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Data show that ovulation is defective in females lacking tyramine beta-hydroxylase, resulting in blockage of mature oocytes within the ovaries.
Recombinant tyramine beta-monooxygenase requires copper for activity and has a typical type 2 copper electron spin resonance (EPR (show EREG ELISA Kits)) spectrum.
Octopamine is not the natural signal for flight initiation because flies lacking octopamine [tyramine-beta-hydroxylase null mutants] can fly, though they show markedly different flight-initiation and -maintenance capabilities compared to wild-type flies.
the tyramine beta-monooxygenase mechanism is different from that of the mammalian enzyme, dopamine beta-monooxygenase
In mice, hepatic Dbh mRNA levels correlated with cardiovascular risk phenotypes.
Dbh-deficient mice exhibit shorter latencies to loss of righting reflex and longer durations of hypersensitivity to general anesthesia.
our results suggest that DBH knockout mice have normal levels of dopamine 2 receptors in the high-affinity state and that additional mechanisms contribute to their behavioral sensitivity to psychostimulants
These results strongly suggest that the norepinephrine defect in Mecp2(-/Y) mice is likely to result from deficient expression of not only tyrosine hydroxylase (show TH ELISA Kits) but also DBH without significant loss of catecholaminergic neurons in the locus coeruleus.
Dbh-/- animals were hypersensitive to the behavioral effects of amphetamine.
A mutation in the ATP7B (show ATP7B ELISA Kits) copper transporter causes reduced levels of this enzyme and norepinephrine in the mouse adrenal gland.
The response of mice deficient in this gene to cholecystokinin (show CCK ELISA Kits)-8 induced satiety
Data show how deficiency of dopamine-beta-hydroxylase (DBH) and CRH (show CRH ELISA Kits) affects tyrosine hydroxylase (show TH ELISA Kits), DBH, and phenylethanolamine N-methyltransferase (show PNMT ELISA Kits) gene expression and protein levels in the adrenal medulla and stellate ganglia of control and stressed mice.
This study indicated that DBH5'-Ins (show INS ELISA Kits)/Del polymorphism may not play a role in the susceptibility to tardive dyskinesia and cognitive deficits in schizophrenia with tardive dyskinesia.
DRD2 (show DRD2 ELISA Kits) A2/A1, DRD3 (show DRD3 ELISA Kits) Ser9Gly, DbetaH -1021C>T, OPRM1 (show OPRM1 ELISA Kits) A118G and GRIK1 (show GRIK1 ELISA Kits) rs2832407C>A are not associated with alcoholism alone or in interaction.
Results suggest that interference of cannabis and cocaine with cognitive impulse control and functional corticostriatal connectivity depends on DBH genotype.
Dopamine beta-Hydroxylase Deficiency is associated with Hyperinsulinemia and Insulin (show INS ELISA Kits) Resistance.
The genotype and allele distribution frequencies in rs1611115 were different between Parkinson's disease patients and the healthy control. The TT genotype may lead to a 2.95 times higher risk of Parkinson's disease occurrence compared with the common genotype CC. DBH rs1611115 polymorphism was likely to be associated with the susceptibility to PD, but we did not find that rs732833 is a susceptibility marker
Results suggest that the DBH gene may play an important role in the occurrence of schizophrenia (SCZ). Also, rs1611114 may be associated with SCZ susceptibility and related clinical symptoms in the Chinese Zhuang but not Han Chinese population.
Study found that the functional T allele in DBH SNP rs1611115, which reduces the conversion of dopamine to norepinephrine, corresponds with different BOLD-signal changes in responses to gambling, drug or sad cues in individuals with and without pathological gambling
The p.Val26Met variant in the dopamine beta-hydroxylase gene at 9q34.2 was associated with Lung Cancer.
A DBH gene variant, rs129882, which confers risk to attention deficit hyperactivity disorder, is also associated with reduced in vitro gene expression.
No significant association was found between the DbetaH 5'-Ins (show INS ELISA Kits)/Del polymorphism and patients with chronic schizophrenia.
The present study presents evidence for the conclusion that the catalytic activity of dopamine beta-hydroxylase (DBH; dopamine beta-mono-oxygenase, EC 22.214.171.124) is regulated independently by pH and by anions
dioxygen and substrate activation are tightly coupled in dopamine beta-monooxygenase
The dopamine beta-hydroxylase (DBH) gene maps to chromosome 1q2.13. Polymorphisms within the DBH gene are associated with piglet survivability.
The protein encoded by this gene is an oxidoreductase belonging to the copper type II, ascorbate-dependent monooxygenase family. It is present in the synaptic vesicles of postganglionic sympathetic neurons and converts dopamine to norepinephrine. It exists in both soluble and membrane-bound forms, depending on the absence or presence, respectively, of a signal peptide.
, dopamine beta hydroxylase
, tyramine beta hydroxylase
, tyramine beta-hydroxylase
, tyramine beta-monooxygenase
, tyroside beta-hydroxylase
, dopamine beta-hydroxylase (dopamine beta-monooxygenase)
, dopamine beta-hydroxylase-like
, dopamine beta-monooxygenase
, Dopamine beta hydroxylase (dopamine beta-monooxygenase)