Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1993-9-10
pubmed:abstractText
Studies indicate that G proteins are likely involved in the signal transduction pathway for prolactin's stimulation of mitogenesis in Nb2 cells. In the mammary gland, little is known about the possible role of G proteins in the prolactin (PRL) stimulation of milk product synthesis. Therefore, the effects of cholera and pertussis toxin, enzymes that modify G protein activity, were tested on several actions of prolactin on mouse mammary tissue in culture. At concentration of 0.1-0.5 micrograms/ml, cholera toxin stimulated ornithine decarboxylase activity in a dose-response fashion; when tested in concert, cholera toxin and prolactin caused an additive response. Cholera toxin by itself did not affect the rate of lactose synthesis, but at concentrations above 0.5 micrograms/ml, it attenuated the magnitude of the prolactin stimulation of lactose synthesis. Pertussis toxin (0-0.5 micrograms/ml), both by itself and in concert with PRL, had no effect on ornithine decarboxylase activity. At concentrations of 25 ng/ml and above, pertussis toxin inhibited the PRL stimulation of lactose synthesis, whereas at 0.2 and 0.5 micrograms/ml, pertussis toxin abolished the PRL response. These observations suggest that a G protein, but not Gs, may be involved in prolactin's mechanism of signal transduction in the mouse mammary gland.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0037-9727
pubmed:author
pubmed:issnType
Print
pubmed:volume
203
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
424-7
pubmed:dateRevised
2007-11-2
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Effects of cholera and pertussis toxins on prolactin stimulation of lactose synthesis and ornithine decarboxylase activity in mouse mammary gland explants.
pubmed:affiliation
Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48201.
pubmed:publicationType
Journal Article