pubmed-article:20603072 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C0007610 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C1274040 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C1538577 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C0205210 | lld:lifeskim |
pubmed-article:20603072 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
pubmed-article:20603072 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:20603072 | pubmed:dateCreated | 2010-7-6 | lld:pubmed |
pubmed-article:20603072 | pubmed:abstractText | The abundant nuclear enzyme PARP-1, a multifunctional regulator of chromatin structure, transcription, and genomic integrity, plays key roles in a wide variety of processes in the nucleus. Recent studies have begun to connect the molecular functions of PARP-1 to specific physiological and pathological outcomes, many of which can be altered by an expanding array of chemical inhibitors of PARP enzymatic activity. | lld:pubmed |
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