An enzyme that converts brain gamma-aminobutyric acid (GAMMA-AMINOBUTYRIC ACID) into succinate semialdehyde, which can be converted to succinic acid and enter the citric acid cycle. It also acts on beta-alanine. EC 2.6.1.19.
A subclass of enzymes of the transferase class that catalyze the transfer of an amino group from a donor (generally an amino acid) to an acceptor (generally a 2-keto acid). Most of these enzymes are pyridoxyl phosphate proteins. (Dorland, 28th ed) EC 2.6.1.
Derivatives of BUTYRIC ACID that contain one or more amino groups attached to the aliphatic structure. Included under this heading are a broad variety of acid forms, salts, esters, and amides that include the aminobutryrate structure.
Benzoic acid esters or salts substituted with one or more iodine atoms.
An enzyme that catalyzes the conversion of L-alanine and 2-oxoglutarate to pyruvate and L-glutamate. (From Enzyme Nomenclature, 1992) EC 2.6.1.2.
Amino derivatives of caproic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the amino caproic acid structure.
The 4-aminomethyl form of VITAMIN B 6. During transamination of amino acids, PYRIDOXAL PHOSPHATE is transiently converted into pyridoxamine phosphate.
A family of compounds containing an oxo group with the general structure of 1,5-pentanedioic acid. (From Lehninger, Principles of Biochemistry, 1982, p442)
Enzymes of the transferase class that catalyze the conversion of L-aspartate and 2-ketoglutarate to oxaloacetate and L-glutamate. EC 2.6.1.1.
An enzyme that plays a role in the GLUTAMATE and butanoate metabolism pathways by catalyzing the oxidation of succinate semialdehyde to SUCCINATE using NAD+ as a coenzyme. Deficiency of this enzyme, causes 4-hydroxybutyricaciduria, a rare inborn error in the metabolism of the neurotransmitter 4-aminobutyric acid (GABA).
This is the active form of VITAMIN B 6 serving as a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into pyridoxamine phosphate (PYRIDOXAMINE).
A family of plasma membrane neurotransmitter transporter proteins that regulates extracellular levels of the inhibitory neurotransmitter GAMMA-AMINOBUTYRIC ACID. They differ from GABA RECEPTORS, which signal cellular responses to GAMMA-AMINOBUTYRIC ACID. They control GABA reuptake into PRESYNAPTIC TERMINALS in the CENTRAL NERVOUS SYSTEM through high-affinity sodium-dependent transport.
A PYRIDOXAL PHOSPHATE containing enzyme that catalyzes the reversible transfer of an amino group between D-Alanine and alpha-ketoglutarate to form PYRUVATE and D-GLUTAMATE, respectively. It plays a role in the synthesis of the bacterial CELL WALL. This enzyme was formerly classified as EC 2.6.1.10.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
The most common inhibitory neurotransmitter in the central nervous system.
Derivatives of GLUTAMIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the 2-aminopentanedioic acid structure.
Proteins involved in the transport of organic anions. They play an important role in the elimination of a variety of endogenous substances, xenobiotics and their metabolites from the body.
The rate dynamics in chemical or physical systems.

A correlation between changes in gamma-aminobutyric acid metabolism and seizures induced by antivitamin B6. (1/160)

The effects of DL-penicillamine (DL-PeA), hydrazine and toxopyrimidine (TXP, 2-methyl-6-amino-5-hydroxymethylpyrimidine) on gamma-aminobutyric acid (GABA) metabolism in mouse brain were studied. All these compounds inhibited the activity of glutamate decarboxylase [EC 4.1.1.15] (GAD) and slightly inhibited that of 4-aminobutyrate: 2-oxoglutarate aminotransferase [EC 2.6.1.19] (GABA-T). In contrast, very different effects were observed on GABA levels; hydrazine caused a marked increase, DL-PeA had no effect, and TXP caused a slight decrease in the content of the amino acid. These results could be described by an equation which related the excitable state to changes in the flux of the GABA bypass. Since the values obtained from the equation clearly reflect the seizure activity, it is suggested that the decreased GABA flux might be a cause of convulsions induced by these drugs.  (+info)

The irreversible gamma-aminobutyric acid (GABA) transaminase inhibitor gamma-vinyl-GABA blocks cocaine self-administration in rats. (2/160)

gamma-Vinyl gamma-aminobutyric acid (GABA) (GVG) is an irreversible inhibitor of GABA transaminase, the primary enzyme involved in GABA metabolism. Acute administration of GVG increases brain GABA levels and blocks cocaine-induced locomotor activity, cocaine-induced lowering of brain stimulation reward thresholds, and cocaine-induced conditioned place preference. To further evaluate the effects of GVG on cocaine-induced reward, we examined its effects on cocaine self-administration in male Wistar rats on fixed ratio 5 and progressive ratio schedules of reinforcement. Additionally, the effects of GVG on operant responding for a food reward were examined on the same two schedules to determine whether the effects of GVG were specific to cocaine reward or generalized to other types of reward. GVG dose dependently decreased responding for cocaine on both schedules of reinforcement, suggesting that GVG attenuated the reward value of the cocaine. Responding for food was also decreased by GVG, suggesting that the effects of increased GABA levels induced by GVG may have a general effect on central reward systems. Data from this and other studies indicate that GVG does not induce motor impairment, decrease spontaneous locomotor activity, or induce catalepsy. Taken together, these data suggest that increases in GABAergic activity induced by GVG have an attenuating effect on centrally mediated reward systems and that the GABA system may be a useful target in the development of new therapeutic strategies for cocaine addiction.  (+info)

The mature size of rat 4-aminobutyrate aminotransferase is different in liver and brain. (3/160)

The amino acid sequence predicted from a rat liver cDNA library indicated that the precursor of beta-AlaAT I (4-aminobutyrate aminotransferase, beta-alanine-oxoglutarate aminotransferase) consists of a mature enzyme of 466 amino acid residues and a 34-amino acid terminal segment, with amino acids attributed to the leader peptide. However, the mass of beta-AlaAT I from rat brain was larger than that from rat liver and kidney, as assessed by Western-blot analysis, mass spectroscopy and N-terminal sequencing. The mature form of beta-AlaAT I from the brain had an ISQAAAK- peptide on the N-terminus of the liver mature beta-AlaAT I. Brain beta-AlaAT I was cleaved to liver beta-AlaAT I when incubated with fresh mitochondrial extract from rat liver. These results imply that mature rat liver beta-AlaAT I is proteolytically cleaved in two steps. The first cleavage of the motif XRX( downward arrow)XS is performed by a mitochondrial processing peptidase, yielding an intermediate-sized protein which is the mature brain beta-AlaAT I. The second cleavage, which generates the mature liver beta-AlaAT I, is also carried out by a mitochondrial endopeptidase. The second peptidase is active in liver but lacking in brain.  (+info)

Effects of blocking GABA degradation on corticotropin-releasing hormone gene expression in selected brain regions. (4/160)

PURPOSE: The gamma-aminobutyric acid (GABA) degradation blocker gamma-vinyl-GABA (VGB) is used clinically to treat seizures in both adult and immature individuals. The mechanism by which VGB controls developmental seizures is not fully understood. Specifically, whether the anticonvulsant properties of VGB arise only from its elevation of brain GABA levels and the resulting activation of GABA receptors, or also from associated mechanisms, remains unresolved. Corticotropin-releasing hormone (CRH), a neuropeptide present in many brain regions involved in developmental seizures, is a known convulsant in the immature brain and has been implicated in some developmental seizures. In certain brain regions, it has been suggested that CRH synthesis and release may be regulated by GABA. Therefore we tested the hypothesis that VGB decreases CRH gene expression in the immature rat brain, consistent with the notion that VGB may decrease seizures also by reducing the levels of the convulsant molecule, CRH. METHODS: VGB was administered to immature, 9-day-old rats in clinically relevant doses, whereas littermate controls received vehicle. RESULTS: In situ hybridization histochemistry demonstrated a downregulation of CRH mRNA levels in the hypothalamic paraventricular nucleus but not in other limbic regions of VGB-treated pups compared with controls. In addition, VGB-treated pups had increased CRH peptide levels in the anterior hypothalamus, as shown by radioimmunoassay. CONCLUSIONS: These findings are consistent with a reduction of both CRH gene expression and secretion in the hypothalamus, but do not support an indirect anticonvulsant mechanism of VGB via downregulation of CRH levels in limbic structures. However, the data support a region-specific regulation of CRH gene expression by GABA.  (+info)

