Defective regulation of vasopressin gene expression in Brattleboro rats

Defective regulation of vasopressin gene expression in Brattleboro rats MAJZOUB, JOSEPH A., ENRIQUE J. CARRAZANA, JANE S. SHULMAN, KAREN J. BAKER, AND RODICA L. EMANUEL. Defective of expression . Am. J. Physiol. 252 (Endocrol. Metab. 15): E637-E642, 1987.-The rat has severe diabetes sipidus due to an autosomal recessive trait resultg the ability to synthesize detectable amounts of hypothalamic . To determe whether this abnormality is due to a regulatory defect the rat’s , we studied changes the hypothalamic content of mRNA normal Long-Evans and homozygous subjected to osmotic stress and correlated these changes with systemic responses to water deprivation. We report that the rat does have a marked defect the of expression consistg of an ability to crease hypothalamic mRNA content response to severe osmotic stress. diabetes sipidus; Rattus norvegicus neuropeptide; messenger ribonucleic acid; METHODS RAT carries as a recessive trait the ability to synthesize detectable amounts of its magnocellular hypothalamic neurons (30). Homozygous have severe diabetes sipidus, which is corrected by replacement therapy (6). tic studies suggest that a sgle autosomal is responsible for the observed phenotype (25). Recently the DNA sequence of a obtaed from a rat has been reported (28). This lacks a sgle guanose residue the second exon of the prote-codg region, givg http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

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Publisher
The American Physiological Society
Copyright
Copyright © 1987 the American Physiological Society
ISSN
0193-1849
eISSN
1522-1555
Publisher site
See Article on Publisher Site

Abstract

MAJZOUB, JOSEPH A., ENRIQUE J. CARRAZANA, JANE S. SHULMAN, KAREN J. BAKER, AND RODICA L. EMANUEL. Defective of expression . Am. J. Physiol. 252 (Endocrol. Metab. 15): E637-E642, 1987.-The rat has severe diabetes sipidus due to an autosomal recessive trait resultg the ability to synthesize detectable amounts of hypothalamic . To determe whether this abnormality is due to a regulatory defect the rat’s , we studied changes the hypothalamic content of mRNA normal Long-Evans and homozygous subjected to osmotic stress and correlated these changes with systemic responses to water deprivation. We report that the rat does have a marked defect the of expression consistg of an ability to crease hypothalamic mRNA content response to severe osmotic stress. diabetes sipidus; Rattus norvegicus neuropeptide; messenger ribonucleic acid; METHODS RAT carries as a recessive trait the ability to synthesize detectable amounts of its magnocellular hypothalamic neurons (30). Homozygous have severe diabetes sipidus, which is corrected by replacement therapy (6). tic studies suggest that a sgle autosomal is responsible for the observed phenotype (25). Recently the DNA sequence of a obtaed from a rat has been reported (28). This lacks a sgle guanose residue the second exon of the prote-codg region, givg

Journal

AJP - Endocrinology and MetabolismThe American Physiological Society

Published: May 1, 1987

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