|Pro- & Anti- apoptotic||Tumor Protein 53 (TP53)||
Transcriptionally regulates target genes that induce cell cycle|
arrest, apoptosis, senescence, DNA repair, or changes in
metabolism in response to cellular stresses.
Tumor Necrosis Factor
Binds and functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR to regulate cell proliferation, differentiation,|
|PRKCQ||Protein kinase C family member; substrate for Caspase-3; phosphorylates BAD and required to activate NFκB (via CARD11 phosphorylation) and AP-1.|
|Pro-apoptotic||FAS & FAS Ligand (FASL)||
Death domain-containing receptor, binding of FASL to FAS|
allows the formation of a death-inducing signaling complex.
Gene family involved in the execution of apoptosis. There are 2|
classes of caspases, which include: initiators (e.g., CASP2, CASP8, CASP9, and CASP10) and effectors (e.g., CASP3, CASP6, CASP7). Initiator caspases activate pro-forms of effector caspases,
enabling effectors to trigger the apoptosis process.
family, member 8)
CARD family protein; involved in various pathways which|
regulate caspases or NFκB; isoforms interact with caspases to
|BCL2-associated X (BAX)||
Forms a heterodimer with BCL2 and functions as an apoptotic|
activator involved mitochondrial release of cytochrome c.
Induces apoptosis by increasing cytochrome c release; interacts|
with the TP53 after exposure to cell stress.
BCL2-associated agonist of
cell death (BAD)
|Forms heterodimers with BCLXL and BCL2 to reverse their death repressor activity.|
|BCL2-like 10 (BCL2L10)||
Interacts with BCL2 proteins (e.g., BCL2, BCL2L1/BCLXL, and|
|BCL2-like 11 (BCL2L11)||
(aka BIM); Interacts with other members of the BCL2 protein|
family (e.g., BCL2, BCL2L1/BCLXL, and MCL1) to act as an
|BCL2-like 14 (BCL2L14)||
Apoptosis facilitator; interacts with BCL2 family members; p53-|
BH3 interacting domain
death agonist (BID)
Induced by CASP8; CASP8 cleaves the protein encoded by this|
gene, and the COOH-terminal part translocates to mitochondria,
which triggers cytochrome c release.
Interacts with survival-promoting proteins to enhance|
programmed cell death.
19 kDa interacting protein
(aka NIX); BCL2/adenovirus E1B 19 kd-interacting protein (BNIP)
gene that may function simultaneously with BNIP3 and play a
role in tumor suppression.
Translocates into nucleus during apoptosis. Nuclear PRKCD|
regulates initiation of cytosolic apoptosis machinery, and
subsequent caspase activation and DNA fragmentation.
Phosphorylate and inactivate BAD. Activates NFκB via IκB kinase regulation. Regulates cell signals in response to insulin and|
|B-cell CL/lymphoma 2 (BCL2)||
Blocks the release of pro-apoptotic cytochrome c and caspase|
Inhibit caspases 3, 6, 7 stimulation via IAP (inhibitor of|
Interacts with growth factor receptors; activates AKT3; target|
|RAF1||Inhibits BIM and BAD activation via ERK1/2 stimulation.|
|BCL2-related protein A1 (BCL2A1)||
Reduces cytochrome c release from mitochondria and blocks|
|Baculoviral IAP repeat-containing 2 (BIRC2)||
(aka CIAP1); Inhibits apoptosis by binding to tumor necrosis|
factor receptor-associated factors TRAF1 and TRAF2.
Blocks mitochondrial-dependent caspase activation;|
phosphorylates and activates RAF-1; phosphorylates and
inactivates BAD; activates AKT via DNA-dependent protein kinase
|IKBKE||Induces BCL-2 expression via NFκB signaling and interaction.|