Effect of gonadal steroids and gamma-aminobutyric acid on LH release and dopamine expression and activity in the zona incerta in rats. (5/160)

A dopaminergic system in the zona incerta stimulates LH release and may mediate the positive feedback effects of the gonadal steroids on LH release. In this study the mechanisms by which steroids might increase dopamine activity in the zona incerta were investigated. In addition, experiments were conducted to determine whether the inhibitory effects of gamma-aminobutyric acid (GABA) on LH release in the zona incerta are due to suppression of dopamine activity in this area or conversely whether the stimulatory effects of dopamine on LH release are due to suppression of a tonic inhibitory GABAergic system. Ovariectomized rats were treated s.c. with oil, 5 micrograms oestradiol benzoate or 5 micrograms oestradiol benzoate followed 48 h later by 0.5 mg progesterone, and killed 54 h after the oestradiol benzoate injection. At this time the LH concentrations were suppressed in the oestradiol benzoate group and increased in the group treated with oestradiol benzoate and progesterone. The ratio of tyrosine hydroxylase:beta-actin mRNA in the zona incerta was significantly increased by the oestradiol benzoate treatment, but the addition of progesterone resulted in values similar to those in the control group. At the same time, the progesterone treatment increased tyrosine hydroxylase activity in the zona incerta as indicated by an increase in L-dihydroxyphenylalanine (L-DOPA) accumulation after 100 mg 3-hydroxybenzylhydrazine hydrochloric acid (NSD1015) kg-1 and an increase in dopamine release as indicated by a increase in dihydroxyphenylacetic acid (DOPAC) concentrations (one of the major metabolites of dopamine). Ovariectomized rats treated with oestradiol benzoate plus progesterone were also injected i.p. with 75 mg gamma-acetylenic GABA kg-1 (a GABA transaminase inhibitor) to increase GABA concentrations in the brain. This treatment had no effect on the ratio of tyrosine hydroxylase:beta-actin mRNA but decreased L-DOPA accumulation and DOPAC concentrations in the zona incerta, indicating a post-translational inhibition of dopamine synthesis and release. Treatment of ovariectomized rats with oestradiol benzoate followed by 100 mg L-DOPA i.p. to increase dopamine concentrations in the whole brain had no effect on glutamic acid decarboxylase mRNA expression in the zona incerta, although it increased the glutamic acid decarboxylase:beta-actin mRNA ratio in other hypothalamic areas (that is, the medical preoptic area, ventromedial nucleus and arcuate nucleus). In conclusion, the steroids act to increase dopamine activity in different ways: oestrogen increases tyrosine hydroxylase mRNA expression and progesterone acts after translation to increase tyrosine hydroxylase activity and dopamine release (as indicated by increases in DOPAC concentrations). This latter effect may be due to progesterone removing a tonic GABAergic inhibition from the dopaminergic system.  (+info)

The inhibitory effects of (gamma)-aminobutyric acid (GABA) on growth hormone secretion in the goldfish are modulated by sex steroids. (6/160)

