pubmed-article:7683518 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C0036536 | lld:lifeskim |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C0036537 | lld:lifeskim |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C0007595 | lld:lifeskim |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C0074825 | lld:lifeskim |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
pubmed-article:7683518 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:7683518 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:7683518 | pubmed:dateCreated | 1993-6-9 | lld:pubmed |
pubmed-article:7683518 | pubmed:abstractText | The ability of IGF binding proteins (IGFBP) to modulate cell growth and IGF-I responsiveness of epithelial cells was examined using the Madin-Darby bovine kidney (MDBK) cell line. The predominant IGFBP present in conditioned media (CM) of untreated cells was found to be IGFBP-2. Following exposure to forskolin, the abundance of IGFBP-2 in CM was decreased, while IGFBP-3 and -4 were induced. These changes corresponded with alterations in mRNA abundance. Growth of MDBK cells in serum-free media was stimulated by addition of 2.5 to 50 ng/ml of IGF-I in a dose responsive manner. Coincubation with equimolar amounts of IGF-I and exogenous bovine IGFBP-3 potentiated the growth response observed with IGF-I alone. In order to alter endogenous IGFBP-3 secretion, cells were exposed to transfection with an expression vector containing sense IGFBP-3 cDNA. Following selection and amplification with methotrexate, cells underwent a permanent alteration in cell morphology, exhibiting characteristics of transporting epithelia. This was associated with secretion of IGFBP-3 under basal conditions. Secretion of IGFBP-3 was due to expression of endogenous IGFBP-3 and not to expression of the transgene. Cells expressing IGFBP-3 under basal conditions grew slower in serum, but were more responsive to 100 ng/ml of IGF-1 in serum-free media compared to wild-type MDBK cells. The role of IGFBP-3 in mediating these responses requires further study. | lld:pubmed |
pubmed-article:7683518 | pubmed:language | eng | lld:pubmed |
pubmed-article:7683518 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7683518 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7683518 | pubmed:month | Mar | lld:pubmed |
pubmed-article:7683518 | pubmed:issn | 0956-523X | lld:pubmed |
pubmed-article:7683518 | pubmed:author | pubmed-author:ClemmonsD RDR | lld:pubmed |
pubmed-article:7683518 | pubmed:author | pubmed-author:CohickW SWS | lld:pubmed |
pubmed-article:7683518 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7683518 | pubmed:volume | 3 | lld:pubmed |
pubmed-article:7683518 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7683518 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7683518 | pubmed:pagination | 20-3 | lld:pubmed |
pubmed-article:7683518 | pubmed:dateRevised | 2004-11-17 | lld:pubmed |
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pubmed-article:7683518 | pubmed:year | 1993 | lld:pubmed |
pubmed-article:7683518 | pubmed:articleTitle | Regulation of IGFBP secretion and modulation of cell growth in MDBK cells. | lld:pubmed |
pubmed-article:7683518 | pubmed:affiliation | University of North Carolina School of Medicine, Division of Endocrinology, Chapel Hill 27599-7170. | lld:pubmed |
pubmed-article:7683518 | pubmed:publicationType | Journal Article | lld:pubmed |