Dopamine beta-Hydroxylase is an enzyme that catalyzes the conversion of dopamine to norepinephrine, a crucial step in the synthesis of catecholamines within the adrenal glands and central nervous system.
A mitochondrial cytochrome P450 enzyme that catalyzes the 11-beta-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11B1 gene, is important in the synthesis of CORTICOSTERONE and HYDROCORTISONE. Defects in CYP11B1 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D2-class receptor genes contain INTRONS, and the receptors inhibit ADENYLYL CYCLASES.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D1-class receptor genes lack INTRONS, and the receptors stimulate ADENYLYL CYCLASES.
Drugs that bind to and activate dopamine receptors.
Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.
Cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behavior of cells.
An enzyme of the oxidoreductase class that catalyzes the formation of L-TYROSINE, dihydrobiopterin, and water from L-PHENYLALANINE, tetrahydrobiopterin, and oxygen. Deficiency of this enzyme may cause PHENYLKETONURIAS and PHENYLKETONURIA, MATERNAL. EC 1.14.16.1.

Long-term effects of N-2-chlorethyl-N-ethyl-2-bromobenzylamine hydrochloride on noradrenergic neurones in the rat brain and heart. (1/584)

1 N-2-Chlorethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP 4) 50 mg/kg intraperitoneally, produced a long-term decrease in the capacity of brain homogenates to accumulate noradrenaline with significant effect 8 months after the injection. It had no effect on the noradrenaline uptake in homogenates from the striatum (dopamine neurones) and on the uptake of 5-hydroxytryptamine (5-HT) in various brain regions. 2 In vitro DSP 4 inhibited the noradrenaline uptake in a cortical homogenate with an IC50 value of 2 muM but was more than ten times less active on the dopamine uptake in a striatal homogenate and the 5-HT uptake in a cortical homogenate. 3 DSP 4 (50 mg/kg i.p.) inhibited the uptake of noradrenaline in the rat heart atrium in vitro but this action was terminated within 2 weeks. 4 DSP 4 (50 mg/kg i.p.) cuased a decrease in the dopamine-beta-hydroxylase (DBH) activity in the rat brain and heart. The onset of this effect was slow; in heart a lag period of 2-4 days was noted. In brain the DBH-activity in cerebral cortex was much more decreased than that in hypothalamus which was only slightly affected. A significant effect was still found 8 months after the injection. The noradrenaline concentration in the brain was greatly decreased for at least two weeks, whereas noradrenaline in heart was only temporarily reduced. 5 The long-term effects of DSP 4 on the noradrenaline accumulation, the DBH activity and noradrenaline concentration in the rat brain were antagonized by desipramine (10 mg/kg i.p.). 6 It is suggested that DSP 4 primarily attacks the membranal noradrenaline uptake sites forming a covalent bond and that the nerve terminals, as a result of this binding, degenerate.  (+info)

Dopamine beta-hydroxylase deficiency impairs cellular immunity. (2/584)

Norepinephrine, released from sympathetic neurons, and epinephrine, released from the adrenal medulla, participate in a number of physiological processes including those that facilitate adaptation to stressful conditions. The thymus, spleen, and lymph nodes are richly innervated by the sympathetic nervous system, and catecholamines are thought to modulate the immune response. However, the importance of this modulatory role in vivo remains uncertain. We addressed this question genetically by using mice that lack dopamine beta-hydroxylase (dbh-/- mice). dbh-/- mice cannot produce norepinephrine or epinephrine, but produce dopamine instead. When housed in specific pathogen-free conditions, dbh-/- mice had normal numbers of blood leukocytes, and normal T and B cell development and in vitro function. However, when challenged in vivo by infection with the intracellular pathogens Listeria monocytogenes or Mycobacterium tuberculosis, dbh-/- mice were more susceptible to infection, exhibited extreme thymic involution, and had impaired T cell function, including Th1 cytokine production. When immunized with trinitrophenyl-keyhole limpet hemocyanin, dbh-/- mice produced less Th1 cytokine-dependent-IgG2a antitrinitrophenyl antibody. These results indicate that physiological catecholamine production is not required for normal development of the immune system, but plays an important role in the modulation of T cell-mediated immunity to infection and immunization.  (+info)

Specification of neurotransmitter identity by Phox2 proteins in neural crest stem cells. (3/584)

We have investigated the specification of noradrenergic neurotransmitter identity in neural crest stem cells (NCSCs). Retroviral expression of both wild-type and dominant-negative forms of the paired homeodomain transcription factor Phox2a indicates a crucial and direct role for this protein (and/or the closely related Phox2b) in the regulation of endogenous tyrosine hydroxylase (TH) and dopamine-beta hydroxylase (DBH) gene expression in these cells. In collaboration with cAMP, Phox2a can induce expression of TH but not of DBH or of panneuronal genes. Phox2 proteins are, moreover, necessary for the induction of both TH and DBH by bone morphogenetic protein 2 (BMP2) (which induces Phox2a/b) and forskolin. They are also necessary for neuronal differentiation. These data suggest that Phox2a/b coordinates the specification of neurotransmitter identity and neuronal fate by cooperating environmental signals in sympathetic neuroblasts.  (+info)

Dehydrodicaffeic acid dilactone, an inhibitor of catechol-O-methyl transferase. (4/584)

In the screening of catechol-O-methyltransferase inhibitors, three compounds were isolated from the culture filtrate of a mushroom, Inonotus sp. One was 3,4-dihydroxycinnamic acid (caffeic acid) which had been reported as an inhibitor of this enzyme. The others were the dextrorotatory 2,6-bis-(3',4'-dihydroxyphenyl)-3,7-dioxabicyclo-[3,3,0]-octane 4,8-dione (dehydrodicaffeic acid dilactone) andits antipode. These new compounds inhibited both dopamine beta-hydroxylase and dopa decarboxylase and showed hypotensive activity in the SH rat.  (+info)

Enhanced contractility and decreased beta-adrenergic receptor kinase-1 in mice lacking endogenous norepinephrine and epinephrine. (5/584)

