pubmed-article:2854946 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C0178719 | lld:lifeskim |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C0052088 | lld:lifeskim |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C0300926 | lld:lifeskim |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C1158430 | lld:lifeskim |
pubmed-article:2854946 | lifeskim:mentions | umls-concept:C0597484 | lld:lifeskim |
pubmed-article:2854946 | pubmed:dateCreated | 1989-7-3 | lld:pubmed |
pubmed-article:2854946 | pubmed:abstractText | NIH3T3 cells were transfected with activated Ha-ras and the corresponding proto-oncogene was subjected to transcriptional control by recombination in vitro with MMTV-LTR. Induction of p21ras expression in quiescent cells by dexamethasone causes an increased turnover of phosphatidylinositol 4,5-bisphosphate with a concomitant rise in inositol phosphates, and an activation of the Na+/H+-antiporter. Addition of serum growth factors to dexamethasone treated cells does not result in an additional stimulation of phosphatidylinositol metabolism or Na+/H+-exchange. There is also a desensitization to exogenous growth factors of the intracellular Ca2+-mobilizing system, leading to a depression of the transitory increase in cytosolic Ca2+ after addition of serum growth factors. None of these effects are seen after expression of the Ha-ras proto-oncogene. Results are discussed as indicating a constitutive growth factor independent activation of growth factor signal transduction by the activated Ha-ras. | lld:pubmed |
pubmed-article:2854946 | pubmed:language | eng | lld:pubmed |
pubmed-article:2854946 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:2854946 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2854946 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2854946 | pubmed:issn | 0065-2571 | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:GrunickeHH | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:GronerBB | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:MalyKK | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:DopplerWW | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:OberhuberHH | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:KEMPHJ AJA | lld:pubmed |
pubmed-article:2854946 | pubmed:author | pubmed-author:HoflacherJJ | lld:pubmed |
pubmed-article:2854946 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2854946 | pubmed:volume | 27 | lld:pubmed |
pubmed-article:2854946 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2854946 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2854946 | pubmed:pagination | 121-31 | lld:pubmed |
pubmed-article:2854946 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:meshHeading | pubmed-meshheading:2854946-... | lld:pubmed |
pubmed-article:2854946 | pubmed:year | 1988 | lld:pubmed |
pubmed-article:2854946 | pubmed:articleTitle | Effect of Ha-ras on phosphatidylinositol metabolism, Na+/H+-antiporter and mobilization of intracellular calcium. | lld:pubmed |
pubmed-article:2854946 | pubmed:affiliation | Institute of Medical Chemistry and Biochemistry, University of Innsbruck, Austria. | lld:pubmed |
pubmed-article:2854946 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2854946 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |