BAX|S163_unk|T167_unk:BCL2-XL*@Mitochondrial outer membrane
a_re1405:( Apoptosis ) PMID:16608847
By immunoprecipitation and yeast two-hybrid select studies, it appears that Bax may form homodimers or heterodimers with either Bcl2 or BCL2L1 (so-called BCL-XL)
Formation of Bax homodimers has been proposed to promote cell death, and this could be blocked by Bax heterodimerization with BCL2 or BCL2L1.
Based on Bax overexpression and dimerization studies, it has been postulated that the relative ratio of Bax homodimers to heterodimers may serve as a key sensory switch that dictates the initiation of apoptosis
Bax homodimerizes and forms heterodimers with BCL2 in vivo.
Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line.
Overexpressed Bax also counters the death repressor activity of BCL2.
These data suggest a model in which the ratio of BCL2 to Bax determines survival or death following an apoptotic stimulus.
Interactions of the BCL2 protein with itself and other members of the BCL2 family, including BCL2L1 (so-called BCL-XL) and Bax, were explored with a yeast two-hybrid system.
This approach gave evidence for BCL2 protein homodimerization.
BCL2 also interacted with BCL2L1 with the dominant inhibitors Bax.
Bax undergoes a concurrent inhibition and priming by BCL2L1
Derepressor (such as Bad or Noxa), is sufficient to trigger apoptosis through interaction with antiapoptotic proteins.
e_re429( EMT ):
The Bcl2 family proteins regulate and mediate the mitochondrial outer membrane permeabilization, a crucial event in the mitochondrial pathway of apoptosis in vertebrates.
The regulation of apoptosis is governed largely by interactions between the pro-survival and pro-death members of the Bcl2 protein family.
Some members of this family (e.g., Bax, Bak, and Bid: pro-apoptotic protines) promote apoptosis, while others such as BCL2, BCL2L1, BCL2L2 (anti-apoptotic protines)work against programmed cell death.
The BCL2 family proteins are characterized by regions of specific sequence homology named as BCL2 homology (BH) motifs that number from 1 to 4 and are critical for function.
Especially a helical BH3 motif of pro-apoptotic proteins occupy and form strong interactions with hydrophobic groove of anti-apoptotic BCL2 family proteins which leads to the activation of the essential death mediators Bax and Bak, thereby committing cells to apoptosis
BCL2L1 (BCL-X) promotes survival of adult and developing retinal ganglion cells.
The activation of the pro-death family member BAX is often the final step before cell death in neurons.
Pro-survival family members such as BCL2L1 act to inhibit BAX activation
Participates in complexes:
In compartment: Mitochondria
In compartment: Mitochondrial outer membrane
Participates in reactions:
As Reactant or Product:
- BCL2-XL*@Mitochondrial outer membrane + BAX|S163_unk|T167_unk@Mitochondrial outer membrane → BAX|S163_unk|T167_unk:BCL2-XL*@Mitochondrial outer membrane
- BCL2-XL*@Mitochondria + BAX@Cytoplasm → BAX:BCL2-XL*@Mitochondria
- BAX@Cytoplasm + BCL2-XL*@Cytoplasm → BAX:BCL2-XL*@Mitochondria
- BAX:BCL2-XL*@Mitochondria + BAX_sub_TRUNC_endsub_*@Cytoplasm → s_s_wnc2_s64 + BAX@Cytoplasm