Identifiers
NAME:BAX:BCL2
Maps_Modules
HMC:RESISTING_CELL_DEATH
Regulated Cell Death / APOPTOSIS
Regulated Cell Death / ER_STRESS
References
PMID:23850759
Identifiers
NAME:BAX:BCL2
References
PMID:23377657
rc_re1811( Regulated Cell Death ):
PMID:16227588
PMID:17891140
Identifiers
NAME:BAX:BCL2
Identifiers
NAME:BAX:BCL2
Maps_Modules
HMC:ACTIVATING_INVASION_AND_METASTASIS
EMT Senescence / EMT_REGULATORS
References
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 proteins) promote apoptosis, while others such as BCL2, BCL2L1, BCL2L2 (anti-apoptotic proteins) 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:9872359
A oncogene-derived protein, Bcl2, confers negative control in the pathway of cellular suicide machinery.
A Bcl2-homologous protein, Bax, promotes cell death by competing with Bcl2.
While Bax???Bax homodimers act as apoptosis inducers, Bcl2??? Bax heterodimer formation evokes a survival signal for the cells.
Both Bcl2 and Bax are transcriptional targets for the tumour suppressor protein, p53, which induces cell cycle arrest or apoptosis in response to DNA damage.
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.
+ BCL2@Mitochondria → BAX:BCL2@Mitochondria
+ BAX|S163_unk|T167_unk@Cytosol → BAX|S163_unk|T167_unk:BCL2@Cytosol
→ Apoptotic death@Cytosol
+ BAX@Endopasmic Reticulum → BAX:BCL2@Endopasmic Reticulum
+ BAX|S163_unk|T167_unk@Mitochondrial inner membrane → BAX|S163_unk|T167_unk:BCL2@Mitochondrial inner membrane