apoptotic dna-fragmentation and tissue homeostasis
| PAG Title | apoptotic dna-fragmentation and tissue homeostasis |
| PAG ID | WAG000657 |
| Type | P |
| Source Link |  BioCarta |
| Publication Reference | NA |
| PAG Description | Apoptotic cell death can be triggered by many different cellular stimuli, resulting in activation of apoptotic sigling pathways including caspases (see Caspase Cascade pathway) and mitochondria (see Role of Mitochondria in Apoptotic Sigling pathway). A cellular response that is characteristic of apoptosis is fragmentation of the nuclear genome to create a nucleosomal ladder. This activity is conducted by multiple nucleases activated by apoptotic sigling pathways. One nuclease involved in apoptosis is D fragmentation factor (DFF), a caspase-activated Dse (CAD). DFF/CAD is activated through cleavage of its associated inhibitor ICAD by caspases proteases during apoptosis. DFF/CAD interacts with chromatin components such as topo II and histone H1 to condense chromatin structure and perhaps recruit CAD to chromatin. Another apoptosis activated protease is endonuclease G, EndoG. EndoG is encoded in the nuclear genome but is localized to mitochondria in normal cells. EndoG may play a role in the replication of the mitochondrial genome, as well as in apoptosis. Apoptotic sigling causes the release of EndoG from mitochondria. Mitochondria are involved in apoptotic sigling in other ways as well, through the release of cytochrome c induced by Bid to activate the caspase protease cascade. These pathways are independent since the EndoG pathway still occurs in cells lacking DFF. |
| Species | Homo sapiens |
| Quality Metric Scores | nCoCo Score: 914 |
| Information Content | Rich |
| Other IDs | |
| Base PAG ID | WAG000657 |
| Human Phenotyte Annotation | |
| Curator | PAGER curation team |
| Curator Contact | PAGER-contact@googlegroups.com |
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