BACKGROUND: Elevated circulating norepinephrine (NE) has been implicated in causing the profound beta-adrenergic receptor (betaAR) downregulation and receptor uncoupling that are characteristic of end-stage human dilated cardiomyopathy, a process mediated in part by increased levels of beta-adrenergic receptor kinase (betaARK1). To explore whether chronic sustained NE stimulation is a primary stimulus that promotes deterioration in cardiac signaling, we characterized a gene-targeted mouse in which activation of the sympathetic nervous system cannot lead to an elevation in plasma NE and epinephrine. METHODS AND RESULTS: Gene-targeted mice that lack dopamine beta-hydroxylase (dbh-/-), the enzyme needed to convert dopamine to NE, were created by homologous recombination. In vivo contractile response to the beta1AR agonist dobutamine, measured by a high-fidelity left ventricular micromanometer, was enhanced in mice lacking the dbh gene. In unloaded adult myocytes isolated from dbh-/- mice, basal contractility was significantly increased compared with control cells. Furthermore, the increase in betaAR responsiveness and enhanced cellular contractility were associated with a significant reduction in activity and protein level of betaARK1 and increased high-affinity agonist binding without changes in betaAR density or G-protein levels. CONCLUSIONS: Mice that lack the ability to generate NE or epinephrine show increased contractility associated primarily with a decrease in the level of betaARK1 protein and kinase activity. This animal model will be valuable in testing whether NE is required for the pathogenesis of heart failure through mating strategies that cross the dbh-/- mouse into genetically engineered models of heart failure.  (+info)

Regulation of basal expression of catecholamine-synthesizing enzyme genes by PACAP. (6/584)

We have previously reported that the cAMP/protein kinase A (PKA) pathway is important in the gene regulation of both induction and basal expressions of the catecholamine synthesizing enzymes tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH). The neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) has been shown to activate the intracellular cAMP/PKA pathway. In the present study, using primary cultured bovine adrenal medullary cells, we determined whether the basal activity of the PACAP receptor might play a role in the maintenance of the basal expression of these enzyme genes via the cAMP/PKA pathway. The potent PACAP receptor antagonist PACAP (6-38) caused a reduction of TH and DBH mRNA levels in a dose dependent manner as well as their enzyme activities and TH protein level. The effects of PACAP (6-38) and the PKA inhibitor H-89 exhibited generally similar trends, and were not additive in the reduction of TH and DBH gene expression and activities, suggesting that they take a common intracellular signaling pathway. The antagonist also caused decreases in the intracellular norepinephrine and epinephrine levels similar to the effect of H-89. Taken together, the data suggests that PACAP is involved in the regulation of maintenance of the catecholamine synthesizing enzymes TH and DBH by utilizing the cAMP/PKA pathway.  (+info)

Acetylcholinesterase activity, and neurofilament protein, and catecholamine synthesizing enzymes immunoreactivities in the mouse adrenal gland during postnatal development. (7/584)

The present study showed the acetylcholinesterase (AChE) activity, and neurofilament protein (NFP), catecholamine-synthesizing enzymes, dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) immunoreactivities in the mouse adrenal gland during postnatal development. From birth to postnatal-1-day, AChE activity was weakly and diffusely found in some medullary cells and in very few nerve fibers whereas strong NFP immunoreactivity was seen in a few ganglion cells and in remarkably numerous nerve fibers in the medulla. Almost all meduallary cells were reactive for both DBH and PNMT during this period. From postnatal-2- or -3-day to postnatal-1-week, strong AChE activity was observed in a few large ganglion cells, but the reaction was weak in clusters of chromaffin cells, and the number of strong AChE-active nerve fibers in the medulla was rapidly increased. From postnatal-2-day onwards, the number of NFP-immunoreactive nerve fibers in the medulla were remarkably numerous. Numerous chromaffin cells were reactive for both DBH and PNMT whereas some chromaffin cells were reactive for only DBH from postnatal-2-day onwards. These results suggest that drastic changes such as an increase of acetylcholine in the nerve fibers, differentiation of noradrenaline and adrenaline cells of the medulla may occur during this period. From postnatal-2-week to postnatal-3-week, weak AChE activity was seen in the clusters of several chromaffin cells and a few ganglion cells, and the number of AChE-active nerve fibers in the medulla was gradually increased. From postnatal-4-week to postnatal-8-week (adult), the distribution and frequency of AChE activity in the adrenal gland were similar to those at postnatal-3-week. In the adult, AChE activity was weakly seen in the clusters of several chromaffin cells showing noradrenaline fluorescence in the adrenal medulla. The noradrenaline cells were contacted by denser AChE-reactive nerve fibers than adrenaline cells. These results suggest that the development of cholinergic nervous system in the mouse adrenal medulla may be completed by postnatal-3-week.  (+info)

Kinetic parameters for dimeric and tetrameric forms of bovine dopamine beta-monooxygenase and their relationship to non-Michaelis-Menten behavior. (8/584)

Bovine dopamine beta-monooxygenase has been assayed over a 10,000-fold range in protein concentration, to approximate conditions where the enzyme was shown to be a dimer or tetramer. Michaelis-Menten kinetics are observed with k(cat) and k(cat)/Km for dissociated enzyme reduced 30% and 200-300% relative to tetramer. Addition of chloride ions to very dilute enzyme or the use of intermediate enzyme concentrations causes non-Michaelis-Menten behavior, attributed to an equilibration between dimer and tetramer. This is not expected to contribute to activity within the chromaffin vesicle, where enzyme and chloride ions are at high levels.  (+info)

Dopamine beta-hydroxylase (DBH) is an enzyme that plays a crucial role in the synthesis of catecholamines, which are important neurotransmitters and hormones in the human body. Specifically, DBH converts dopamine into norepinephrine, another essential catecholamine.

DBH is primarily located in the adrenal glands and nerve endings of the sympathetic nervous system. It requires molecular oxygen, copper ions, and vitamin C (ascorbic acid) as cofactors to perform its enzymatic function. Deficiency or dysfunction of DBH can lead to various medical conditions, such as orthostatic hypotension and neuropsychiatric disorders.