Double-labelling studies at the electron microscopic level demonstrated that gamma-aminobutyric acid (GABA)-immunoreactive nerve endings are associated with growth-hormone-secreting cells in the proximal pars distalis of the goldfish pituitary gland, suggesting that GABA may be important for the control of growth hormone release in this species. An in vitro assay for GABA-transaminase activity demonstrated that the pituitary is a site for the metabolism of GABA to succinic acid. In vitro, GABA or the GABA antagonists bicuculline and saclofen did not affect the rate of growth hormone release from dispersed pituitary cells in static incubation. In contrast, intracerebroventricular injection of GABA reduced serum growth hormone levels within 30 min. During the seasonal gonadal cycle, intraperitoneal injection of GABA was without effect in sexually regressed goldfish, but caused a significant decrease in serum growth hormone levels in sexually recrudescent animals. Intraperitoneal implantation of solid silastic pellets containing oestradiol increased serum GH levels fivefold in sexually regressed and recrudescent goldfish; in both groups, GABA suppressed the oestradiol-stimulated increase in circulating growth hormone levels. The effect of oestradiol on basal serum growth hormone levels was specific since progesterone and testosterone were without effect. However, in recrudescent animals treated with progesterone and testosterone, the inhibitory effects of GABA on serum growth hormone levels were absent, indicating a differential role for these steroids in growth hormone release. Taken together, these results demonstrate that GABA has an inhibitory effect on growth hormone release in goldfish.  (+info)

Recovery of visual field constriction following discontinuation of vigabatrin. (7/160)

Epilepsy patients treated with vigabatrin may develop symptomatic or asymptomatic concentric visual field constriction due to GABA-associated retinal dysfunction. The prevalence and course of this side effect are not established yet; in previously reported adult patients the visual disturbances seem to be irreversible. We present two patients with a significant improvement of visual field constriction and retinal function after the discontinuation of vigabatrin. These findings suggest that vigabatrin-associated retinal changes are at least partly reversible in some patients, and that these patients may benefit significantly from a withdrawal of vigabatrin. Larger scale clinical studies are needed to identify predictive factors both for the occurrence and reversibility of vigabatrin-associated visual field defects.  (+info)

Increased mesolimbic GABA concentration blocks heroin self-administration in the rat. (8/160)

Opiate reinforcement has been hypothesized to be mediated by an inhibition of mesolimbic gamma-aminobutyric acid (GABA) release that subsequently disinhibits ventral tegmental area (VTA) dopamine neurons. In support of this hypothesis, this study demonstrates that when administered directly into the lateral ventricle, the VTA, or the ventral pallidum, but not the nucleus accumbens, gamma-vinyl-GABA (GVG, an irreversible GABA-transaminase inhibitor, 20-50 microg) dose dependently blocked heroin (0.06 mg/kg) self-administration (SA), as assessed by an increase in heroin SA at low doses of GVG and an initial increase followed 1 to 2 h later by a blockade of heroin SA at higher GVG doses. This effect lasted 3 to 5 days. In drug-naive rats, intra-VTA GVG pretreatment also prevented or delayed acquisition of heroin SA for 2 days. This GVG effect was prevented or reversed by systemic or intra-VTA pretreatment with the GABA(B) antagonist 2-hydroxysaclofen, but not the GABA(A) antagonist bicuculline. Similarly, coadministration of heroin with aminooxy-acetic acid (1-4 mg/kg) or ethanolamine-O-sulfate (50-100 mg/kg), two reversible GABA transaminase inhibitors, dose dependently reduced heroin reinforcement. Coadministration of (+/-)-nipecotic acid (0.1-5 mg/kg) with heroin, or intra-VTA or -ventral pallidum pretreatment with (+/-)-nipecotic acid (10 microg) or NO-711 (2 microg), two GABA uptake inhibitors, significantly increased heroin SA behavior, an effect also blocked by systemic 2-hydroxysaclofen, but not bicuculline. Taken together, these experiments, for the first time, demonstrate that pharmacological elevation of mesolimbic GABA concentration blocks heroin reinforcement by activating GABA(B) receptors, supporting the GABAergic hypothesis of opiate reinforcement and the incorporation of GABA agents in opiate abuse treatment.  (+info)

4-Aminobutyrate transaminase (GABA transaminase or GABA-T) is an enzyme that catalyzes the reversible transfer of an amino group from 4-aminobutyrate (GABA) to 2-oxoglutarate, forming succinic semialdehyde and glutamate. This enzyme plays a crucial role in the metabolism of the major inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the central nervous system. Inhibition of GABA transaminase is a therapeutic strategy for the treatment of various neurological disorders, such as epilepsy and anxiety, due to its ability to increase GABA levels in the brain.

