Linked Life Data

11259135

Source:http://linkedlifedata.com/resource/pubmed/id/11259135

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-3-22
pubmed:abstractText
The development of a mouse line deficient in the PRL receptor (PRLR) would be an ideal means to better understand the multiple functions of prolactin. We were worried initially that removal of the PRLR from the mouse genome might be lethal and were surprised to find this not to be the case. We identified numerous deficiencies in PRLR knockout (KO) animals. Female homozygous mice are completely infertile and lack normal mammary development, while hemizygotes are unable to lactate following their first pregnancy. PRLR KO males and females have markedly elevated (30- to 100-fold) serum prolactin levels and in some instances pituitary hyperplasia is present. Maternal behavior is severely affected in both hemizygous and heterozygous animals. Bone formation is reduced in young animals and adults (males and females). Recently, we noticed that older KO animals show a slight reduction in body weight which appears to be due to reduced abdominal fat deposition.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0091-3022
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
140-5
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Implications of multiple phenotypes observed in prolactin receptor knockout mice.
pubmed:affiliation
INSERM Unité 344-Endocrinologie Moléculaire, Faculté de Médecine Necker, 156 rue de Vaugirard, Paris Cedex, 75730, France. kelly@necker.fr
pubmed:publicationType
Journal Article, Review