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Table 1 Selected genes involved in the regulation of apoptosis

From: Interaction among apoptosis-associated sequence variants and joint effects on aggressive prostate cancer

  Gene Function*
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
(TNF)
Binds and functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR to regulate cell proliferation, differentiation,
and apoptosis.
  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.
  CASPASE (CASP) 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.
  CARD8 (Caspase
recruitment domain
family, member 8)
CARD family protein; involved in various pathways which
regulate caspases or NFκB; isoforms interact with caspases to
signal apoptosis.
  BCL2-associated X (BAX) Forms a heterodimer with BCL2 and functions as an apoptotic
activator involved mitochondrial release of cytochrome c.
  BCL2-antagonist/killer 1
(BAK1)
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
BAX).
  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
apoptosis activator.
  BCL2-like 14 (BCL2L14) Apoptosis facilitator; interacts with BCL2 family members; p53-
target gene.
  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.
  BCL2-interacting killer
(BIK)
Interacts with survival-promoting proteins to enhance
programmed cell death.
  BCL2/adenovirus E1B
19 kDa interacting protein
3-like (BNIP3L)
(aka NIX); BCL2/adenovirus E1B 19 kd-interacting protein (BNIP)
gene that may function simultaneously with BNIP3 and play a
role in tumor suppression.
  PRKCD Translocates into nucleus during apoptosis. Nuclear PRKCD
regulates initiation of cytosolic apoptosis machinery, and
subsequent caspase activation and DNA fragmentation.
Anti-apoptotic AKT3 Phosphorylate and inactivate BAD. Activates NFκB via IκB kinase regulation. Regulates cell signals in response to insulin and
growth factors.
  B-cell CL/lymphoma 2 (BCL2) Blocks the release of pro-apoptotic cytochrome c and caspase
activation.
  NFκB Inhibit caspases 3, 6, 7 stimulation via IAP (inhibitor of
apoptosis) activation.
  PIK3CB Interacts with growth factor receptors; activates AKT3; target
for PRKC.
  RAF1 Inhibits BIM and BAD activation via ERK1/2 stimulation.
  BCL2-related protein A1 (BCL2A1) Reduces cytochrome c release from mitochondria and blocks
caspase activation.
  Baculoviral IAP repeat-containing 2 (BIRC2) (aka CIAP1); Inhibits apoptosis by binding to tumor necrosis
factor receptor-associated factors TRAF1 and TRAF2.
  PRKCE Blocks mitochondrial-dependent caspase activation;
phosphorylates and activates RAF-1; phosphorylates and
inactivates BAD; activates AKT via DNA-dependent protein kinase
(DNA-PK).
  IKBKE Induces BCL-2 expression via NFκB signaling and interaction.
  1. *Gene functions based on NCBI and/or selected publications (as indicated in the manuscript)