Steroid 11-beta-hydroxylase is a crucial enzyme involved in the steroidogenesis pathway, specifically in the synthesis of cortisol and aldosterone, which are vital hormones produced by the adrenal glands. This enzyme is encoded by the CYP11B1 gene in humans.

The enzyme's primary function is to catalyze the conversion of 11-deoxycortisol to cortisol and 11-deoxycorticosterone to aldosterone through the process of hydroxylation at the 11-beta position of the steroid molecule. Cortisol is a critical glucocorticoid hormone that helps regulate metabolism, immune response, and stress response, while aldosterone is a mineralocorticoid hormone responsible for maintaining electrolyte and fluid balance in the body.

Deficiencies or mutations in the CYP11B1 gene can lead to various disorders, such as congenital adrenal hyperplasia (CAH), which may result in impaired cortisol and aldosterone production, causing hormonal imbalances and associated symptoms.

Dopamine is a type of neurotransmitter, which is a chemical messenger that transmits signals in the brain and nervous system. It plays several important roles in the body, including:

* Regulation of movement and coordination
* Modulation of mood and motivation
* Control of the reward and pleasure centers of the brain
* Regulation of muscle tone
* Involvement in memory and attention

Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area. It is released by neurons (nerve cells) and binds to specific receptors on other neurons, where it can either excite or inhibit their activity.

Abnormalities in dopamine signaling have been implicated in several neurological and psychiatric conditions, including Parkinson's disease, schizophrenia, and addiction.

Dopamine D2 receptor is a type of metabotropic G protein-coupled receptor that binds to the neurotransmitter dopamine. It is one of five subtypes of dopamine receptors (D1-D5) and is encoded by the gene DRD2. The activation of D2 receptors leads to a decrease in the activity of adenylyl cyclase, which results in reduced levels of cAMP and modulation of ion channels.

D2 receptors are widely distributed throughout the central nervous system (CNS) and play important roles in various physiological functions, including motor control, reward processing, emotion regulation, and cognition. They are also involved in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, drug addiction, and Tourette syndrome.

D2 receptors have two main subtypes: D2 short (D2S) and D2 long (D2L). The D2S subtype is primarily located in the presynaptic terminals and functions as an autoreceptor that regulates dopamine release, while the D2L subtype is mainly found in the postsynaptic neurons and modulates intracellular signaling pathways.

Antipsychotic drugs, which are used to treat schizophrenia and other psychiatric disorders, work by blocking D2 receptors. However, excessive blockade of these receptors can lead to side effects such as extrapyramidal symptoms (EPS), tardive dyskinesia, and hyperprolactinemia. Therefore, the development of drugs that selectively target specific subtypes of dopamine receptors is an active area of research in the field of neuropsychopharmacology.

Dopamine D1 receptors are a type of G protein-coupled receptor that bind to the neurotransmitter dopamine. They are classified as D1-like receptors, along with D5 receptors, and are activated by dopamine through a stimulatory G protein (Gs).

D1 receptors are widely expressed in the central nervous system, including the striatum, prefrontal cortex, hippocampus, and amygdala. They play important roles in various physiological functions, such as movement control, motivation, reward processing, working memory, and cognition.

Activation of D1 receptors leads to increased levels of intracellular cyclic adenosine monophosphate (cAMP) and activation of protein kinase A (PKA), which in turn modulate the activity of various downstream signaling pathways. Dysregulation of dopamine D1 receptor function has been implicated in several neurological and psychiatric disorders, including Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder (ADHD), and drug addiction.

Dopamine agonists are a class of medications that mimic the action of dopamine, a neurotransmitter in the brain that regulates movement, emotion, motivation, and reinforcement of rewarding behaviors. These medications bind to dopamine receptors in the brain and activate them, leading to an increase in dopaminergic activity.

Dopamine agonists are used primarily to treat Parkinson's disease, a neurological disorder characterized by motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and postural instability. By increasing dopaminergic activity in the brain, dopamine agonists can help alleviate some of these symptoms.

Examples of dopamine agonists include:

1. Pramipexole (Mirapex)
2. Ropinirole (Requip)
3. Rotigotine (Neupro)
4. Apomorphine (Apokyn)

Dopamine agonists may also be used off-label to treat other conditions, such as restless legs syndrome or certain types of dopamine-responsive dystonia. However, these medications can have significant side effects, including nausea, dizziness, orthostatic hypotension, compulsive behaviors (such as gambling, shopping, or sexual addiction), and hallucinations. Therefore, they should be used with caution and under the close supervision of a healthcare provider.

Dopamine antagonists are a class of drugs that block the action of dopamine, a neurotransmitter in the brain associated with various functions including movement, motivation, and emotion. These drugs work by binding to dopamine receptors and preventing dopamine from attaching to them, which can help to reduce the symptoms of certain medical conditions such as schizophrenia, bipolar disorder, and gastroesophageal reflux disease (GERD).

There are several types of dopamine antagonists, including:

1. Typical antipsychotics: These drugs are primarily used to treat psychosis, including schizophrenia and delusional disorders. Examples include haloperidol, chlorpromazine, and fluphenazine.
2. Atypical antipsychotics: These drugs are also used to treat psychosis but have fewer side effects than typical antipsychotics. They may also be used to treat bipolar disorder and depression. Examples include risperidone, olanzapine, and quetiapine.
3. Antiemetics: These drugs are used to treat nausea and vomiting. Examples include metoclopramide and prochlorperazine.
4. Dopamine agonists: While not technically dopamine antagonists, these drugs work by stimulating dopamine receptors and can be used to treat conditions such as Parkinson's disease. However, they can also have the opposite effect and block dopamine receptors in high doses, making them functionally similar to dopamine antagonists.

Common side effects of dopamine antagonists include sedation, weight gain, and movement disorders such as tardive dyskinesia. It's important to use these drugs under the close supervision of a healthcare provider to monitor for side effects and adjust the dosage as needed.

