node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
Bak1 | Bax | ENSMUSP00000077757 | ENSMUSP00000033093 | 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 BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 0.985 |
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 | Bcl2a1a | ENSMUSP00000077757 | ENSMUSP00000096086 | 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-related protein A1; Retards apoptosis induced by IL-3 deprivation. May function in the response of hemopoietic cells to external signals and in maintaining endothelial survival during infection. Can inhibit apoptosis induced by serum starvation in the mammary epithelial cell line HC11 ; Belongs to the Bcl-2 family. | 0.987 |
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 | 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 | Cyct | ENSMUSP00000077757 | ENSMUSP00000028430 | 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. | Cytochrome c, testis-specific; Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. | 0.964 |
Bak1 | Gm10053 | ENSMUSP00000077757 | ENSMUSP00000072829 | 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. | Cytochrome c, somatic; Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. | 0.967 |
Bak1 | Mcl1 | ENSMUSP00000077757 | ENSMUSP00000044048 | 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. | Induced myeloid leukemia cell differentiation protein Mcl-1 homolog; Involved in the regulation of apoptosis versus cell survival, and in the maintenance of viability but not of proliferation. Mediates its effects by interactions with a number of other regulators of apoptosis. Isoform 2 has antiapoptotic activity. | 0.983 |
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 |
Bax | Bak1 | ENSMUSP00000033093 | ENSMUSP00000077757 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 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. | 0.985 |
Bax | Bcl2 | ENSMUSP00000033093 | ENSMUSP00000108371 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 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. | 0.998 |
Bax | Bcl2l1 | ENSMUSP00000033093 | ENSMUSP00000105445 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 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. | 0.990 |
Bax | Bcl2l11 | ENSMUSP00000033093 | ENSMUSP00000105970 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 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. | 0.997 |
Bax | Bid | ENSMUSP00000033093 | ENSMUSP00000004560 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 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. | 0.997 |
Bax | Cyct | ENSMUSP00000033093 | ENSMUSP00000028430 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | Cytochrome c, testis-specific; Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. | 0.986 |
Bax | Gm10053 | ENSMUSP00000033093 | ENSMUSP00000072829 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | Cytochrome c, somatic; Electron carrier protein. The oxidized form of the cytochrome c heme group can accept an electron from the heme group of the cytochrome c1 subunit of cytochrome reductase. Cytochrome c then transfers this electron to the cytochrome oxidase complex, the final protein carrier in the mitochondrial electron-transport chain. | 0.986 |
Bax | Mcl1 | ENSMUSP00000033093 | ENSMUSP00000044048 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | Induced myeloid leukemia cell differentiation protein Mcl-1 homolog; Involved in the regulation of apoptosis versus cell survival, and in the maintenance of viability but not of proliferation. Mediates its effects by interactions with a number of other regulators of apoptosis. Isoform 2 has antiapoptotic activity. | 0.899 |
Bax | Trp53 | ENSMUSP00000033093 | ENSMUSP00000104298 | Apoptosis regulator BAX; Accelerates programmed cell death by binding to, and antagonizing the apoptosis repressor BCL2 or its adenovirus homolog E1B 19k protein. Under stress conditions, undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis. Promotes activation of CASP3, and thereby apoptosis. BAX deficiency leads to lymphoid hyperplasia and male sterility, because of the cessation of sperm production; Belongs to the Bcl-2 family. | 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 [...] | 0.979 |
Bcl2 | Bak1 | ENSMUSP00000108371 | ENSMUSP00000077757 | 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. | 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. | 0.996 |