node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
ATF2 | ATF3 | ENSP00000264110 | ENSP00000344352 | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | 0.997 |
ATF2 | BCL2 | ENSP00000264110 | ENSP00000329623 | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | B-cell CLL/lymphoma 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) | 0.941 |
ATF2 | HRK | ENSP00000264110 | ENSP00000257572 | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | harakiri, BCL2 interacting protein (contains only BH3 domain); Promotes apoptosis | 0.906 |
ATF2 | JUN | ENSP00000264110 | ENSP00000360266 | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | jun proto-oncogene; Transcription factor that recognizes and binds to the enhancer heptamer motif 5’-TGA[CG]TCA-3’. Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signaling pathway stimulation | 0.999 |
ATF2 | MAPK10 | ENSP00000264110 | ENSP00000352157 | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | mitogen-activated protein kinase 10; Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress- activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and AT [...] | 0.997 |
ATF2 | STAT1 | ENSP00000264110 | ENSP00000354394 | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | signal transducer and activator of transcription 1, 91kDa | 0.418 |
ATF3 | ATF2 | ENSP00000344352 | ENSP00000264110 | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | 0.997 |
ATF3 | BCL2 | ENSP00000344352 | ENSP00000329623 | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | B-cell CLL/lymphoma 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) | 0.458 |
ATF3 | HRK | ENSP00000344352 | ENSP00000257572 | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | harakiri, BCL2 interacting protein (contains only BH3 domain); Promotes apoptosis | 0.824 |
ATF3 | JUN | ENSP00000344352 | ENSP00000360266 | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | jun proto-oncogene; Transcription factor that recognizes and binds to the enhancer heptamer motif 5’-TGA[CG]TCA-3’. Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signaling pathway stimulation | 0.999 |
ATF3 | MAPK10 | ENSP00000344352 | ENSP00000352157 | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | mitogen-activated protein kinase 10; Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress- activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and AT [...] | 0.770 |
ATF3 | STAT1 | ENSP00000344352 | ENSP00000354394 | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | signal transducer and activator of transcription 1, 91kDa | 0.747 |
BCL2 | ATF2 | ENSP00000329623 | ENSP00000264110 | B-cell CLL/lymphoma 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) | activating transcription factor 2; Transcriptional activator, probably constitutive, which binds to the cAMP-responsive element (CRE) (consensus- 5’- GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Interaction with JUN redirects JUN to bind to CRES preferentially over the 12-O-tetradecanoylphorbol-13-acetate response elements (TRES) as part of an ATF2/JUN complex | 0.941 |
BCL2 | ATF3 | ENSP00000329623 | ENSP00000344352 | B-cell CLL/lymphoma 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) | activating transcription factor 3; This protein binds the cAMP response element (CRE) (consensus- 5’-GTGACGT[AC][AG]-3’), a sequence present in many viral and cellular promoters. Represses transcription from promoters with ATF sites. It may repress transcription by stabilizing the binding of inhibitory cofactors at the promoter. Isoform 2 activates transcription presumably by sequestering inhibitory cofactors away from the promoters | 0.458 |
BCL2 | BCL2L1 | ENSP00000329623 | ENSP00000302564 | B-cell CLL/lymphoma 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) | BCL2-like 1; Potent inhibitor of cell death. Inhibits activation of caspases (By similarity). 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 | 0.996 |
BCL2 | BIK | ENSP00000329623 | ENSP00000216115 | B-cell CLL/lymphoma 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) | BCL2-interacting killer (apoptosis-inducing); Accelerates programmed cell death. Association to the apoptosis repressors Bcl-X(L), BHRF1, Bcl-2 or its adenovirus homolog E1B 19k protein suppresses this death-promoting activity. Does not interact with BAX | 0.999 |
BCL2 | HRK | ENSP00000329623 | ENSP00000257572 | B-cell CLL/lymphoma 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) | harakiri, BCL2 interacting protein (contains only BH3 domain); Promotes apoptosis | 0.987 |
BCL2 | JUN | ENSP00000329623 | ENSP00000360266 | B-cell CLL/lymphoma 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) | jun proto-oncogene; Transcription factor that recognizes and binds to the enhancer heptamer motif 5’-TGA[CG]TCA-3’. Promotes activity of NR5A1 when phosphorylated by HIPK3 leading to increased steroidogenic gene expression upon cAMP signaling pathway stimulation | 0.988 |
BCL2 | MAPK10 | ENSP00000329623 | ENSP00000352157 | B-cell CLL/lymphoma 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) | mitogen-activated protein kinase 10; Serine/threonine-protein kinase involved in various processes such as neuronal proliferation, differentiation, migration and programmed cell death. Extracellular stimuli such as proinflammatory cytokines or physical stress stimulate the stress- activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. In this cascade, two dual specificity kinases MAP2K4/MKK4 and MAP2K7/MKK7 phosphorylate and activate MAPK10/JNK3. In turn, MAPK10/JNK3 phosphorylates a number of transcription factors, primarily components of AP-1 such as JUN and AT [...] | 0.799 |
BCL2 | MCL1 | ENSP00000329623 | ENSP00000358022 | B-cell CLL/lymphoma 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) | myeloid cell leukemia sequence 1 (BCL2-related) | 0.986 |