Dopamine receptors are a type of G protein-coupled receptor that bind to and respond to the neurotransmitter dopamine. There are five subtypes of dopamine receptors (D1-D5), which are classified into two families based on their structure and function: D1-like (D1 and D5) and D2-like (D2, D3, and D4).

Dopamine receptors play a crucial role in various physiological processes, including movement, motivation, reward, cognition, emotion, and neuroendocrine regulation. They are widely distributed throughout the central nervous system, with high concentrations found in the basal ganglia, limbic system, and cortex.

Dysfunction of dopamine receptors has been implicated in several neurological and psychiatric disorders, such as Parkinson's disease, schizophrenia, attention deficit hyperactivity disorder (ADHD), drug addiction, and depression. Therefore, drugs targeting dopamine receptors have been developed for the treatment of these conditions.

Phenylalanine Hydroxylase (PAH) is an enzyme that plays a crucial role in the metabolism of the essential amino acid phenylalanine. This enzyme is primarily found in the liver and is responsible for converting phenylalanine into tyrosine, another amino acid. PAH requires a cofactor called tetrahydrobiopterin (BH4) to function properly.

Defects or mutations in the gene that encodes PAH can lead to a genetic disorder known as Phenylketonuria (PKU). In PKU, the activity of PAH is significantly reduced or absent, causing an accumulation of phenylalanine in the body. If left untreated, this condition can result in severe neurological damage and intellectual disability due to the toxic effects of high phenylalanine levels on the developing brain. A strict low-phenylalanine diet and regular monitoring of blood phenylalanine levels are essential for managing PKU and preventing associated complications.

