Apoptosis PCR array
| 【Numbering】BKMI100015 | 【CAS】CAS | ||
| 【Item No.】BKMI100015-1 | 【specification】 | ||
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[Main advantages] Apoptosis is a morphological phenomenon. When observed by optical or electron microscopy, features of apoptotic cells include stained nuclei rupture, plasma membrane foaming, or cell ruffling. Eventually, the cells divide into apoptotic bodies that are cleared by phagocytosis without triggering an inflammatory response.
Apoptosis consists of two different pathways: the extrinsic pathway (death receptor pathway) and the intrinsic pathway (mitochondrial pathway).
1. extrinsic pathway (death receptor pathway)
The extrinsic pathway is initiated by the death receptors and the related ligand on the cell surface. Death receptors consists of TNFR family members (TNFR 1 / 2, Fas, DR3 / 4 / 5, etc.), and their related ligands include TNF- α, FasL, TRAIL, TWEAK, etc. Ligand binding induces receptor activation, leading to the formation of a death-inducing signaling complex (DISC), which activates pro-caspase. Members of this complex include the bridging proteins FADD and TRADD, which recruit and activate caspase-8 / caspase-10 and can then activate the downstream effectors caspase (caspase-3, caspase-7). The activated caspase can directly degrade structural and functional proteins in cells, causing apoptosis.
2. Internal pathway (mitochondrial pathway)
The Intrinsic apoptotic pathway involves many conserved signaling proteins and depends on mitochondrial integrity. This process is tightly regulated by the balance between the protein activities in the Bcl-2 family, and the Bcl-2 family consists of pro-apoptotic (Bax, Bak, Bad, Bid, Puma, Bim, and Noxa) and anti-apoptotic (Bcl-2 Bcl-2, Bcl-xL, Bcl-w, Mcl-1) factors. Apoptosis is triggered when members of the proapoptotic family with BH 3 domains (eg, BAD, BID, and BIM) are activated during cellular stress by expression changes or by post-translational modifications. Then the pro-apoptotic proteins BAX and BAK induce changes in the mitochondrial outer membrane permeability (MOMP), leading to the release of cytochrome c from the intermembrane space of the organelle. Free cytochrome c then forms a complex with Apaf-1, which activates caspase-9 and triggers a series of apoptotic events.
Both the intrinsic and extrinsic pathways ultimately depend on the protease activity of specific members of the caspase family. These caspases fall into two major groups."Initiators" caspases-2, -8, -9, -10 and-12 are tightly coupled to upstream pro-apoptotic signals and act by cleavage and activating downstream "executors" caspases-3, -6 and-7, modifying the proteins ultimately responsible for cellular breakdown
Message
Apoptosis consists of two different pathways: the extrinsic pathway (death receptor pathway) and the intrinsic pathway (mitochondrial pathway).
1. extrinsic pathway (death receptor pathway)
The extrinsic pathway is initiated by the death receptors and the related ligand on the cell surface. Death receptors consists of TNFR family members (TNFR 1 / 2, Fas, DR3 / 4 / 5, etc.), and their related ligands include TNF- α, FasL, TRAIL, TWEAK, etc. Ligand binding induces receptor activation, leading to the formation of a death-inducing signaling complex (DISC), which activates pro-caspase. Members of this complex include the bridging proteins FADD and TRADD, which recruit and activate caspase-8 / caspase-10 and can then activate the downstream effectors caspase (caspase-3, caspase-7). The activated caspase can directly degrade structural and functional proteins in cells, causing apoptosis.
2. Internal pathway (mitochondrial pathway)
The Intrinsic apoptotic pathway involves many conserved signaling proteins and depends on mitochondrial integrity. This process is tightly regulated by the balance between the protein activities in the Bcl-2 family, and the Bcl-2 family consists of pro-apoptotic (Bax, Bak, Bad, Bid, Puma, Bim, and Noxa) and anti-apoptotic (Bcl-2 Bcl-2, Bcl-xL, Bcl-w, Mcl-1) factors. Apoptosis is triggered when members of the proapoptotic family with BH 3 domains (eg, BAD, BID, and BIM) are activated during cellular stress by expression changes or by post-translational modifications. Then the pro-apoptotic proteins BAX and BAK induce changes in the mitochondrial outer membrane permeability (MOMP), leading to the release of cytochrome c from the intermembrane space of the organelle. Free cytochrome c then forms a complex with Apaf-1, which activates caspase-9 and triggers a series of apoptotic events.
Both the intrinsic and extrinsic pathways ultimately depend on the protease activity of specific members of the caspase family. These caspases fall into two major groups."Initiators" caspases-2, -8, -9, -10 and-12 are tightly coupled to upstream pro-apoptotic signals and act by cleavage and activating downstream "executors" caspases-3, -6 and-7, modifying the proteins ultimately responsible for cellular breakdown
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