Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-2-22
pubmed:abstractText
Bone morphogenetic protein (BMP) controls osteoblast proliferation and differentiation through Smad proteins. Here we show that Tob, a member of the emerging family of antiproliferative proteins, is a negative regulator of BMP/Smad signaling in osteoblasts. Mice carrying a targeted deletion of the tob gene have a greater bone mass resulting from increased numbers of osteoblasts. Orthotopic bone formation in response to BMP2 is elevated in tob-deficient mice. Overproduction of Tob represses BMP2-induced, Smad-mediated transcriptional activation. Finally, Tob associates with receptor-regulated Smads (Smad1, 5, and 8) and colocalizes with these Smads in the nuclear bodies upon BMP2 stimulation. The results indicate that Tob negatively regulates osteoblast proliferation and differentiation by suppressing the activity of the receptor-regulated Smad proteins.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Bmp2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Protein 2, http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Protein 7, http://linkedlifedata.com/resource/pubmed/chemical/Bone Morphogenetic Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Ligands, http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins, http://linkedlifedata.com/resource/pubmed/chemical/SMAD8 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Smad Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Smad1 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Smad1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Smad5 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Smad5 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Smad8 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Smad9 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Tob1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0092-8674
pubmed:author
pubmed:issnType
Print
pubmed:day
22
pubmed:volume
103
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1085-97
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11163184-Alleles, pubmed-meshheading:11163184-Animals, pubmed-meshheading:11163184-Bone Morphogenetic Protein 2, pubmed-meshheading:11163184-Bone Morphogenetic Protein 7, pubmed-meshheading:11163184-Bone Morphogenetic Proteins, pubmed-meshheading:11163184-Bone Remodeling, pubmed-meshheading:11163184-Carrier Proteins, pubmed-meshheading:11163184-Cell Differentiation, pubmed-meshheading:11163184-Cell Division, pubmed-meshheading:11163184-Cell Size, pubmed-meshheading:11163184-DNA-Binding Proteins, pubmed-meshheading:11163184-Gene Expression, pubmed-meshheading:11163184-Germ-Line Mutation, pubmed-meshheading:11163184-Ligands, pubmed-meshheading:11163184-Mice, pubmed-meshheading:11163184-Mice, Inbred C57BL, pubmed-meshheading:11163184-Mice, Knockout, pubmed-meshheading:11163184-Osteoblasts, pubmed-meshheading:11163184-Phosphoproteins, pubmed-meshheading:11163184-Signal Transduction, pubmed-meshheading:11163184-Skull, pubmed-meshheading:11163184-Smad Proteins, pubmed-meshheading:11163184-Smad1 Protein, pubmed-meshheading:11163184-Smad5 Protein, pubmed-meshheading:11163184-Smad8 Protein, pubmed-meshheading:11163184-Trans-Activators, pubmed-meshheading:11163184-Transcription, Genetic, pubmed-meshheading:11163184-Transforming Growth Factor beta
pubmed:year
2000
pubmed:articleTitle
Negative regulation of BMP/Smad signaling by Tob in osteoblasts.
pubmed:affiliation
Department of Oncology, The Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't