... pyrocatechol beta-oxidase dopa beta-hydroxylase dopamine beta-oxidase dopamine hydroxylase phenylamine beta-hydroxylase (3,4- ... dopamine beta-monooxygenase dopamine beta-hydroxylase membrane-associated dopamine beta-monooxygenase (MDBH) soluble dopamine ... GeneReviews/NIH/NCBI/UW entry on Dopamine Beta-Hydroxylase Deficiency Dopamine+beta-Hydroxylase at the U.S. National Library of ... Dopamine beta-hydroxylase (DBH), also known as dopamine beta-monooxygenase, is an enzyme (EC 1.14.17.1) that in humans is ...
... hydroxylase deficiency is a condition that affects the autonomic nervous system, which controls involuntary body processes such ... medlineplus.gov/genetics/condition/dopamine-beta-hydroxylase-deficiency/ Dopamine beta-hydroxylase deficiency. ... Mutations in the dopamine beta-hydroxylase gene are associated with human norepinephrine deficiency. Am J Med Genet. 2002 Mar 1 ... Dopamine beta (β)-hydroxylase deficiency is a condition that affects the autonomic nervous system, which controls involuntary ...
View our 5 Dopamine beta-Hydroxylase products for your research including Dopamine beta-Hydroxylase Primary Antibodies, ... Dopamine beta-Hydroxylase: Products. Dopamine β-hydroxylase (DβH; also dopamine β-monooxygenase) is a 73 - 77 kDa member of the ... The first is an N-terminal 120 aa DOMON domain (dopamine β-monooxygenase N-terminal) that may either bind DβH to the cell ... converts dopamine into norepinepherine.. Human DβH is a copper-containing disulfide-linked homodimer that is found in neurons ...
Dopamine Beta Hydroxylase antibody LS-C6444 is an unconjugated sheep polyclonal antibody to human Dopamine Beta Hydroxylase ( ... Dopamine Beta Hydroxylase antibody LS-C6444 is an unconjugated sheep polyclonal antibody to human Dopamine Beta Hydroxylase ( ... IHC‑plus™ DBH/Dopamine Beta Hydroxylase Antibody (aa437‑448) LS‑B9552 Species: Human, Mouse, Rat, Bovine, Guinea pig, Hamster, ... Dopamine Beta Hydroxylase (DbH) C-terminal. By immunoblot the antibody specifically reacts with a single (or double) band (s) ...
Nepicastat hydrochloride is a potent and selective inhibitor of both bovine and human dopamine-β-hydroxylase with IC50 of 8.5 ...
Dopamine Beta-hydroxylase Deficiency. In Encyclopedia. https://encyclopedia.pub/entry/5417 Yin, Nicole. "Dopamine Beta- ... Mutations in the dopamine beta-hydroxylase gene are associated with humannorepinephrine deficiency. Am J Med Genet. 2002 Mar 1; ... Dopamine beta (β)-hydroxylase deficiency is a condition that affects the autonomic nervous system, which controls involuntary ... Garland EM, Biaggioni I. Dopamine Beta-Hydroxylase Deficiency. 2003 Sep 4[updated 2019 Apr 25]. In: Adam MP, Ardinger HH, Pagon ...
DBH: dopamine beta-hydroxylase. *DBT: dihydrolipoamide branched chain transacylase E2. *DCAF17: DDB1 and CUL4 associated factor ...
... we used antibodies directed against dopamine beta-hydroxylase (DβH), the synthetic enzyme for NE, or against two different ... or against two different isoforms of the beta-adrenergic receptors (βARs), one that predominately recognizes neurons (βAR 248) ... isoforms of the beta-adrenergic receptors (βARs), one that predominately recognizes neurons (βAR 248) and the other astrocytes ... we used antibodies directed against dopamine beta-hydroxylase (DβH), the synthetic enzyme for NE, ...
Polymorphisms of the gene encoding dopamine beta hydroxylase (DBH) have been reported to be associated with ADHD; however, ... Reduced DBH expression would be consistent with decreased conversion of dopamine to noradrenaline and thus with a relative hypo ... Identification and functional characterisation of a novel dopamine beta hydroxylase gene variant associated with attention ...
Recently, we obtained evidence that the SHR harbors a variant in the gene for dopamine beta hydroxylase (Dbh) that is ... Effects of transgenic expression of dopamine beta hydroxylase (Dbh) gene on blood pressure in spontaneously hypertensive rats. ... Effects of transgenic expression of dopamine beta hydroxylase (Dbh) gene on blood pressure ... Pressão Sanguínea/genética; Dopamina beta-Hidroxilase/biossíntese; Dopamina beta-Hidroxilase/genética; Hipertensão/genética; ...
Kanda T, Gotoh F, Yamamoto M, Sakai F, Takeoka T, Takagi Y: Serum dopamine beta-hydroxylase activity in acute stroke. Stroke ... Wilson AF, ElstonRC, Siervogel RM ,Tran LD: Linkage of a gene regulating dopamine- beta-hydroxylase activity and the ABO blood ... Zhang H, Cotecchia S, Thomas SA, Tanoue A, Tsujimoto G, Faber JE: Gene deletion of dopamine beta-hydroxylase and alpha1- ... Miyata S, Nagata H, Yamao S, Nakamura S, Kameyama M: Dopamine-beta-hydroxylase activities in serum and cerebrospinal fluid of ...
Urinary catecholamine excretion and plasma dopamine-beta-hydroxylase activity during mental work performed in some periods of ...
Possible control of dopamine beta-hydroxylase via a codominant mechanism associated with the polymorphic (GT)n repeat at its ... Dive into the research topics of Possible control of dopamine beta-hydroxylase via a codominant mechanism associated with the ...
Enzymes: choline acetyltransferase; dopamine beta-hydroxylase; GABA transaminase; glutamic acid decarboxylase; glutaminergic; ... Two targets, the mu-opiate receptor and the dopamine transporter, have been extensively pursued in medication discovery efforts ... such as the dopamine receptor, an indirect site of action for cocaine and amphetamine, or ligand gated ion channels, such as ... dopamine: D1, D3, D4, D5; estrogen; GABA A subunits; GABA ion channel; GABA B; glutamatergic, glycine site; metabotropic ...
Deficiency of dopamine-beta-hydroxylase leads to reduced catecholamine levels. Decreased ascorbic acid oxidase activity leads ... and dopamine beta hydroxylase. The deficiency or impaired function of these enzyme systems is thought to be responsible for the ... Phi Beta Kappa, Society for Neuroscience. Disclosure: Nothing to disclose. ...
Rush, R.A.; Geffen, L.B. Dopamine beta-hydroxylase in health and disease. Crit. Rev. Clin. Lab. Sci. 1980, 12, 241-277. [Google ... The Cu-containing enzyme dopamine β-hydroxylase catalyses the conversion of dopamine to norepinephrine [14,59,60] and vitamin C ... the enzyme cofactor for the tyrosine hydroxylase that produces dopamine [64]. Dopamine is a neurotransmitter important for ... Levine, M. Ascorbic acid specifically enhances dopamine beta-monooxygenase activity in resting and stimulated chromaffin cells ...
