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Literature summary for 1.14.17.1 extracted from
- Alpha-synuclein interferes with cAMP/PKA-dependent upregulation of dopamine beta-hydroxylase and is associated with abnormal adaptive responses to immobilization stress (2014), Exp. Neurol., 252, 63-74 .
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| dopamine + ascorbate + O2 | Homo sapiens | - |
noradrenaline + dehydroascorbate + H2O | - |
? |  |
| dopamine + ascorbate + O2 | Mus musculus | - |
noradrenaline + dehydroascorbate + H2O | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | P09172 | - |
- |
| Mus musculus | Q64237 | - |
- |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| brain | - |
Mus musculus | - |
| neuroblastoma cell | - |
Homo sapiens | - |
| SK-N-BE(2) cell | - |
Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| dopamine + ascorbate + O2 | - |
Homo sapiens | noradrenaline + dehydroascorbate + H2O | - |
? | |
| dopamine + ascorbate + O2 | - |
Mus musculus | noradrenaline + dehydroascorbate + H2O | - |
? | |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| DBH | - |
Homo sapiens |
| DBH | - |
Mus musculus |
| dopamine beta-hydroxylase | - |
Homo sapiens |
| dopamine beta-hydroxylase | - |
Mus musculus |
Cofactor
| Cofactor | Comment | Organism | Structure |
|---|---|---|---|
| ascorbate | - |
Homo sapiens | |
| ascorbate | - |
Mus musculus | |
Expression
| Organism | Comment | Expression |
|---|---|---|
| Mus musculus | A53T Tg mice that express human A53T variant alpha-synuclein under the direction of the mouse prion protein promoter show decreased DBH expression. A53T Tg mice exhibit anxiety-like behaviors and abnormal adaptive responses following the repeated immobilization stress | down |
| Homo sapiens | alpha-SYN enters the nucleus and binds directly to the DBH promoter region. alpha-Syn atteniúates the forskolin-induced DBH upregulation in SK-N-BE(2) cells | down |
| Homo sapiens | forskolin, dexamethasone, ionomycin, and 17-beta-estradiol all induce a significant increase in DBH promoter activity, the most significant 15.8fold upregulation of DBH transcription is observed in forskolin-treated cells The forskolin-induced DBH upregulation in SK-N-BE(2) cells is attenuated by alpha-Syn. CRE-mediated transcriptional regulation of tyrosine hydroxylase and enzyme DBH plays a crucial role in stress response | up |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | dopamine beta-hydroxylase catalyzes the conversion of dopamine to norepinephrine in the biosynthesis of catecholamines. Effect of wild-type and mutant alpha-SYN on cAMP response element (CRE)-mediated regulation of the norepinephrine-synthesizing enzyme dopamine beta-hydroxylase (DBH): overexpression of wild-type or mutant human alpha-SYN interfers with CRE-mediated regulation of DBH transcription in norepinephrine-producing SK-N-BE(2) cells. Upon entering the nucleus, alpha-SYN interacts with the DBH promoter region encompassing the CRE, which interfered with forskolin-induced CREB binding to the CRE region. Mutant A53T alpha-SYN shows much higher tendency to nuclear translocation and interaction with the DBH promoter region encompassing the CRE than wild-type. CRE-mediated transcriptional regulation of tyrosine hydroxylase and enzyme DBH plays a crucial role in stress response | Homo sapiens |
| physiological function | dopamine beta-hydroxylase catalyzes the conversion of dopamine to norepinephrine in the biosynthesis of catecholamines. Effect of wild-type and mutant human alpha-SYN on cAMP response element (CRE)-mediated regulation of the norepinephrine-synthesizing enzyme dopamine beta-hydroxylase (DBH), stress-induced DBH regulation is modulated in the brains of A53T transgenic mice (A53T Tg). Overexpression of wild-type or mutant human alpha-SYN interfers with CRE-mediated regulation of DBH transcription in murine brains of A53T transgenic mice (A53T Tg). Upon entering the nucleus, alpha-SYN interacts with the DBH promoter region encompassing the CRE, which interfers with forskolin-induced CREB binding to the CRE region. Mutant A53T alpha-SYN shows much higher tendency to nuclear translocation and interaction with the DBH promoter region encompassing the CRE than wild-type | Mus musculus |
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