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Literature summary extracted from

  • Kim, S.; Park, J.; Moon, J.; Choi, H.
    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 .
    View publication on PubMed

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
1.14.17.1 dopamine + ascorbate + O2 Homo sapiens
-
 noradrenaline + dehydroascorbate + H2O
-
 ?
1.14.17.1 dopamine + ascorbate + O2 Mus musculus
-
 noradrenaline + dehydroascorbate + H2O
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
1.14.17.1 Homo sapiens P09172
-
-
1.14.17.1 Mus musculus Q64237
-
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.14.17.1 brain
-
 Mus musculus
-
1.14.17.1 neuroblastoma cell
-
 Homo sapiens
-
1.14.17.1 SK-N-BE(2) cell
-
 Homo sapiens
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
1.14.17.1 dopamine + ascorbate + O2
-
 Homo sapiens noradrenaline + dehydroascorbate + H2O
-
 ?
1.14.17.1 dopamine + ascorbate + O2
-
 Mus musculus noradrenaline + dehydroascorbate + H2O
-
 ?

Synonyms

EC Number Synonyms Comment Organism
1.14.17.1 DBH
-
 Homo sapiens
1.14.17.1 DBH
-
 Mus musculus
1.14.17.1 dopamine beta-hydroxylase
-
 Homo sapiens
1.14.17.1 dopamine beta-hydroxylase
-
 Mus musculus

Cofactor

EC Number Cofactor Comment Organism Structure
1.14.17.1 ascorbate
-
 Homo sapiens
1.14.17.1 ascorbate
-
 Mus musculus

Expression

EC Number Organism Comment Expression
1.14.17.1 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
1.14.17.1 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
1.14.17.1 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

EC Number General Information Comment Organism
1.14.17.1 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
1.14.17.1 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