Apoptosis pathway · HTML
Apoptosis — death-receptor, mitochondrial & cytotoxic-granule pathways. Three input routes converge on the executioner caspases. The extrinsic arm (FasL, TNF, TRAIL → Fas/TNFR1/DR4/DR5 → FADD/DISC → caspase-8/-10), the intrinsic arm (BH3-only proteins tipping the BAX/BAK vs Bcl-2 balance → cytochrome c → apoptosome → caspase-9), and the cytotoxic-granule arm (perforin-delivered granzyme B from NK / CTL / CAR-T cells) all activate caspase-3/7, cleaving PARP and unleashing CAD to fragment DNA. A caspase-independent branch (AIF, EndoG) and the RIPK1→MLKL necroptosis switch are shown alongside. Click any protein for the matching Assay Genie In Vivo antibody or ELISA kit.
Extrinsic (death-receptor) pathway. Death ligands — FasL, TNF, TRAIL — cluster their receptors Fas, TNFR1, DR4, DR5, which recruit FADD (and TRADD) to build the death-inducing signalling complex (DISC). This activates the initiator caspases caspase-8 and caspase-10, restrained by c-FLIP. They cleave executioner caspases directly and cleave Bid to tBid, wiring into the mitochondrial arm. At TNFR1 a survival complex (TRADD–RIPK1–TRAF2–cIAP1/2) instead drives NF-κB; when caspase-8 is blocked, RIPK1 engages RIPK3→MLKL to trigger necroptosis.
Intrinsic (mitochondrial) pathway. Stress and DNA damage act through p53 and BH3-only proteins (Bim, Bad, Puma, Noxa, tBid), which neutralise the guardians Bcl-2 / Bcl-xL / Mcl-1 and unleash BAX/BAK/BOK. Pore formation (MOMP) releases cytochrome c — which nucleates the APAF1 apoptosome and caspase-9 — plus SMAC and HtrA2, which neutralise the IAPs XIAP and survivin, and AIF / EndoG, which drive a caspase-independent route to the nucleus. Survival signals oppose this: AKT inactivates Bad; NF-κB induces FLIP, XIAP and Bcl-xL.
Cytotoxic-granule & execution. NK, CTL and CAR-T cells release perforin, which delivers granzyme B into the target to cleave Bid and caspase-3 directly. All routes converge on caspase-3 and caspase-7, which cleave PARP, inactivate ICAD to release the CAD nuclease, and dismantle the cell — DNA fragmentation, blebbing and phosphatidylserine exposure. This is the effector mechanism behind cytotoxic killing and depleting-antibody clearance. Assay Genie’s In Vivo anti-TNF blocks the death ligand, and every caspase, Bcl-2-family member, IAP, granzyme and adaptor is covered by an ELISA kit. For research use only; not for diagnostic or therapeutic procedures. Mouse targets shown where available.
Every protein node links to a product: In Vivo anti-TNF for the death ligand; the receptors, caspases, Bcl-2 family, IAPs, granzymes, adaptors and nucleases open the matching ELISA kit or antibody.