Transaminases, also known as aminotransferases, are a group of enzymes found in various tissues of the body, particularly in the liver, heart, muscle, and kidneys. They play a crucial role in the metabolism of amino acids, the building blocks of proteins.

There are two major types of transaminases: aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Both enzymes are normally present in low concentrations in the bloodstream. However, when tissues that contain these enzymes are damaged or injured, such as during liver disease or muscle damage, the levels of AST and ALT in the blood may significantly increase.

Measurement of serum transaminase levels is a common laboratory test used to assess liver function and detect liver injury or damage. Increased levels of these enzymes in the blood can indicate conditions such as hepatitis, liver cirrhosis, drug-induced liver injury, heart attack, and muscle disorders. It's important to note that while elevated transaminase levels may suggest liver disease, they do not specify the type or cause of the condition, and further diagnostic tests are often required for accurate diagnosis and treatment.

Aminobutyrates are compounds that contain an amino group (-NH2) and a butyric acid group (-CH2-CH2-CH2-COOH). The most common aminobutyrate is gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating brain excitability and is involved in various physiological processes, including sleep, memory, and anxiety regulation. Abnormalities in GABAergic neurotransmission have been implicated in several neurological and psychiatric disorders, such as epilepsy, anxiety disorders, and chronic pain. Other aminobutyrates may also have important biological functions, but their roles are less well understood than that of GABA.

Iodobenzoates are organic compounds that consist of a benzoic acid molecule with an iodine atom substituted at the carboxyl group. Specifically, an iodobenzoate is an ester derived from benzoic acid and iodine, in which the hydrogen atom of the carboxylic acid group (-COOH) has been replaced by an iodine atom.

The general formula for an iodobenzoate can be represented as C6H4(IO)CO2R, where R represents an alkyl or aryl group. Iodobenzoates have various applications in organic synthesis and pharmaceuticals, including the production of dyes, drugs, and other chemical intermediates.

It's worth noting that iodobenzoates are not a medical condition or diagnosis but rather a class of chemical compounds with potential uses in medical research and therapeutics.

Alanine transaminase (ALT) is a type of enzyme found primarily in the cells of the liver and, to a lesser extent, in the cells of other tissues such as the heart, muscles, and kidneys. Its primary function is to catalyze the reversible transfer of an amino group from alanine to another alpha-keto acid, usually pyruvate, to form pyruvate and another amino acid, usually glutamate. This process is known as the transamination reaction.

When liver cells are damaged or destroyed due to various reasons such as hepatitis, alcohol abuse, nonalcoholic fatty liver disease, or drug-induced liver injury, ALT is released into the bloodstream. Therefore, measuring the level of ALT in the blood is a useful diagnostic tool for evaluating liver function and detecting liver damage. Normal ALT levels vary depending on the laboratory, but typically range from 7 to 56 units per liter (U/L) for men and 6 to 45 U/L for women. Elevated ALT levels may indicate liver injury or disease, although other factors such as muscle damage or heart disease can also cause elevations in ALT.

Aminocaproates are a group of chemical compounds that contain an amino group and a carboxylic acid group, as well as a straight or branched alkyl chain with 6-10 carbon atoms. They are often used in medical settings as anti-fibrinolytic agents, which means they help to prevent the breakdown of blood clots.

One example of an aminocaproate is epsilon-aminocaproic acid (EACA), which is a synthetic analogue of the amino acid lysine. EACA works by inhibiting the activation of plasminogen to plasmin, which is an enzyme that breaks down blood clots. By doing so, EACA can help to reduce bleeding and improve clot stability in certain medical conditions, such as hemophilia or following surgery.

