ATP-dependent chromatin remodeling enzymes are a rapidly emerging therapeutic target. Components of SWI/SNF, the most commonly studied chromatin remodeling complex, are mutated in ~20% of all human cancers. Traditional assays used to identify chromatin remodeling inhibitors indirectly measure ATP consumption. This makes them prone to identification of nonspecific inhibitors of ATP-dependent enzymes. Further, these assays do not directly monitor chromatin remodeling activity. Therefore, there is a need in the field for defined nucleosome substrates that can be used to directly quantify chromatin remodeling activity.
|ARID1A||Ovarian, hepatocellular, bladder, gastric, endometrioid, pancreatic, colon, lung, neuroblastoma, Burkitt lymphoma|
|ARID1B||Melanoma, neuroblastoma, hepatocellular, pancreatic, liver|
|PBRM1||Renal cell carcinoma, breast, gastic, pancreatic|
|SMARCA2||Lung, colon, breast|
|SMARCA4||Lung medulloblastoma, Burkitt lymphoma, SCCOHT|
|SMARCB1||Rhabdoid tumor, familial schwannomatosis|
|Adapted from Heming et al.|
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