dopamine beta-hydroxylase. ISO. SMPDB. SMP:00012. NCBI chr 3:10,488,260...10,505,245 Ensembl chr 3:10,488,260...10,505,248 ... dopamine beta-hydroxylase. ISO. RGD. PMID:19342614. RGD:4139904. NCBI chr 3:10,488,260...10,505,245 Ensembl chr 3:10,488,260... ... dopamine beta-hydroxylase. ISO. RGD. PMID:19342614. RGD:4139904. NCBI chr 3:10,488,260...10,505,245 Ensembl chr 3:10,488,260... ... beta-carotene oxygenase 1. ISO. IEA. TAS. SMPDB. KEGG. RGD. PMID:21569862 PMID:21718801. SMP:00074 rno:00830, RGD:6903956, RGD: ...
Dopamine beta-hydroxylase: Biochemistry and molecular biology. Ann N Y Acad Sci. 493: 342-50. Retrieved August 2, 2007. ... Next is β-oxidation into norepinephrine by dopamine beta hydroxylase.. *Epinephrine then is synthesized from norepinephrine via ... The enzyme phenylalanine hydroxylase (PAH) is fundamental to the process through conversion of amino acid phenylalanine into ... The enzyme phenylalananine hydroxylase (PAH) is necessary to break down phenylalanine. However, a genetic mutation in the gene ...
Dopamine beta-Hydroxylase Deficiency (PathBank: SMP0000498). *Monoamine Oxidase-A Deficiency (MAO-A) (PathBank: SMP0000533) ...
DBH is a gene associated with dopamine beta-hydroxylase deficiency (inheritance: recessive), which is characterized by severe ... Here, we show recessive betas in FinnGen versus UKBB (betas set to 5, when beta , 5). Plot size corresponds to MAF in gnomAD ... DBH is associated with the recessively inherited disease dopamine beta-hydroxylase deficiency, which is characterized by severe ... a common mechanism that may explain protection against falciparum malaria in sickle trait and beta-thalassemia trait. Blood 104 ...
dopamine beta-hydroxylase deficiency DYSOSTOSIS MULTIPLEX, AIN-NAZ TYPE Efavirenz, Poor Metabolism of ... Genes Community Projects (beta) QTLs Strains Markers Genome Information Ontologies Cell Lines References Download Submit Data ... OntoMate (Literature Search) JBrowse (Genome Browser) Synteny Browser (VCMap) (beta) Variant Visualizer Multi-Ontology ...
Check Hydroxylases pathway , inhibitors reviews and assay information. ... Hydroxylases Inhibitors on signaling pathway are available at Adooq Bioscience. ... Nepicastat hydrochloride is an inhibitor of dopamine beta-hydroxylase, an enzyme that catalyzes the conversion of dopamine to ... Nepicastat is an inhibitor of dopamine beta-hydroxylase, an enzyme that catalyzes the conversion of dopamine to norepinephrine ...
Pathogenic - Dopamine Beta-Hydroxylase Deficiency. 16.05.2022 00:16 If you have the gene mutation "CT" or "TC" you are an ... On the super rare chance you are homozygous "CC", you have the extremely rare condition Dopamine Beta-Hydroxylase Deficiency. ... unaffected carrier of Dopamine Beta-Hydroxylase Deficiency. ...
MOST FB+ NEURONS STAINED FOR DOPAMINE BETA HYDROXYLASE (DBH); ONE-THIRD TO ONE-QUARTER STAINED FOR SOMATOSTATIN (SOM), ... Most FB+ neurons stained for dopamine beta hydroxylase (DBH); one-third to one-quarter stained for somatostatin (SOM), ...
miR-375 inhibits catecholamine biogenesis by reducing the expression of tyrosine hydroxylase and dopamine-beta-hydroxylase in ... miR-375 maintains normal pancreatic alpha- and beta-cell mass. Proc Natl Acad Sci U S A (2009) 106:5813-8. doi:10.1073/pnas. ... Circulating miR-375 as a biomarker of beta-cell death and diabetes in mice. Endocrinology (2013) 154:603-8. doi:10.1210/en.2012 ... miR-375 is specifically expressed in endocrine and neuroendocrine cells, including pancreatic islets beta-cells, pituitary ...
By genetically eliminating the biosynthetic enzyme for NE, dopamine beta-hydroxylase (DBH), mutant mice (Dbh-/-) that ...
Anti-DBH-SAP - targets cells expressing dopamine beta-hydroxylase (Cat. #IT-03) ...
1997) Distribution of dopamine beta-hydroxylase-like immunoreactive fibers within the shell subregion of the nucleus accumbens ... BETA: Related publications Publications. You can help our author matching system! If you notice any publications incorrectly ... 1996) Modulation of forebrain electroencephalographic activity in halothane-anesthetized rat via actions of noradrenergic beta- ... 1996) Enhancement of behavioral and electroencephalographic indices of waking following stimulation of noradrenergic beta- ...
  • Mutations identified in dopamine beta hydroxylase deficiency and non-synonymous SNPs such as rs6271 in this gene were found to cause defective secretion of the protein from the endoplasmic reticulum. (wikipedia.org)
  • Inadequate DBH is called dopamine beta hydroxylase deficiency. (wikipedia.org)
  • Dopamine beta (β)-hydroxylase deficiency is a condition that affects the autonomic nervous system, which controls involuntary body processes such as the regulation of blood pressure and body temperature. (medlineplus.gov)
  • Individuals with dopamine β-hydroxylase deficiency typically experience a sharp drop in blood pressure upon standing ( orthostatic hypotension ), which can cause dizziness, blurred vision, or fainting. (medlineplus.gov)
  • People with dopamine β-hydroxylase deficiency experience extreme fatigue during exercise (exercise intolerance) due to their problems maintaining a normal blood pressure. (medlineplus.gov)
  • Dopamine β-hydroxylase deficiency is a very rare disorder. (medlineplus.gov)
  • Mutations in the DBH gene cause dopamine β-hydroxylase deficiency. (medlineplus.gov)
  • The lack of norepinephrine causes difficulty with regulating blood pressure and other autonomic nervous system problems seen in dopamine β-hydroxylase deficiency. (medlineplus.gov)
  • Garland EM, Biaggioni I. Dopamine Beta-Hydroxylase Deficiency. (medlineplus.gov)
  • Mutations in the dopamine beta-hydroxylase gene are associated with human norepinephrine deficiency. (medlineplus.gov)
  • Senard JM, Rouet P. Dopamine beta-hydroxylase deficiency. (medlineplus.gov)
  • Dopamine Beta-hydroxylase Deficiency" Encyclopedia , https://encyclopedia.pub/entry/5417 (accessed December 02, 2023). (encyclopedia.pub)
  • Other features of dopamine β-hydroxylase deficiency include droopy eyelids (ptosis), nasal congestion, and an inability to stand for a prolonged period of time. (encyclopedia.pub)
  • Phenylketonuria (PKU) is a genetic disorder characterized by a deficiency in, or problem with the proper activity of, the enzyme phenylalanine hydroxylase (PAH), which is necessary to metabolize the amino acid phenylalanine to the amino acid tyrosine . (newworldencyclopedia.org)
  • If you have the gene mutation "CT" or "TC" you are an unaffected carrier of Dopamine Beta-Hydroxylase Deficiency. (opensnp.org)
  • On the super rare chance you are homozygous "CC", you have the extremely rare condition Dopamine Beta-Hydroxylase Deficiency. (opensnp.org)
