Name | Number of supported studies | Average coverage | |
---|---|---|---|
epithelial cell of proximal tubule | 8 studies | 31% ± 8% | |
hepatocyte | 3 studies | 68% ± 14% | |
glutamatergic neuron | 3 studies | 25% ± 1% |
Insufficient scRNA-seq data for expression of ACMSD at tissue level.
Tissue | GTEx Coverage | GTEx Average TPM | GTEx Number of samples | TCGA Coverage | TCGA Average TPM | TCGA Number of samples |
---|---|---|---|---|---|---|
liver | 100% | 3395.32 | 226 / 226 | 95% | 47.73 | 385 / 406 |
kidney | 100% | 3259.26 | 89 / 89 | 87% | 51.45 | 786 / 901 |
pancreas | 96% | 15.27 | 314 / 328 | 15% | 1.77 | 26 / 178 |
adrenal gland | 96% | 13.97 | 248 / 258 | 0% | 0.02 | 1 / 230 |
thymus | 86% | 6.42 | 559 / 653 | 0% | 0 | 0 / 605 |
ovary | 84% | 5.27 | 151 / 180 | 0% | 0 | 0 / 430 |
breast | 66% | 6.44 | 301 / 459 | 10% | 0.95 | 108 / 1118 |
lung | 63% | 3.86 | 367 / 578 | 7% | 0.68 | 77 / 1155 |
prostate | 65% | 2.81 | 160 / 245 | 0% | 0.01 | 1 / 502 |
uterus | 62% | 2.61 | 105 / 170 | 1% | 0.08 | 4 / 459 |
spleen | 52% | 4.54 | 125 / 241 | 0% | 0 | 0 / 0 |
stomach | 44% | 1.43 | 159 / 359 | 3% | 0.27 | 9 / 286 |
intestine | 45% | 2.64 | 434 / 966 | 2% | 0.20 | 11 / 527 |
peripheral blood | 46% | 10.67 | 430 / 929 | 0% | 0 | 0 / 0 |
brain | 43% | 2.02 | 1136 / 2642 | 1% | 0.06 | 6 / 705 |
bladder | 43% | 1.10 | 9 / 21 | 1% | 0.09 | 4 / 504 |
skin | 42% | 1.48 | 766 / 1809 | 0% | 0 | 0 / 472 |
esophagus | 37% | 1.28 | 532 / 1445 | 1% | 0.08 | 2 / 183 |
adipose | 37% | 1.85 | 445 / 1204 | 0% | 0 | 0 / 0 |
muscle | 33% | 0.96 | 263 / 803 | 0% | 0 | 0 / 0 |
blood vessel | 31% | 0.96 | 418 / 1335 | 0% | 0 | 0 / 0 |
heart | 29% | 0.94 | 248 / 861 | 0% | 0 | 0 / 0 |
abdomen | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
bone marrow | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
diaphragm | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
eye | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 80 |
gingiva | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
lymph node | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 29 |
nasal cavity | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nasopharynx | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
nose | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
placenta | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
spinal column | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 0 |
tonsil | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 45 |
ureter | 0% | 0 | 0 / 0 | 0% | 0 | 0 / 1 |
GO_0019748 | Biological process | secondary metabolic process |
GO_1904985 | Biological process | negative regulation of quinolinate biosynthetic process |
GO_0006569 | Biological process | tryptophan catabolic process |
GO_1905012 | Biological process | regulation of 'de novo' NAD biosynthetic process from tryptophan |
GO_1905004 | Biological process | picolinic acid biosynthetic process |
GO_0005829 | Cellular component | cytosol |
GO_0005737 | Cellular component | cytoplasm |
GO_0001760 | Molecular function | aminocarboxymuconate-semialdehyde decarboxylase activity |
GO_0016787 | Molecular function | hydrolase activity |
GO_0005515 | Molecular function | protein binding |
GO_0008270 | Molecular function | zinc ion binding |
Gene name | ACMSD |
Protein name | 2-amino-3-carboxymuconate-6-semialdehyde decarboxylase (EC 4.1.1.45) (Picolinate carboxylase) |
Synonyms | |
Description | FUNCTION: 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. . FUNCTION: 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. . FUNCTION: 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. . |
Accessions | A0A0S2Z681 A0A0S2Z630 ENST00000356140.10 [Q8TDX5-1] Q8TDX5 ENST00000392928.5 [Q8TDX5-2] |