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http://purl.uniprot.org/citations/16311053http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16311053http://www.w3.org/2000/01/rdf-schema#comment"The roles of insulin-like growth factors (IGFs) in regulating growth and their modulation by six IGF binding proteins (IGFBP) are well established. IGFBP-5, the most abundant IGFBP stored in bone, is an important regulator of bone formation via IGF-dependent and -independent mechanisms. Two new proteins, four and a half lim (FHL)-2, a transcription modulator that interacts with IGFBP-5, and a disintegrin and metalloprotease (ADAM)-9, an IGFBP-5 protease, have been identified as potential regulators of IGFBP-5 action in bone. We tested the hypothesis that agents which modulate bone formation by regulating IGFBP-5 expression would also regulate FHL-2 and ADAM-9 expression in a coordinated manner. We evaluated the expression of IGFBP-5, FHL-2, and ADAM-9 by real-time reverse transcriptase (RT)-PCR during differentiation of mouse bone marrow stromal cells into osteoblasts and in response to treatment with bone formation modulators in the LSaOS human osteosarcoma cell line. IGFBP-5 and FHL-2 increased 4.3- and 3.0-fold (P < or = 0.01), respectively, during osteoblast differentiation. Dexamethasone (Dex), an inhibitor of bone formation, decreased IGFBP-5 and FHL-2 and increased ADAM-9 in LSaOS cells (P < or = 0.05). Bone morphogenic protein (BMP)-7, a stimulator of bone formation, increased IGFBP-5 and decreased ADAM-9 (P<0.01). To determine if BMP-7 would eliminate Dex inhibition of IGFBP-5, cells were treated with Dex+BMP-7. The BMP-7-induced increase in IGFBP-5 was reduced, but not eliminated, in the presence of Dex (P < or = 0.01), indicating that BMP-7 and Dex may regulate IGFBP-5 via different mechanisms. Transforming growth factor (TGF)-beta, a stimulator of bone formation, increased IGFBP-5 and FHL-2 expression (P < or = 0.01). IGF-I and TNF-alpha decreased expression of ADAM-9 (P<0.05). In conclusion, our findings are consistent with the hypothesis that FHL-2 and ADAM-9 are important modulators of IGFBP-5 actions and are, in part, regulated in a coordinated manner in bone."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.org/dc/terms/identifier"doi:10.1016/j.ghir.2005.10.001"xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/author"Mohan S."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/author"Winter E."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/author"Kramer A."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/author"Baylink D.J."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/author"Govoni K.E."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/author"Amaar Y.G."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/name"Growth Horm IGF Res"xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/pages"49-56"xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/title"Regulation of insulin-like growth factor binding protein-5, four and a half lim-2, and a disintegrin and metalloprotease-9 expression in osteoblasts."xsd:string
http://purl.uniprot.org/citations/16311053http://purl.uniprot.org/core/volume"16"xsd:string
http://purl.uniprot.org/citations/16311053http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16311053
http://purl.uniprot.org/citations/16311053http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16311053
http://purl.uniprot.org/uniprot/Q61072#attribution-B39B87279191B632E3F47E6BCD8D32D3http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/P11087#attribution-F35E632943A3BCE3F64EB3B1F13A01AFhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/O70433#attribution-F35E632943A3BCE3F64EB3B1F13A01AFhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/P05017#attribution-F35E632943A3BCE3F64EB3B1F13A01AFhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/P47878#attribution-F35E632943A3BCE3F64EB3B1F13A01AFhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/Q07079#attribution-F35E632943A3BCE3F64EB3B1F13A01AFhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/P09535#attribution-F35E632943A3BCE3F64EB3B1F13A01AFhttp://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/#_D3Z7M4-mappedCitation-16311053http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16311053
http://purl.uniprot.org/uniprot/#_A0A087WR06-mappedCitation-16311053http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16311053