| pubmed-article:1830205 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C1704256 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C0014442 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C0017636 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C0597304 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C1515406 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C1707455 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:1830205 | lifeskim:mentions | umls-concept:C0205275 | lld:lifeskim |
| pubmed-article:1830205 | pubmed:dateCreated | 1991-8-21 | lld:pubmed |
| pubmed-article:1830205 | pubmed:abstractText | Transforming growth factor-beta (TGF-beta), a regulator of cell growth and differentiation, is secreted by most cultured cells in latent form (L-TGF-beta). Activation of L-TGF-beta can be achieved by various physico-chemical treatments, including acidification, alkalinization, heating and chaotropic agents. Proposed physiological activators include proteinases and glycosidases, which, however, only lead to limited activation (15-20% of the total TGF-beta activity after acidic activation). In the present study L-TGF-beta 1 partially purified from human platelets was not activated by treatment with neuraminidase or the proteinases plasmin, endoproteinase Arg-C, elastase and chymotrypsin. The mechanism of activation of L-TGF-beta was further assessed by using the human glioblastoma cell line 308, which releases biologically active TGF-beta 2. Factor(s) secreted by 308 glioblastoma cells were found to be able to activate partially purified L-TGF-beta 1 from human platelets. Our finding may prove to constitute a physiologically relevant mechanism for the activation of latent forms of TGF-beta in vivo. | lld:pubmed |
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| pubmed-article:1830205 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1830205 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1830205 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1830205 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1830205 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1830205 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1830205 | pubmed:issn | 0264-6021 | lld:pubmed |
| pubmed-article:1830205 | pubmed:author | pubmed-author:FontanaAA | lld:pubmed |
| pubmed-article:1830205 | pubmed:author | pubmed-author:HuberDD | lld:pubmed |
| pubmed-article:1830205 | pubmed:author | pubmed-author:BodmerSS | lld:pubmed |
| pubmed-article:1830205 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1830205 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1830205 | pubmed:volume | 277 ( Pt 1) | lld:pubmed |
| pubmed-article:1830205 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1830205 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1830205 | pubmed:pagination | 165-73 | lld:pubmed |
| pubmed-article:1830205 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:1830205 | pubmed:meshHeading | pubmed-meshheading:1830205-... | lld:pubmed |
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| pubmed-article:1830205 | pubmed:meshHeading | pubmed-meshheading:1830205-... | lld:pubmed |
| pubmed-article:1830205 | pubmed:meshHeading | pubmed-meshheading:1830205-... | lld:pubmed |
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| pubmed-article:1830205 | pubmed:meshHeading | pubmed-meshheading:1830205-... | lld:pubmed |
| pubmed-article:1830205 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1830205 | pubmed:articleTitle | Activation of human platelet-derived latent transforming growth factor-beta 1 by human glioblastoma cells. Comparison with proteolytic and glycosidic enzymes. | lld:pubmed |
| pubmed-article:1830205 | pubmed:affiliation | Department of Internal Medicine, University Hospital of Zürich, Switzerland. | lld:pubmed |
| pubmed-article:1830205 | pubmed:publicationType | Journal Article | lld:pubmed |
