node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
Bad | Bak1 | ENSMUSP00000025910 | ENSMUSP00000077757 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | 0.698 |
Bad | Bbc3 | ENSMUSP00000025910 | ENSMUSP00000002152 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Bcl-2-binding component 3; Essential mediator of p53/TP53-dependent and p53/TP53- independent apoptosis. Functions by promoting partial unfolding of BCL2L1 and dissociation of BCL2L1 from p53/TP53 (By similarity). Regulates ER stress-induced neuronal apoptosis; Belongs to the Bcl-2 family. | 0.552 |
Bad | Bcl2 | ENSMUSP00000025910 | ENSMUSP00000108371 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Apoptosis regulator Bcl-2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release. | 0.997 |
Bad | Bcl2l1 | ENSMUSP00000025910 | ENSMUSP00000105445 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Bcl-2-like protein 1; Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage- dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis. Isoform Bcl-X(S) promotes apoptosis; Belongs to the Bcl-2 family. | 0.999 |
Bad | Bcl2l11 | ENSMUSP00000025910 | ENSMUSP00000105970 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Bcl-2-like protein 11; Induces apoptosis and anoikis. The isoforms vary in cytotoxicity with isoform BimS being the most potent and isoform BimEL being the least potent; Belongs to the Bcl-2 family. | 0.890 |
Bad | Bid | ENSMUSP00000025910 | ENSMUSP00000004560 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | BH3-interacting domain death agonist p11; Induces caspases and apoptosis. Counters the protective effect of Bcl-2. The major proteolytic product p15 BID allows the release of cytochrome c. | 0.844 |
Bad | Hrk | ENSMUSP00000025910 | ENSMUSP00000057532 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Activator of apoptosis harakiri; Promotes apoptosis. | 0.459 |
Bad | Pmaip1 | ENSMUSP00000025910 | ENSMUSP00000025399 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Phorbol-12-myristate-13-acetate-induced protein 1; Promotes activation of caspases and apoptosis. Promotes mitochondrial membrane changes and efflux of apoptogenic proteins from the mitochondria. Contributes to p53/TP53-dependent apoptosis after radiation exposure. Promotes proteasomal degradation of MCL1. Competes with BIM/BCL2L11 for binding to MCL1 and can displace BIM/BCL2L11 from its binding site on MCL1 (By similarity). Competes with BAK1 for binding to MCL1 and can displace BAK1 from its binding site on MCL1. | 0.489 |
Bad | Trp53 | ENSMUSP00000025910 | ENSMUSP00000104298 | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | Cellular tumor antigen p53; Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its intera [...] | 0.498 |
Bak1 | Bad | ENSMUSP00000077757 | ENSMUSP00000025910 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | 0.698 |
Bak1 | Bbc3 | ENSMUSP00000077757 | ENSMUSP00000002152 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Bcl-2-binding component 3; Essential mediator of p53/TP53-dependent and p53/TP53- independent apoptosis. Functions by promoting partial unfolding of BCL2L1 and dissociation of BCL2L1 from p53/TP53 (By similarity). Regulates ER stress-induced neuronal apoptosis; Belongs to the Bcl-2 family. | 0.954 |
Bak1 | Bcl2 | ENSMUSP00000077757 | ENSMUSP00000108371 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Apoptosis regulator Bcl-2; Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release. | 0.996 |
Bak1 | Bcl2l1 | ENSMUSP00000077757 | ENSMUSP00000105445 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Bcl-2-like protein 1; Potent inhibitor of cell death. Inhibits activation of caspases. Appears to regulate cell death by blocking the voltage- dependent anion channel (VDAC) by binding to it and preventing the release of the caspase activator, CYC1, from the mitochondrial membrane. Also acts as a regulator of G2 checkpoint and progression to cytokinesis during mitosis. Isoform Bcl-X(S) promotes apoptosis; Belongs to the Bcl-2 family. | 0.998 |
Bak1 | Bcl2l11 | ENSMUSP00000077757 | ENSMUSP00000105970 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Bcl-2-like protein 11; Induces apoptosis and anoikis. The isoforms vary in cytotoxicity with isoform BimS being the most potent and isoform BimEL being the least potent; Belongs to the Bcl-2 family. | 0.980 |
Bak1 | Becn1 | ENSMUSP00000077757 | ENSMUSP00000119369 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Beclin-1-C 35 kDa; Plays a central role in autophagy. Acts as core subunit of different PI3K complex forms that mediate formation of phosphatidylinositol 3-phosphate and are believed to play a role in multiple membrane trafficking pathways: PI3KC3-C1 is involved in initiation of autophagosomes and PI3KC3-C2 in maturation of autophagosomes and endocytosis. Involved in regulation of degradative endocytic trafficking and required for the abcission step in cytokinesis, probably in the context of PI3KC3-C2 (By similarity). Essential for the formation of PI3KC3-C2 but not PI3KC3-C1 PI3K comp [...] | 0.636 |
Bak1 | Bid | ENSMUSP00000077757 | ENSMUSP00000004560 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | BH3-interacting domain death agonist p11; Induces caspases and apoptosis. Counters the protective effect of Bcl-2. The major proteolytic product p15 BID allows the release of cytochrome c. | 0.994 |
Bak1 | Hrk | ENSMUSP00000077757 | ENSMUSP00000057532 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Activator of apoptosis harakiri; Promotes apoptosis. | 0.568 |
Bak1 | Pmaip1 | ENSMUSP00000077757 | ENSMUSP00000025399 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Phorbol-12-myristate-13-acetate-induced protein 1; Promotes activation of caspases and apoptosis. Promotes mitochondrial membrane changes and efflux of apoptogenic proteins from the mitochondria. Contributes to p53/TP53-dependent apoptosis after radiation exposure. Promotes proteasomal degradation of MCL1. Competes with BIM/BCL2L11 for binding to MCL1 and can displace BIM/BCL2L11 from its binding site on MCL1 (By similarity). Competes with BAK1 for binding to MCL1 and can displace BAK1 from its binding site on MCL1. | 0.888 |
Bak1 | Trp53 | ENSMUSP00000077757 | ENSMUSP00000104298 | Bcl-2 homologous antagonist/killer; In the presence of an appropriate stimulus, accelerates programmed cell death by binding to, and antagonizing the anti- apoptotic action of BCL2. | Cellular tumor antigen p53; Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its intera [...] | 0.983 |
Bbc3 | Bad | ENSMUSP00000002152 | ENSMUSP00000025910 | Bcl-2-binding component 3; Essential mediator of p53/TP53-dependent and p53/TP53- independent apoptosis. Functions by promoting partial unfolding of BCL2L1 and dissociation of BCL2L1 from p53/TP53 (By similarity). Regulates ER stress-induced neuronal apoptosis; Belongs to the Bcl-2 family. | Bcl2-associated agonist of cell death; Promotes cell death. Successfully competes for the binding to Bcl-X(L), Bcl-2 and Bcl-W, thereby affecting the level of heterodimerization of these proteins with BAX. Can reverse the death repressor activity of Bcl-X(L), but not that of Bcl-2. Appears to act as a link between growth factor receptor signaling and the apoptotic pathways. | 0.552 |