| node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
| BAK1 | BAX | ENSP00000363591 | ENSP00000293288 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | 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; Belongs to the Bcl-2 family | 0.952 |
| BAK1 | BCL2 | ENSP00000363591 | ENSP00000381185 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; 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; BCL2 family | 0.984 |
| BAK1 | BCL2A1 | ENSP00000363591 | ENSP00000267953 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | 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 (By similarity). Can inhibit apoptosis induced by serum starvation in the mammary epithelial cell line HC11 (By similarity); BCL2 family | 0.938 |
| BAK1 | BCL2L1 | ENSP00000363591 | ENSP00000302564 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; 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; Belongs to the Bcl-2 family | 0.998 |
| BAK1 | BCL2L2 | ENSP00000363591 | ENSP00000250405 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | Bcl-2-like protein 2; Promotes cell survival. Blocks dexamethasone-induced apoptosis. Mediates survival of postmitotic Sertoli cells by suppressing death-promoting activity of BAX; Belongs to the Bcl-2 family | 0.734 |
| BAK1 | C22orf29 | ENSP00000363591 | ENSP00000384924 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | Protein Bop; Could induce apoptosis in a BH3 domain-dependent manner. The direct interaction network of Bcl-2 family members may play a key role in modulation RTL10/BOP intrinsic apoptotic signaling activity | 0.666 |
| BAK1 | MCL1 | ENSP00000363591 | ENSP00000358022 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | Induced myeloid leukemia cell differentiation protein Mcl-1; 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 1 inhibits apoptosis. Isoform 2 promotes apoptosis; Belongs to the Bcl-2 family | 0.965 |
| BAK1 | VDAC1 | ENSP00000363591 | ENSP00000265333 | 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | Voltage-dependent anion-selective channel protein 1; Forms a channel through the mitochondrial outer membrane and also the plasma membrane. The channel at the outer mitochondrial membrane allows diffusion of small hydrophilic molecules; in the plasma membrane it is involved in cell volume regulation and apoptosis. It adopts an open conformation at low or zero membrane potential and a closed conformation at potentials above 30-40 mV. The open state has a weak anion selectivity whereas the closed state is cation-selective. May participate in the formation of the permeability transition p [...] | 0.882 |
| BAX | BAK1 | ENSP00000293288 | ENSP00000363591 | 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; 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | 0.952 |
| BAX | BCL2 | ENSP00000293288 | ENSP00000381185 | 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; 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; BCL2 family | 0.967 |
| BAX | BCL2A1 | ENSP00000293288 | ENSP00000267953 | 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; Belongs to the Bcl-2 family | 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 (By similarity). Can inhibit apoptosis induced by serum starvation in the mammary epithelial cell line HC11 (By similarity); BCL2 family | 0.609 |
| BAX | BCL2L1 | ENSP00000293288 | ENSP00000302564 | 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; 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; Belongs to the Bcl-2 family | 0.998 |
| BAX | BCL2L2 | ENSP00000293288 | ENSP00000250405 | 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; Belongs to the Bcl-2 family | Bcl-2-like protein 2; Promotes cell survival. Blocks dexamethasone-induced apoptosis. Mediates survival of postmitotic Sertoli cells by suppressing death-promoting activity of BAX; Belongs to the Bcl-2 family | 0.749 |
| BAX | C22orf29 | ENSP00000293288 | ENSP00000384924 | 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; Belongs to the Bcl-2 family | Protein Bop; Could induce apoptosis in a BH3 domain-dependent manner. The direct interaction network of Bcl-2 family members may play a key role in modulation RTL10/BOP intrinsic apoptotic signaling activity | 0.637 |
| BAX | MCL1 | ENSP00000293288 | ENSP00000358022 | 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; Belongs to the Bcl-2 family | Induced myeloid leukemia cell differentiation protein Mcl-1; 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 1 inhibits apoptosis. Isoform 2 promotes apoptosis; Belongs to the Bcl-2 family | 0.996 |
| BAX | VDAC1 | ENSP00000293288 | ENSP00000265333 | 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; Belongs to the Bcl-2 family | Voltage-dependent anion-selective channel protein 1; Forms a channel through the mitochondrial outer membrane and also the plasma membrane. The channel at the outer mitochondrial membrane allows diffusion of small hydrophilic molecules; in the plasma membrane it is involved in cell volume regulation and apoptosis. It adopts an open conformation at low or zero membrane potential and a closed conformation at potentials above 30-40 mV. The open state has a weak anion selectivity whereas the closed state is cation-selective. May participate in the formation of the permeability transition p [...] | 0.891 |
| BCL2 | BAK1 | ENSP00000381185 | ENSP00000363591 | 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; BCL2 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 or its adenovirus homolog E1B 19k protein. Low micromolar levels of zinc ions inhibit the promotion of apoptosis; Belongs to the Bcl-2 family | 0.984 |
| BCL2 | BAX | ENSP00000381185 | ENSP00000293288 | 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; BCL2 family | 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; Belongs to the Bcl-2 family | 0.967 |
| BCL2 | BCL2A1 | ENSP00000381185 | ENSP00000267953 | 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; BCL2 family | 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 (By similarity). Can inhibit apoptosis induced by serum starvation in the mammary epithelial cell line HC11 (By similarity); BCL2 family | 0.913 |
| BCL2 | BCL2L1 | ENSP00000381185 | ENSP00000302564 | 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; BCL2 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; Belongs to the Bcl-2 family | 0.991 |
