abbreviation: Am. J. Physiol. Renal Physiol.

ISSN: 0363-6127

DAY: 19

MONTH: 09

YEAR: 2006

Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901990

Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Keywords Mesh Terms:

KEYWORDS: Renal Aminoacidurias

MESH TERMS: physiopathology

Chemical & Substance for Abstract: Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin. Information

Substance Name: Tmem27 protein, mouse

Registry Number: 0

Grant and Affiliation Information for Aminoaciduria and altered renal expression of luminal amino acid transporters in mice lacking novel gene collectrin.

AFFILIATION: Dept. of Medicine, Duke University, Durham, NC, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: 2T32-DK-007731-12

ACRONYM: DK

MEDLINETA: Am J Physiol Renal Physiol

REFSOURCE: Am J Physiol Renal Physiol. 2007 Feb;292

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