Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-4-21
pubmed:abstractText
At weaning the mammary gland undergoes a reductive remodelling process (involution) which is associated with the cessation of milk protein gene expression and programmed cell death of milk-producing epithelial cells. Elevated nuclear protein kinase A (PKA) activity was observed from one day post-lactation, paralleled by increased c-fos, junB, junD and to a lesser extent c-jun mRNA levels. AP-1 DNA binding activity was transiently induced and the AP-1 complex was shown to consist principally of cFos/JunD. Oct-1 DNA binding activity and Oct-1 protein were gradually lost from the gland over the first 4 days of involution, whereas Oct-1 mRNA levels remained unchanged. Comparing nuclear extracts from normal mammary glands with nuclear extracts from glands which had been cleared of all epithelial cells 3 weeks after birth, revealed that PKA activation, AP-1 induction and Oct-1 inactivation all are dependent on the presence of the epithelial compartment. The increased Fos/Jun expression and the inactivation of Oct-1 may be consequences of the increased PKA activity. A similar induction of AP-1 (cFos/JunD) was also observed in the involuting rat ventral prostate pointing to a possible role for AP-1 in programmed cell death.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Caseins, http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP-Dependent Protein Kinases, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Hcfc1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Host Cell Factor C1, http://linkedlifedata.com/resource/pubmed/chemical/Milk Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Octamer Transcription Factor-1, http://linkedlifedata.com/resource/pubmed/chemical/Pou2f1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Pou2f1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-fos, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/whey protein
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1213-23
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:8134124-Animals, pubmed-meshheading:8134124-Apoptosis, pubmed-meshheading:8134124-Base Sequence, pubmed-meshheading:8134124-Caseins, pubmed-meshheading:8134124-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:8134124-DNA-Binding Proteins, pubmed-meshheading:8134124-Down-Regulation, pubmed-meshheading:8134124-Gene Expression Regulation, pubmed-meshheading:8134124-Host Cell Factor C1, pubmed-meshheading:8134124-Lactation, pubmed-meshheading:8134124-Male, pubmed-meshheading:8134124-Mammary Glands, Animal, pubmed-meshheading:8134124-Mice, pubmed-meshheading:8134124-Mice, Inbred BALB C, pubmed-meshheading:8134124-Milk Proteins, pubmed-meshheading:8134124-Molecular Sequence Data, pubmed-meshheading:8134124-Octamer Transcription Factor-1, pubmed-meshheading:8134124-Prostate, pubmed-meshheading:8134124-Protein Binding, pubmed-meshheading:8134124-Proto-Oncogene Proteins c-fos, pubmed-meshheading:8134124-Proto-Oncogene Proteins c-jun, pubmed-meshheading:8134124-Rats, pubmed-meshheading:8134124-Rats, Wistar, pubmed-meshheading:8134124-Transcription Factors, pubmed-meshheading:8134124-Weaning
pubmed:year
1994
pubmed:articleTitle
Protein kinase A and AP-1 (c-Fos/JunD) are induced during apoptosis of mouse mammary epithelial cells.
pubmed:affiliation
Laboratory for Clinical and Experimental Research, University of Bern, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't