Other aminocaproates include tranexamic acid (TXA) and 4-aminoethylbenzoic acid (AEBA), which also have anti-fibrinolytic properties and are used in similar clinical settings. However, it's important to note that these medications can increase the risk of thrombosis (blood clots) if not used properly, so they should only be administered under the close supervision of a healthcare provider.

Pyridoxamine is a form of vitamin B6, which is a water-soluble vitamin that plays an essential role in the body's protein metabolism, neurotransmitter synthesis, and hemoglobin production. Pyridoxamine is a specific chemical compound that is a derivative of pyridoxine, another form of vitamin B6.

Pyridoxamine functions as a cofactor for various enzymes involved in the metabolism of amino acids, the building blocks of proteins. It helps to convert harmful homocysteine into the essential amino acid methionine, which is important for maintaining normal levels of homocysteine and supporting cardiovascular health.

Pyridoxamine has been studied for its potential role in treating or preventing certain medical conditions, such as diabetic nephropathy and neurodegenerative diseases, due to its antioxidant properties and ability to protect against protein glycation, a process that can damage tissues and contribute to aging and disease. However, more research is needed to establish its safety and efficacy for these uses.

Alpha-ketoglutaric acid, also known as 2-oxoglutarate, is not an acid in the traditional sense but is instead a key molecule in the Krebs cycle (citric acid cycle), which is a central metabolic pathway involved in cellular respiration. Alpha-ketoglutaric acid is a crucial intermediate in the process of converting carbohydrates, fats, and proteins into energy through oxidation. It plays a vital role in amino acid synthesis and the breakdown of certain amino acids. Additionally, it serves as an essential cofactor for various enzymes involved in numerous biochemical reactions within the body. Any medical conditions or disorders related to alpha-ketoglutaric acid would typically be linked to metabolic dysfunctions or genetic defects affecting the Krebs cycle.

Aspartate aminotransferases (ASTs) are a group of enzymes found in various tissues throughout the body, including the heart, liver, and muscles. They play a crucial role in the metabolic process of transferring amino groups between different molecules.

In medical terms, AST is often used as a blood test to measure the level of this enzyme in the serum. Elevated levels of AST can indicate damage or injury to tissues that contain this enzyme, such as the liver or heart. For example, liver disease, including hepatitis and cirrhosis, can cause elevated AST levels due to damage to liver cells. Similarly, heart attacks can also result in increased AST levels due to damage to heart muscle tissue.

It is important to note that an AST test alone cannot diagnose a specific medical condition, but it can provide valuable information when used in conjunction with other diagnostic tests and clinical evaluation.

Succinate-semialdehyde dehydrogenase (SSDH) is an enzyme involved in the metabolism of the neurotransmitter gamma-aminobutyric acid (GABA). Specifically, SSDH catalyzes the conversion of succinic semialdehyde to succinate in the final step of the GABA degradation pathway. This enzyme plays a critical role in maintaining the balance of GABA levels in the brain and is therefore essential for normal neurological function. Deficiencies or mutations in SSDH can lead to neurological disorders, including developmental delays, intellectual disability, and seizures.

Pyridoxal phosphate (PLP) is the active form of vitamin B6 and functions as a cofactor in various enzymatic reactions in the human body. It plays a crucial role in the metabolism of amino acids, carbohydrates, lipids, and neurotransmitters. Pyridoxal phosphate is involved in more than 140 different enzyme-catalyzed reactions, making it one of the most versatile cofactors in human biochemistry.

As a cofactor, pyridoxal phosphate helps enzymes carry out their functions by facilitating chemical transformations in substrates (the molecules on which enzymes act). In particular, PLP is essential for transamination, decarboxylation, racemization, and elimination reactions involving amino acids. These processes are vital for the synthesis and degradation of amino acids, neurotransmitters, hemoglobin, and other crucial molecules in the body.

