| pubmed-article:1549349 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0031511 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0027754 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0085262 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0027752 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0376315 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:1549349 | lifeskim:mentions | umls-concept:C0439831 | lld:lifeskim |
| pubmed-article:1549349 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1549349 | pubmed:dateCreated | 1992-4-20 | lld:pubmed |
| pubmed-article:1549349 | pubmed:abstractText | The ras gene product (p21) is thought to transduce signals from various growth and differentiation factors. p21 is a GTP-binding protein, and its activity is regulated by the bound GDP/GTP ratio. We analysed p21-bound nucleotides in cell lysates of rat pheochromocytoma cell line PC12 cells stimulated with various factors. Nerve growth factors (NGF) rapidly increased the relative amount of active p21-GTP complex to as much as 20% of the total amount of p21 within 2 min. The amount of p21-GTP then declined to 8% after 10 min, and this level was sustained for at least 2 h. Epidermal growth factor (EGF) also stimulated a rapid accumulation of p21-GTP to the same extent as seen with NGF, but the amount of p21-GTP declined to 5% after 10 min and gradually returned to the basal level within 60 min. In contrast, basic fibroblast growth factor, interleukin 6 and dibutyryl cAMP, which induce neuronal differentiation of PC12 cells, did not stimulate the accumulation of p21-GTP at any time point examined. Phorbol 12-myristate 13-acetate also had no effect. Interestingly, the protein kinase inhibitor K-252a specifically suppressed the NGF-induced accumulation of p21-GTP, but did not suppress the EGF-induced response. These results strongly suggest that an active p21-GTP complex transduces the differentiation signal from NGF. It may also be suggested that the process of activating p21 is mediated by a K-252a-sensitive protein kinase(s). | lld:pubmed |
| pubmed-article:1549349 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1549349 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1549349 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1549349 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1549349 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:1549349 | pubmed:issn | 0950-9232 | lld:pubmed |
| pubmed-article:1549349 | pubmed:author | pubmed-author:NakamuraSS | lld:pubmed |
| pubmed-article:1549349 | pubmed:author | pubmed-author:HattoriSS | lld:pubmed |
| pubmed-article:1549349 | pubmed:author | pubmed-author:MuroyaKK | lld:pubmed |
| pubmed-article:1549349 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1549349 | pubmed:volume | 7 | lld:pubmed |
| pubmed-article:1549349 | pubmed:geneSymbol | ras | lld:pubmed |
| pubmed-article:1549349 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1549349 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1549349 | pubmed:pagination | 277-81 | lld:pubmed |
| pubmed-article:1549349 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:1549349 | pubmed:meshHeading | pubmed-meshheading:1549349-... | lld:pubmed |
| pubmed-article:1549349 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1549349 | pubmed:articleTitle | Nerve growth factor induces rapid accumulation of the GTP-bound form of p21ras in rat pheochromocytoma PC12 cells. | lld:pubmed |
| pubmed-article:1549349 | pubmed:affiliation | Division of Biochemistry and Cellular Biology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. | lld:pubmed |
| pubmed-article:1549349 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1549349 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1549349 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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