  • NORTHERA is indicated for the treatment of orthostatic dizziness, lightheadedness, or the "feeling that you are about to black out" in adult patients with symptomatic neurogenic orthostatic hypotension (nOH) caused by primary autonomic failure (Parkinson's disease [PD], multiple system atrophy, and pure autonomic failure), dopamine beta-hydroxylase deficiency, and non-diabetic autonomic neuropathy. (nih.gov)
  • The dopamine β-hydroxylase deficiency is a very rare inherited disorder that is characterized in the blood by the lack of norepinephrine and epinephrine. (sciencedict.com)
  • What is dopamine β-hydroxylase deficiency? (sciencedict.com)
  • A dopamine-β-hydroxylase deficiency is characterized not only by an increased concentration of dopamine but also by a lack of neurotransmitters and hormones noradrenaline and adrenaline. (sciencedict.com)
  • In the case of dopamine β-hydroxylase deficiency, the first reaction step does not take place or takes place only inadequately. (sciencedict.com)
  • Because it only occurs once in each of them, the parents do not suffer from dopamine β-hydroxylase deficiency. (sciencedict.com)
  • The symptoms of a dopamine-β-hydroxylase deficiency correspond to the failure of the functions of the two hormones noradrenaline and adrenaline. (sciencedict.com)
  • Orthostatic hypotension and various cardiovascular disorders are among the most important symptoms of dopamine β-hydroxylase deficiency. (sciencedict.com)
  • In addition, newborns with dopamine β-hydroxylase deficiency often suffer from hypothermia, muscle hypotension and hypoglycaemia. (sciencedict.com)
  • When diagnosing dopamine β-hydroxylase deficiency, it is not enough to just determine the enzyme dopamine β-hydroxylase. (sciencedict.com)
  • The dopamine beta hydroxylase deficiency market is expected to witness market growth at a rate of 6.00% in the forecast period of 2022 to 2029. (biiut.com)
  • Dopamine beta-hydroxylase deficiency (or norepinephrine deficiency) is caused by mutation in the gene encoding dopamine beta-hydroxylase. (smpdb.ca)
  • Dopamine beta-hydroxylase (DBH), also known as dopamine beta-monooxygenase, is an enzyme (EC 1.14.17.1) that in humans is encoded by the DBH gene. (wikipedia.org)
  • The three substrates of the enzyme are dopamine, vitamin C (ascorbate), and O2. (wikipedia.org)
  • for example, the human DBH enzyme catalyzes the beta-hydroxylation of amphetamine and para-hydroxyamphetamine, producing norephedrine and para-hydroxynorephedrine respectively. (wikipedia.org)
  • The systematic name of this enzyme class is 3,4-dihydroxyphenethylamine, ascorbate:oxygen oxidoreductase (beta-hydroxylating). (wikipedia.org)
  • The DBH gene provides instructions for producing the enzyme dopamine β-hydroxylase. (medlineplus.gov)
  • DBH gene mutations result in the production of a nonfunctional dopamine β-hydroxylase enzyme. (medlineplus.gov)
  • To understand better the cellular mechanisms of NE and its adrenergic receptors in the LA, we used antibodies directed against dopamine beta-hydroxylase (DβH), the synthetic enzyme for NE, or against two different isoforms of the beta-adrenergic receptors (βARs), one that predominately recognizes neurons (βAR 248) and the other astrocytes (βAR 404), to characterize the microenvironments of DβH and βAR. (frontiersin.org)
  • To understand better the cellular mechanisms of NE's contributions to fear learning, we examined the anatomical organization of NE terminals and βARs in the LA. In this study, we employed immunoelectron microscopy to determine whether terminals immunoreactive for dopamine beta-hydroxylase (DβH), the synthetic enzyme for NE, form synaptic junctions in the LA and if so, examine these synapses and identify the post-synaptic targets on NE terminals. (frontiersin.org)
  • Tryosine, one of the main precursors of catecholamines, is created from phenylalanine by hydroxylation via the enzyme phenylalanine hydroxylase. (newworldencyclopedia.org)
  • The enzyme phenylalanine hydroxylase (PAH) is fundamental to the process through conversion of amino acid phenylalanine into the amino acid tyrosine. (newworldencyclopedia.org)
  • The enzyme phenylalananine hydroxylase (PAH) is necessary to break down phenylalanine. (newworldencyclopedia.org)
  • Nepicastat is an inhibitor of dopamine beta-hydroxylase, an enzyme that catalyzes the conversion of dopamine to norepinephrine. (adooq.com)
  • 4-Chloro-DL-phenylalanine is a selective and irreversible inhibitor of tryptophan hydroxylase, a rate-limiting enzyme in the biosynthesis of serotonin (5-HYDROXYTRYPTAMINE). (adooq.com)
  • By genetically eliminating the biosynthetic enzyme for NE, dopamine beta-hydroxylase (DBH), mutant mice (Dbh-/-) that completely lack NE and epinephrine were created. (upenn.edu)
  • The enzyme dopamine beta-hydroxylase, which catalyzes the formation of norepinephrine from dopamine, requires copper. (hairanalysisprogram.com)
  • However, a defective enzyme dopamine-β-hydroxylase prevents its formation. (sciencedict.com)
  • Dopamine beta-hydroxylase catalyzes the conversion of dopamine to norepinephrine. (wikipedia.org)
  • People who lack functional dopamine β-hydroxylase cannot convert dopamine to norepinephrine, which leads to a shortage of norepinephrine in the body. (medlineplus.gov)
  • We found modestly increased adrenal expression of Dbh in transgenic rats versus SHR non-transgenic controls that was associated with reduced adrenal levels of dopamine and increased plasma levels of norepinephrine and epinephrine . (bvsalud.org)
  • The Cloninger trait of Persistence has been associated with dopamine neurotransmission and is likely related to the ABO/DBH linkage via the role of DBH in determining the dopamine:norepinephrine ratio. (hy-ls.org)
  • Low DBH is known to be associated with trait Impulsiveness so it would appear that impulsiveness may be related to a higher dopamine to norepinephrine ratio, and based on research demonstrating the role of dopamine neurotransmission in the expression of motivation as well as trait Persistence, the likely situation is that lower tonic dopaminergic transmission produces Persistent action and higher tonic dopaminergic transmission produces Impulsive action. (hy-ls.org)
  • The intricate coordination of systems in the human body is seen in the process, catalyzed by enzymes , by which phenylalanine is degraded into tyrosine, which in turn is converted into the vitally important neurotransmitters and hormones dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline). (newworldencyclopedia.org)
  • L-tyrosine, in turn, is converted into L-DOPA, which is further converted into dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline). (newworldencyclopedia.org)
  • Dopamine, norepinephrine, and epinephrine are known as catecholamines . (newworldencyclopedia.org)
