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- Bb88dc7c20cf1e590423d233a049c13d1 NCIT_P378 "NCI" @default.
- Bb88dc7c20cf1e590423d233a049c13d1 type Axiom @default.
- Bb88dc7c20cf1e590423d233a049c13d1 annotatedProperty IAO_0000115 @default.
- Bb88dc7c20cf1e590423d233a049c13d1 annotatedSource NCIT_C182011 @default.
- Bb88dc7c20cf1e590423d233a049c13d1 annotatedTarget "An orally bioavailable, small molecule, dual inhibitor of ataxia telangiectasia mutated kinase (ATM) and DNA-dependent protein kinase (DNA-PK), with potential radio-sensitizing and antineoplastic activities. Upon oral administration, ATM kinase/DNA-PK inhibitor XRD-0394 selectively targets, binds to and inhibits the activity of ATM and DNA-PK. This inhibits ATM-mediated signaling, which may prevent DNA damage checkpoint activation, disrupt DNA damage repair and induce tumor cell apoptosis. By disrupting DNA damage repair, this agent may sensitize tumor cells to radiotherapy and increase its anti-tumor activity. In addition, by inhibiting the activity of DNA-PK, this agent interferes with the non-homologous end joining (NHEJ) process which may prevent the repair of DNA double strand breaks (DSBs) caused by ionizing radiation. This may also increase radiotherapy cytotoxicity leading to enhanced tumor cell death. ATM, a serine/threonine protein kinase upregulated in a variety of cancer cell types, is activated in response to DNA damage and plays a key role in DNA-strand repair. DNA-PK plays a key role in the NHEJ pathway and DSB repair. The enhanced ability of tumor cells to repair DNA damage plays a major role in the resistance of tumor cells to radiotherapy." @default.