BCL2:p53*@Mitochondrial outer membrane
a_re1406( Apoptosis ):
unphosphorylated TP53 from coIP experiments with okadaic acid (PKC inhibitor) or ceramide C2 (potent inductor of PP1/2A
Fraction of induced p53 translocates to the mitochondria of apoptosing tumor cells. Targeting p53 to mitochondria is sufficient to launch apoptosis.
p53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BCL2L1 and BCL2 proteins, resulting in cytochrome c release.
In other hand, cytosolic localization of endogenous p53 was necessary and sufficient for apoptosis. p53 directly activated the pro-apoptotic BCL2 protein Bax in the absence of other proteins to permeabilize mitochondria and engage the apoptotic program.
Binding of BCL2 or BCL2L1 to TP53 therefore antagonizes the activation of BAX via binding to TP53. Like this BCL2 and BCL2L1 also perform their anti-apoptotic effect.
e_re433( EMT ):
p53 induces apoptosis by target gene regulation and transcription-independent signaling.
A fraction of induced p53 translocates to the mitochondria of apoptosing tumor cells. Targeting p53 to mitochondria is sufficient to launch apoptosis.
Evidence that p53 translocation to the mitochondria occurs in vivo in irradiatedthymocytes was shown.
Participates in complexes:
In compartment: Mitochondria
In compartment: Mitochondrial outer membrane
Participates in reactions:
As Reactant or Product:
- BCL2|unk@Mitochondrial outer membrane + p53*|S15_unk@Cytoplasm → BCL2:p53*@Mitochondrial outer membrane
- p53*@Mitochondria + BCL2@Mitochondria → BCL2:p53*@Mitochondria