  • Next is β-oxidation into norepinephrine by dopamine beta hydroxylase. (newworldencyclopedia.org)
  • In the first reaction step, dopamine is oxidized to norepinephrine with the help of the enzymatic support of dopamine-β-hydroxylase with the addition of an additional OH group on the C3 atom. (sciencedict.com)
  • Panaxtriol is a tyrosine hydroxylase inducer. (adooq.com)
  • The neurological properties of N2a-Rα based on AhR activation were evaluated by immunohistochemical analysis of cytoskeletal molecules and by RT-PCR analysis of mRNA expression of neurotransmitter-production related molecules, such as tyrosine hydroxylase (TH). (biomedcentral.com)
  • N2a-Rα cells expressed tyrosine hydroxylase (TH) mRNA as a functional marker of catecholaminergic neurotransmitter production. (biomedcentral.com)
  • Effects of transgenic expression of dopamine beta hydroxylase (Dbh) gene on blood pressure in spontaneously hypertensive rats. (bvsalud.org)
  • Recently, we obtained evidence that the SHR harbors a variant in the gene for dopamine beta hydroxylase (Dbh) that is associated with reduced adrenal expression of Dbh mRNA and reduced DBH enzymatic activity which correlated negatively with blood pressure . (bvsalud.org)
  • The gene for phenylalanine hydroxylase is found on chromosome 12 (Longe 2006). (newworldencyclopedia.org)
  • This is an autosomal recessive mutation of a gene on chromosome 9, which encodes dopamine β-hydroxylase as the DBH gene. (sciencedict.com)
  • The genetic mutation has been isolated to the nerve growth factor beta gene. (medscape.com)
  • Nepicastat hydrochloride is a potent and selective inhibitor of both bovine and human dopamine-β-hydroxylase with IC50 of 8.5 nM and 9 nM, with negligible affinity for twelve other enzymes and thirteen neurotransmitter receptors. (dcchemicals.com)
  • Fusaric acid is a potent dopamine β-hydroxylase inhibitor. (dcchemicals.com)
  • LX 1606 hippurate is an orally bioavailable, small-molecule, tryptophan hydroxylase (TPH) inhibitor with potential antiserotonergic activity. (adooq.com)
  • LX-1031 is a potent, orally available tryptophan 5-hydroxylase (TPH) inhibitor that reduces serotonin (5-HT) synthesis peripherally. (adooq.com)
  • Ro 61-8048 is a potent and competitive kynurenine 3-hydroxylase inhibitor (Ki = 4.8 nM, IC50 = 37 nM). (adooq.com)
  • Metyrapone is an inhibitor of cytochrome P450-mediated ω/ω-1 hydroxylase activity and CYP11B1. (adooq.com)
  • Osilodrostat (LCI699) is a potent inhibitor of human 11β-hydroxylase and aldosterone synthase with IC50 values of 2.5 and 0.7 nM, respectively. (adooq.com)
  • Telotristat (LP-778902) is a potent tryptophan hydroxylase inhibitor with an in vivo IC50 of 0.028 μM. (adooq.com)
  • Rodatristat (KAR5417) is a potent tryptophan hydroxylase 1 (TPH1) and TPH2 inhibitor with IC50s value of 33 nM and 7 nM, respectively, and shows robust reduction of intestinal serotonin (5-HT) levels in mice. (adooq.com)
  • Rodatristat ethyl (KAR5585) is a first-in-class oral tryptophan hydroxylase 1 (TPH1) Inhibitor with nanomolar in vitro potency. (adooq.com)
  • It is both soluble (73 kDa) and membrane-bound (77 kDa) (anchored by an uncleaved signal sequence), and via hydroxylation, converts dopamine into norepinepherine. (rndsystems.com)
  • Dopamine beta-hydroxylase catalyzes the hydroxylation of not only dopamine but also other phenylethylamine derivatives when available. (wikipedia.org)
  • Dopamine Beta Hydroxylase antibody LS-C6444 is an unconjugated sheep polyclonal antibody to human Dopamine Beta Hydroxylase (DBH) (aa596-612). (lsbio.com)
  • One of the catecholamine enzymes, DBH, dopamine beta hydroxylase, is in tight linkage disequilibrium with the ABO locus. (hy-ls.org)
  • Human genetics of plasma dopamine beta-hydroxylase activity: applications to research in psychiatry and neurology. (medlineplus.gov)
  • Advances in AD biomarker research have demonstrated changes in amyloid-beta (Aβ), brain metabolism and other pathophysiologies prior to the onset of memory loss, with some markers possibly changing one or two decades earlier. (researchwithrutgers.com)
  • Tetrahydropapaverine, one of the TIQs and an analogue of salsolinol and tetrahydropapaveroline, has been reported to have neurotoxic effects on dopamine neurons. (adooq.com)
  • Changes in ileal muscle tension were isometrically recorded following 30 μM dopamine or 30 μM SKF38393 (a dopamine receptor 1 (D1R) agonist) or 30 μM bromocriptine (a D2R agonist). (ecco-ibd.eu)
  • pAMPK)] and inhibition [dopamine-beta-hydroxylase GLUT3 MCT2] of protein expression in these cells responses Brefeldin A that were normalized Brefeldin A by insulin plus lactate treatment. (bioskinrevive.com)
  • These two hormones are created in the body when dopamine is converted. (sciencedict.com)
  • The main effect of a putative splice variant in Dopamine beta-hydroxylase namely rs1108580 was found to be associated with Working memory Processing speed in a north Indian Schizophrenia case control study where the G/G genotype of that single-nucleotide polymorphism(SNP) was found to have lower cognitive scores than those with A/A and A/G genotypes. (wikipedia.org)
  • Both Venter and Watson appear to have both non-B ABO blood group and high activity DBH and to have dopamine genotypes consistent with Persistence personality trait research as well as to evidence this trait in publically available biographical information. (hy-ls.org)
  • 1996 ) Modulation of forebrain electroencephalographic activity in halothane-anesthetized rat via actions of noradrenergic beta-receptors within the medial septal region. (neurotree.org)
  • SSRIs antidepressant activity is influenced by G beta 3 variants. (neurotransmitter.net)
  • Human colitis and mouse ileitis affect dopamine machinery in the enteric nervous system. (ecco-ibd.eu)
  • 0.01]), suggesting that dopamine responses are mainly mediated through D1R. (ecco-ibd.eu)
  • Immunofluorescence distribution of Iba1 (a macrophage specific marker), D1R, DBH and dopamine transporter (DAT) were determined in longitudinal muscle-myenteric plexus whole-mount preparations (LMMPs) by confocal microscopy. (ecco-ibd.eu)
  • Data are given on the dopamine beta-hydroxylase levels in the serum of tree planters. (cdc.gov)
  • Dopamine beta-Hydroxylase " has 5 results in Products. (rndsystems.com)
  • Following exposure to radioactive strontium compounds, the most severe non carcinogenic effects seen are the result of incorporation of radioactive strontium, an emitter of beta radiation, into the skeleton, with subsequent irradiation of surrounding tissues (ATSDR 2001e). (cdc.gov)