| pubmed-article:12526804 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12526804 | lifeskim:mentions | umls-concept:C1882071 | lld:lifeskim |
| pubmed-article:12526804 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:12526804 | lifeskim:mentions | umls-concept:C0008546 | lld:lifeskim |
| pubmed-article:12526804 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:12526804 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:12526804 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:12526804 | pubmed:dateCreated | 2003-1-15 | lld:pubmed |
| pubmed-article:12526804 | pubmed:abstractText | We suggest that common principles underlie both cellular signaling networks and chromatin. To exemplify similarities, we focus on signaling complexes that form at membrane receptors and on nucleosomes. Multiple signal-transducing modifications on side chain residues of receptor tyrosine kinases (RTKs) and histone proteins are used to create docking sites that facilitate proximal relations of enzymes and their substrates. We argue that multiple histone modifications, like RTK modifications, promote switch-like behavior and ensure robustness of the signal, and we compare this interpretation with the histone code hypothesis. This view provides insight into chromatin function and epigenetic inheritance. | lld:pubmed |
| pubmed-article:12526804 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12526804 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12526804 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12526804 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12526804 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12526804 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:12526804 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:12526804 | pubmed:author | pubmed-author:SchreiberStua... | lld:pubmed |
| pubmed-article:12526804 | pubmed:author | pubmed-author:BernsteinBrad... | lld:pubmed |
| pubmed-article:12526804 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12526804 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:12526804 | pubmed:volume | 111 | lld:pubmed |
| pubmed-article:12526804 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12526804 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12526804 | pubmed:pagination | 771-8 | lld:pubmed |
| pubmed-article:12526804 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:meshHeading | pubmed-meshheading:12526804... | lld:pubmed |
| pubmed-article:12526804 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12526804 | pubmed:articleTitle | Signaling network model of chromatin. | lld:pubmed |
| pubmed-article:12526804 | pubmed:affiliation | Department of Chemistry and Chemical Biology and Howard Hughes Medical Institute, Harvard University, 12 Oxford Street, Cambridge, MA 02138, USA. sls@slsiris.harvard.edu | lld:pubmed |
| pubmed-article:12526804 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12526804 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12526804 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:12526804 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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