Pyridoxal phosphate is formed from the conversion of pyridoxal (a form of vitamin B6) by the enzyme pyridoxal kinase, using ATP as a phosphate donor. The human body obtains vitamin B6 through dietary sources such as whole grains, legumes, vegetables, nuts, and animal products like poultry, fish, and pork. It is essential to maintain adequate levels of pyridoxal phosphate for optimal enzymatic function and overall health.

GABA (gamma-aminobutyric acid) is the primary inhibitory neurotransmitter in the mammalian central nervous system. GABA plasma membrane transport proteins, also known as GATs (GABA transporters), are a family of membrane-spanning proteins responsible for the uptake of GABA from the extracellular space into neurons and glial cells.

There are four main subtypes of GATs in mammals, named GAT1, GAT2, GAT3, and Betaine/GABA transporter 1 (BGT1). These transport proteins play a crucial role in terminating the synaptic transmission of GABA and regulating its concentration in the extracellular space. They also help maintain the balance between excitation and inhibition in the central nervous system.

GATs are targets for various pharmacological interventions, as modulation of their activity can affect GABAergic neurotransmission and have therapeutic potential in treating several neurological disorders, such as epilepsy, anxiety, and chronic pain.

D-Alanine transaminase (DAT or Dalat) is an enzyme that catalyzes the reversible transfer of an amino group from D-alanine to α-ketoglutarate, producing pyruvate and D-glutamate. It is found in various bacteria and plays a role in their metabolism. However, it is not typically considered a medically significant enzyme in humans, as it is not commonly used as a clinical marker of liver or other organ function.

The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:

1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.

The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.

"Swine" is a common term used to refer to even-toed ungulates of the family Suidae, including domestic pigs and wild boars. However, in a medical context, "swine" often appears in the phrase "swine flu," which is a strain of influenza virus that typically infects pigs but can also cause illness in humans. The 2009 H1N1 pandemic was caused by a new strain of swine-origin influenza A virus, which was commonly referred to as "swine flu." It's important to note that this virus is not transmitted through eating cooked pork products; it spreads from person to person, mainly through respiratory droplets produced when an infected person coughs or sneezes.

Gamma-Aminobutyric Acid (GABA) is a major inhibitory neurotransmitter in the mammalian central nervous system. It plays a crucial role in regulating neuronal excitability and preventing excessive neuronal firing, which helps to maintain neural homeostasis and reduce the risk of seizures. GABA functions by binding to specific receptors (GABA-A, GABA-B, and GABA-C) on the postsynaptic membrane, leading to hyperpolarization of the neuronal membrane and reduced neurotransmitter release from presynaptic terminals.

In addition to its role in the central nervous system, GABA has also been identified as a neurotransmitter in the peripheral nervous system, where it is involved in regulating various physiological processes such as muscle relaxation, hormone secretion, and immune function.

GABA can be synthesized in neurons from glutamate, an excitatory neurotransmitter, through the action of the enzyme glutamic acid decarboxylase (GAD). Once synthesized, GABA is stored in synaptic vesicles and released into the synapse upon neuronal activation. After release, GABA can be taken up by surrounding glial cells or degraded by the enzyme GABA transaminase (GABA-T) into succinic semialdehyde, which is further metabolized to form succinate and enter the Krebs cycle for energy production.

Dysregulation of GABAergic neurotransmission has been implicated in various neurological and psychiatric disorders, including epilepsy, anxiety, depression, and sleep disturbances. Therefore, modulating GABAergic signaling through pharmacological interventions or other therapeutic approaches may offer potential benefits for the treatment of these conditions.

Glutamates are the salt or ester forms of glutamic acid, which is a naturally occurring amino acid and the most abundant excitatory neurotransmitter in the central nervous system. Glutamate plays a crucial role in various brain functions, such as learning, memory, and cognition. However, excessive levels of glutamate can lead to neuronal damage or death, contributing to several neurological disorders, including stroke, epilepsy, and neurodegenerative diseases like Alzheimer's and Parkinson's.

