| node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
| ACMSD | AFMID | ENSP00000348459 | ENSP00000328938 | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | 0.418 |
| ACMSD | HAAO | ENSP00000348459 | ENSP00000294973 | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | 0.987 |
| ACMSD | KMO | ENSP00000348459 | ENSP00000355517 | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | kynurenine 3-monooxygenase (kynurenine 3-hydroxylase); Catalyzes the hydroxylation of L-kynurenine (L-Kyn) to form 3-hydroxy-L-kynurenine (L-3OHKyn). Required for synthesis of quinolinic acid, a neurotoxic NMDA receptor antagonist and potential endogenous inhibitor of NMDA receptor signaling in axonal targeting, synaptogenesis and apoptosis during brain development. Quinolinic acid may also affect NMDA receptor signaling in pancreatic beta cells, osteoblasts, myocardial cells, and the gastrointestinal tract (By similarity) | 0.858 |
| ACMSD | KYNU | ENSP00000348459 | ENSP00000264170 | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | kynureninase; Catalyzes the cleavage of L-kynurenine (L-Kyn) and L-3- hydroxykynurenine (L-3OHKyn) into anthranilic acid (AA) and 3- hydroxyanthranilic acid (3-OHAA), respectively. Has a preference for the L-3-hydroxy form. Also has cysteine-conjugate-beta-lyase activity | 0.815 |
| ACMSD | QPRT | ENSP00000348459 | ENSP00000378782 | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | quinolinate phosphoribosyltransferase; Involved in the catabolism of quinolinic acid (QA) | 0.746 |
| ACMSD | TDO2 | ENSP00000348459 | ENSP00000444788 | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | tryptophan 2,3-dioxygenase; Incorporates oxygen into the indole moiety of tryptophan. Has a broad specificity towards tryptamine and derivatives including D- and L-tryptophan, 5-hydroxytryptophan and serotonin (By similarity) | 0.658 |
| AFMID | ACMSD | ENSP00000328938 | ENSP00000348459 | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | 0.418 |
| AFMID | HAAO | ENSP00000328938 | ENSP00000294973 | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | 0.605 |
| AFMID | IDO2 | ENSP00000328938 | ENSP00000443432 | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | indoleamine 2,3-dioxygenase 2; Catalyzes the first and rate-limiting step in the kynurenine pathway of tryptophan catabolism | 0.938 |
| AFMID | KMO | ENSP00000328938 | ENSP00000355517 | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | kynurenine 3-monooxygenase (kynurenine 3-hydroxylase); Catalyzes the hydroxylation of L-kynurenine (L-Kyn) to form 3-hydroxy-L-kynurenine (L-3OHKyn). Required for synthesis of quinolinic acid, a neurotoxic NMDA receptor antagonist and potential endogenous inhibitor of NMDA receptor signaling in axonal targeting, synaptogenesis and apoptosis during brain development. Quinolinic acid may also affect NMDA receptor signaling in pancreatic beta cells, osteoblasts, myocardial cells, and the gastrointestinal tract (By similarity) | 0.965 |
| AFMID | KYNU | ENSP00000328938 | ENSP00000264170 | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | kynureninase; Catalyzes the cleavage of L-kynurenine (L-Kyn) and L-3- hydroxykynurenine (L-3OHKyn) into anthranilic acid (AA) and 3- hydroxyanthranilic acid (3-OHAA), respectively. Has a preference for the L-3-hydroxy form. Also has cysteine-conjugate-beta-lyase activity | 0.954 |
| AFMID | TDO2 | ENSP00000328938 | ENSP00000444788 | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | tryptophan 2,3-dioxygenase; Incorporates oxygen into the indole moiety of tryptophan. Has a broad specificity towards tryptamine and derivatives including D- and L-tryptophan, 5-hydroxytryptophan and serotonin (By similarity) | 0.706 |
| CAT | HAAO | ENSP00000241052 | ENSP00000294973 | catalase; Occurs in almost all aerobically respiring organisms and serves to protect cells from the toxic effects of hydrogen peroxide. Promotes growth of cells including T-cells, B-cells, myeloid leukemia cells, melanoma cells, mastocytoma cells and normal and transformed fibroblast cells | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | 0.911 |
| CAT | KYNU | ENSP00000241052 | ENSP00000264170 | catalase; Occurs in almost all aerobically respiring organisms and serves to protect cells from the toxic effects of hydrogen peroxide. Promotes growth of cells including T-cells, B-cells, myeloid leukemia cells, melanoma cells, mastocytoma cells and normal and transformed fibroblast cells | kynureninase; Catalyzes the cleavage of L-kynurenine (L-Kyn) and L-3- hydroxykynurenine (L-3OHKyn) into anthranilic acid (AA) and 3- hydroxyanthranilic acid (3-OHAA), respectively. Has a preference for the L-3-hydroxy form. Also has cysteine-conjugate-beta-lyase activity | 0.910 |
| GAD1 | HAAO | ENSP00000350928 | ENSP00000294973 | glutamate decarboxylase 1 (brain, 67kDa); Catalyzes the production of GABA | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | 0.927 |
| HAAO | ACMSD | ENSP00000294973 | ENSP00000348459 | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | aminocarboxymuconate semialdehyde decarboxylase; Converts alpha-amino-beta-carboxymuconate-epsilon- semialdehyde (ACMS) to alpha-aminomuconate semialdehyde (AMS). ACMS can be converted non-enzymatically to quinolate (QA), a key precursor of NAD, and a potent endogenous excitotoxin of neuronal cells which is implicated in the pathogenesis of various neurodegenerative disorders. In the presence of ACMSD, ACMS is converted to AMS, a benign catabolite. ACMSD ultimately controls the metabolic fate of tryptophan catabolism along the kynurenine pathway | 0.987 |
| HAAO | AFMID | ENSP00000294973 | ENSP00000328938 | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | arylformamidase; Catalyzes the hydrolysis of N-formyl-L-kynurenine to L- kynurenine, the second step in the kynurenine pathway of tryptophan degradation. Kynurenine may be further oxidized to nicotinic acid, NAD(H) and NADP(H). Required for elimination of toxic metabolites (By similarity) | 0.605 |
| HAAO | CAT | ENSP00000294973 | ENSP00000241052 | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | catalase; Occurs in almost all aerobically respiring organisms and serves to protect cells from the toxic effects of hydrogen peroxide. Promotes growth of cells including T-cells, B-cells, myeloid leukemia cells, melanoma cells, mastocytoma cells and normal and transformed fibroblast cells | 0.911 |
| HAAO | GAD1 | ENSP00000294973 | ENSP00000350928 | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | glutamate decarboxylase 1 (brain, 67kDa); Catalyzes the production of GABA | 0.927 |
| HAAO | IDO2 | ENSP00000294973 | ENSP00000443432 | 3-hydroxyanthranilate 3,4-dioxygenase; Catalyzes the oxidative ring opening of 3- hydroxyanthranilate to 2-amino-3-carboxymuconate semialdehyde, which spontaneously cyclizes to quinolinate | indoleamine 2,3-dioxygenase 2; Catalyzes the first and rate-limiting step in the kynurenine pathway of tryptophan catabolism | 0.613 |
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