Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2001-4-3
pubmed:abstractText
Various types of collagen have been identified as potential ligands for the two mammalian discoidin domain receptor tyrosine kinases, DDR1 and DDR2. Here, we used a recombinant fusion protein between the extracellular domain of DDR1 and alkaline phosphatase to detect specific receptor binding sites during mouse development. Major sites of DDR1-binding activity, indicative of ligand expression, were found in skeletal bones, the skin, and the urogenital tract. Ligand expression in the uterus during implantation and in the mammary gland during pregnancy colocalized with the expression of the DDR1 receptor. The generation of DDR1-null mice by gene targeting yielded homozygous mutant animals that were viable but smaller in size than control littermates. The majority of mutant females were unable to bear offspring due to a lack of proper blastocyst implantation into the uterine wall. When implantation did occur, the mutant females were unable to lactate. Histological analysis showed that the alveolar epithelium failed to secrete milk proteins into the lumen of the mammary gland. The lactational defect appears to be caused by hyperproliferation and abnormal branching of mammary ducts. These results suggest that DDR1 is a key mediator of the stromal-epithelial interaction during ductal morphogenesis in the mammary gland.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-10352148, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-10380918, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-10647936, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-10681566, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-10783152, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-10970885, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-2065352, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-7522971, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-7635053, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-7845682, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-7845687, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-7848919, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-7937762, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8108131, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8127887, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8226977, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8302582, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8390675, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8397369, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8622863, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8796349, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-8977099, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9009201, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9075249, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9291576, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9291579, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9396043, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9607563, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9630227, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9659899, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9659900, http://linkedlifedata.com/resource/pubmed/commentcorrection/11283268-9684896
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0270-7306
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2906-17
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11283268-Animals, pubmed-meshheading:11283268-Base Sequence, pubmed-meshheading:11283268-Binding Sites, pubmed-meshheading:11283268-Collagen, pubmed-meshheading:11283268-DNA Probes, pubmed-meshheading:11283268-Embryo Implantation, pubmed-meshheading:11283268-Female, pubmed-meshheading:11283268-Gene Expression Regulation, Developmental, pubmed-meshheading:11283268-Lactation, pubmed-meshheading:11283268-Ligands, pubmed-meshheading:11283268-Mammary Glands, Animal, pubmed-meshheading:11283268-Mice, pubmed-meshheading:11283268-Mice, Inbred C57BL, pubmed-meshheading:11283268-Mice, Inbred ICR, pubmed-meshheading:11283268-Mice, Knockout, pubmed-meshheading:11283268-Pregnancy, pubmed-meshheading:11283268-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:11283268-Receptors, Mitogen, pubmed-meshheading:11283268-Recombinant Fusion Proteins
pubmed:year
2001
pubmed:articleTitle
Discoidin domain receptor 1 tyrosine kinase has an essential role in mammary gland development.
pubmed:affiliation
Programme in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5. W.Vogel@em.uni-frankfurt.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't