| pubmed-article:9888429 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9888429 | lifeskim:mentions | umls-concept:C0728866 | lld:lifeskim |
| pubmed-article:9888429 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:9888429 | lifeskim:mentions | umls-concept:C0599956 | lld:lifeskim |
| pubmed-article:9888429 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:9888429 | pubmed:dateCreated | 1999-1-20 | lld:pubmed |
| pubmed-article:9888429 | pubmed:abstractText | Previous studies have identified the cytoskeletal proteins actin and tubulin as potential cellular targets in the trabecular meshwork for novel glaucoma therapy. The authors and others have hypothesized that acto-myosin interactions may be important for outflow function. The current study was conducted to evaluate 2,3-butanedione 2-monoxime (BDM), a compound that interferes with acto-myosin function through the myosin adenosine triphosphatase (ATPase) reaction; 1-(5-isoquinolinylsulfonyl)-2-methyl-piperazine (H-7), a proposed myosin light-chain kinase inhibitor; and the direct actin disrupter, latrunculin B, in an outflow pathway cell culture and perfused excised eye model system. | lld:pubmed |
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| pubmed-article:9888429 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9888429 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9888429 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9888429 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9888429 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:9888429 | pubmed:issn | 0146-0404 | lld:pubmed |
| pubmed-article:9888429 | pubmed:author | pubmed-author:EpsteinD LDL | lld:pubmed |
| pubmed-article:9888429 | pubmed:author | pubmed-author:RobertsB CBC | lld:pubmed |
| pubmed-article:9888429 | pubmed:author | pubmed-author:RowletteL LLL | lld:pubmed |
| pubmed-article:9888429 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9888429 | pubmed:volume | 40 | lld:pubmed |
| pubmed-article:9888429 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9888429 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9888429 | pubmed:pagination | 74-81 | lld:pubmed |
| pubmed-article:9888429 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9888429 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:9888429 | pubmed:articleTitle | Acto-myosin drug effects and aqueous outflow function. | lld:pubmed |
| pubmed-article:9888429 | pubmed:affiliation | Department of Ophthalmology, Duke University Medical Center, Duke University Eye Center, Durham, North Carolina 27710, USA. | lld:pubmed |
| pubmed-article:9888429 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9888429 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9888429 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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