| pubmed-article:2207264 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2207264 | lifeskim:mentions | umls-concept:C0034678 | lld:lifeskim |
| pubmed-article:2207264 | lifeskim:mentions | umls-concept:C0596901 | lld:lifeskim |
| pubmed-article:2207264 | lifeskim:mentions | umls-concept:C0029005 | lld:lifeskim |
| pubmed-article:2207264 | lifeskim:mentions | umls-concept:C0235169 | lld:lifeskim |
| pubmed-article:2207264 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:2207264 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:2207264 | pubmed:dateCreated | 1990-11-21 | lld:pubmed |
| pubmed-article:2207264 | pubmed:abstractText | Two electrode voltage clamp conditions were used to study the early effects on ionic membrane channels of the intracellularly injected proto-oncogenic form of c-Ha-ras (c-ras) and its oncogenic counterpart v-Ha-ras (v-ras). These experiments were conducted on isolated somata of identified fully differentiated neurons of the sea snail Hermissenda. 20 min after c-ras, and 10 min after v-ras intracellular injections into type B medial photoreceptors of Hermissenda, the peak amplitude of two outward potassium currents (IA and IC), across the isolated Type B soma membrane begin to decrease. These two currents have been previously isolated by differences in activation and inactivation kinetics and their response to pharmacological blockers. c- or v-ras injections did not have any effect on a voltage-dependent inward calcium current. Reduction of IA preceded that of IC. Current reductions due to c-ras, but not to v-ras injection reversed spontaneously after 40 min. The voltage dependence of the steady state inactivation of IA shifted toward more negative potentials with ras injections. Ras-mediated cell transformations therefore, could involve, perhaps as initial events, prolonged modification of membrane currents. | lld:pubmed |
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| pubmed-article:2207264 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2207264 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2207264 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2207264 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2207264 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2207264 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:2207264 | pubmed:issn | 0006-3495 | lld:pubmed |
| pubmed-article:2207264 | pubmed:author | pubmed-author:AlkonD LDL | lld:pubmed |
| pubmed-article:2207264 | pubmed:author | pubmed-author:LowyD RDR | lld:pubmed |
| pubmed-article:2207264 | pubmed:author | pubmed-author:CollinCC | lld:pubmed |
| pubmed-article:2207264 | pubmed:author | pubmed-author:PapageorgeA... | lld:pubmed |
| pubmed-article:2207264 | pubmed:author | pubmed-author:SakakibaraMM | lld:pubmed |
| pubmed-article:2207264 | pubmed:author | pubmed-author:HuddieP LPL | lld:pubmed |
| pubmed-article:2207264 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2207264 | pubmed:volume | 58 | lld:pubmed |
| pubmed-article:2207264 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2207264 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2207264 | pubmed:pagination | 785-90 | lld:pubmed |
| pubmed-article:2207264 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2207264 | pubmed:meshHeading | pubmed-meshheading:2207264-... | lld:pubmed |
| pubmed-article:2207264 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2207264 | pubmed:articleTitle | Early regulation of membrane excitability by ras oncogene proteins. | lld:pubmed |
| pubmed-article:2207264 | pubmed:affiliation | National Institutes of Health, Laboratory of Molecular and Cellular Neurobiology, Bethesda, Maryland 20892. | lld:pubmed |
| pubmed-article:2207264 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2207264 | pubmed:publicationType | In Vitro | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2207264 | lld:pubmed |
