Identifiers
NAME:BAX:BCL2-XL*
Maps_Modules
HMC:RESISTING_CELL_DEATH
Regulated Cell Death / ER_STRESS
References
PMID:23850759
Identifiers
NAME:BAX:BCL2-XL*
Maps_Modules
HMC:ACTIVATING_INVASION_AND_METASTASIS
EMT Senescence / EMT_REGULATORS
References
PMID9153240
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
PMID:8358790
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.
PMID:7937747
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.
PMID:11085534
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.
em_emtc_emtc_re429( EMT Senescence ):
PMID:22039431
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
PMID:22836101
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
Identifiers
NAME:BAX:BCL2-XL*
References
rc_re1405:( Regulated Cell Death ) PMID:16608847
+ BAX@Cytosol → BAX:BCL2-XL*@Mitochondria
+ BAX|S163_unk|T167_unk@Mitochondrial inner membrane → BAX|S163_unk|T167_unk:BCL2-XL*@Mitochondrial inner membrane
+ BAX@Endopasmic Reticulum → BAX:BCL2-XL*@Endopasmic Reticulum
+ BCL2-XL*@Cytoplasm → BAX:BCL2-XL*@Mitochondria
+ BAX_sub_TRUNC_endsub_*@Cytoplasm → su_wnc1_s_wnc2_s64 + BAX@Cytoplasm