loading...| Preferred Name | Apoptosis | |
| Synonyms |
PathwayType: signaling Organ: generic Description: Apoptosis is the genetically programmed pathway of cell death. Pathway is built manually using published studies. Pathway_Author: A. Nesterova ORCID:0000-0002-9448-8101 Organ_System: generic Tissue: generic Link: https://mammal-profservices.pathwaystudio.com/app/sd?urn=urn:agi-pathway:uuid-be878e67-d551-45ea-a23d-6170599173a9 NodeType: Pathway Notes: Headnote: Apoptosis is the genetically regulated programmed cell death which occurs in mulaticellular organisms as part of their normal development and functioning. There are at least two broad pathways, extrinsic and intrinsic, leading to apoptosis. In both pathways, the signaling results in activation of caspases which act in a proteolytic cascade to dismantle and remove the dying cell. Signaling description: The extrinsic pathway begins outside the cell and is often related to the signaling of death receptors (DR). The members of the DR family that have been thoroughly studied are TNFRSF10A, TNFRSF10B, TNFRSF1A, TNFRSF25, FAS, EDAR, and NGFR. They are distinguished by a cytoplasmic region termed the death domain (DD). When these receptors are coupled with their corresponding ligands, a number of molecules are recruited to the DD and activate the downstream signaling cascade. FAS, TNFRSF10A, and TNFRSF10B interact with FADD which activates CASP8. CASP10 is activated by a similar mechanism. Active CASP8 then triggers downstream caspases such as CASP3 and CASP7. TNFRSF1A, TNFRSF25, EDAR, and NGFR recruit TRADD as a platform adaptor and, in turn, assemble alternative signaling complexes through secondary adaptors. The intrinsic apoptosis pathway begins when an injury occurs within the cell and is often referred to as the mitochondrial pathway of apoptosis. CASP8, activated through DR signaling, can cleave BID protein which is a member of BCL2 family proteins in the mitochondrial membrane. BCL2 family proteins have an essential role in the life-or-death choice in the cellular fate. The BCL2 family includes both anti- and proapoptotic members and the balance between their activities regulate the release of apoptosis-promoting compounds such as AIFM1, ENDOG, DIABLO, and cytochrome c (CYCS) from mitochondria. In addition to DRs, growth factors also influence mitochondrial apoptosis via PI3K and AKT1 pathways. AKT1 is important in BAD regulation, which is a proapoptotic member of the BCL2 family and is involved in mitochondrial apoptosis. Outcome effects: CYCS is released from mitochondria to bind APAF1. This interaction forms a heptamer protein complex called the apoptosome which can bind to seven molecules of CASP9. Active CASP9 can cleave and consequently activate CASP3. Source: Cell Process CellType: generic |
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| ID |
urn:agi-pathway:uuid-be878e67-d551-45ea-a23d-6170599173a9 |
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| database_cross_reference |
PS:PathwayType PS:Description PS:Tissue PS:Pathway_Author PS:Link PS:CellType PS:Organ_System PS:NodeType PS:Notes PS:Organ PS:Source |
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| has_exact_synonym |
PathwayType: signaling Organ: generic Description: Apoptosis is the genetically programmed pathway of cell death. Pathway is built manually using published studies. Pathway_Author: A. Nesterova ORCID:0000-0002-9448-8101 Organ_System: generic Tissue: generic NodeType: Pathway Notes: Headnote: Apoptosis is the genetically regulated programmed cell death which occurs in mulaticellular organisms as part of their normal development and functioning. There are at least two broad pathways, extrinsic and intrinsic, leading to apoptosis. In both pathways, the signaling results in activation of caspases which act in a proteolytic cascade to dismantle and remove the dying cell. Signaling description: The extrinsic pathway begins outside the cell and is often related to the signaling of death receptors (DR). The members of the DR family that have been thoroughly studied are TNFRSF10A, TNFRSF10B, TNFRSF1A, TNFRSF25, FAS, EDAR, and NGFR. They are distinguished by a cytoplasmic region termed the death domain (DD). When these receptors are coupled with their corresponding ligands, a number of molecules are recruited to the DD and activate the downstream signaling cascade. FAS, TNFRSF10A, and TNFRSF10B interact with FADD which activates CASP8. CASP10 is activated by a similar mechanism. Active CASP8 then triggers downstream caspases such as CASP3 and CASP7. TNFRSF1A, TNFRSF25, EDAR, and NGFR recruit TRADD as a platform adaptor and, in turn, assemble alternative signaling complexes through secondary adaptors. The intrinsic apoptosis pathway begins when an injury occurs within the cell and is often referred to as the mitochondrial pathway of apoptosis. CASP8, activated through DR signaling, can cleave BID protein which is a member of BCL2 family proteins in the mitochondrial membrane. BCL2 family proteins have an essential role in the life-or-death choice in the cellular fate. The BCL2 family includes both anti- and proapoptotic members and the balance between their activities regulate the release of apoptosis-promoting compounds such as AIFM1, ENDOG, DIABLO, and cytochrome c (CYCS) from mitochondria. In addition to DRs, growth factors also influence mitochondrial apoptosis via PI3K and AKT1 pathways. AKT1 is important in BAD regulation, which is a proapoptotic member of the BCL2 family and is involved in mitochondrial apoptosis. Outcome effects: CYCS is released from mitochondria to bind APAF1. This interaction forms a heptamer protein complex called the apoptosome which can bind to seven molecules of CASP9. Active CASP9 can cleave and consequently activate CASP3. Source: Cell Process CellType: generic |
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| id |
urn:agi-pathway:uuid-be878e67-d551-45ea-a23d-6170599173a9 |
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| label |
Apoptosis |
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| notation |
uuid-be878e67-d551-45ea-a23d-6170599173a9 |
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| prefLabel |
Apoptosis |
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| treeView |
urn:agi-folder:a urn:agi-folder:mitochondria urn:agi-folder:apoptosis_and_cell_death urn:agi-folder:generic |
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| subClassOf |
urn:agi-folder:a urn:agi-folder:mitochondria urn:agi-folder:apoptosis_and_cell_death urn:agi-folder:generic |