Glutamates are also commonly found in food as a natural flavor enhancer, often listed under the name monosodium glutamate (MSG). While MSG has been extensively studied, its safety remains a topic of debate, with some individuals reporting adverse reactions after consuming foods containing this additive.

Organic anion transporters (OATs) are membrane transport proteins that are responsible for the cellular uptake and excretion of various organic anions, such as drugs, toxins, and endogenous metabolites. They are found in various tissues, including the kidney, liver, and brain, where they play important roles in the elimination and detoxification of xenobiotics and endogenous compounds.

In the kidney, OATs are located in the basolateral membrane of renal tubular epithelial cells and mediate the uptake of organic anions from the blood into the cells. From there, the anions can be further transported into the urine by other transporters located in the apical membrane. In the liver, OATs are expressed in the sinusoidal membrane of hepatocytes and facilitate the uptake of organic anions from the blood into the liver cells for metabolism and excretion.

There are several isoforms of OATs that have been identified, each with distinct substrate specificities and tissue distributions. Mutations in OAT genes can lead to various diseases, including renal tubular acidosis, hypercalciuria, and drug toxicity. Therefore, understanding the function and regulation of OATs is important for developing strategies to improve drug delivery and reduce adverse drug reactions.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

As a transaminase, GABA-T's role is to move functional groups from an amino acid and a α-keto acid, and vice versa. In the case ... "GABA-TRANSAMINASE DEFICIENCY". www.omim.org. Retrieved 2020-10-18. Fait A, Fromm H, Walter D, Galili G, Fernie AR (January 2008 ... This means that it is in the transferase class of enzymes, the nitrogenous transferase sub-class and the transaminase sub- ... Parviz M, Vogel K, Gibson KM, Pearl PL (November 2014). "Disorders of GABA metabolism: SSADH and GABA-transaminase deficiencies ...
... pyruvate transaminase (EC 2.6.1.96, aminobutyrate aminotransferase, gamma-aminobutyrate aminotransaminase, gamma-aminobutyrate ... aminobutyrate transaminase, GABA aminotransferase, GABA transaminase, GABA transferase, POP2 (gene)) is an enzyme with ... gamma-aminobutyric acid pyruvate transaminase, gamma-aminobutyric acid transaminase, gamma-aminobutyric transaminase, 4- ... and potential functions for an Arabidopsis gamma-aminobutyrate transaminase that utilizes both pyruvate and glyoxylate". ...
Vigabatrin is a drug that is irreparably suppresses GABA transaminase that causes increased amount of GABA in the brain. In a ... Rainesalo S, Saransaari P, Peltola J, Keränen T (March 2003). "Uptake of GABA and activity of GABA-transaminase in platelets ... This gene goes by a number of names, including, GABA transaminase, GABAT, 4-aminobutyrate transaminase, NPD009 etc. This gene ... Jeremiah S, Povey S (July 1981). "The biochemical genetics of human gamma-aminobutyric acid transaminase". Annals of Human ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate transaminase, ...
Under normal conditions, SSADH works with the enzyme GABA transaminase to convert GABA to succinic acid. Succinic acid can then ... Vigabatrin is an irreversible inhibitor of GABA transaminases which leads to decreased levels of GHB and elevation of GABA. ... Parviz, M.; Vogel, K.; Gibson, K.M.; Pearl, P.L. (2014). "Disorders of GABA Metabolism: SSADH and GABA-transaminase ... The absence of SSADH leads to a 30-fold increase of GHB and a 2-4 fold increase of GABA in the brains of patients with SSADH ...
... may refer to: 4-aminobutyrate transaminase, an enzyme GabT RNA motif This disambiguation page lists articles associated ...
It is formed from GABA by the action of GABA transaminase (4-aminobutyrate aminotransferase) and further oxidised to become ... Transaminase (aminotransferase) Succinic semialdehyde dehydrogenase deficiency Lide, David R. (1998), Handbook of Chemistry and ...
... may refer to: Alanine transaminase, an enzyme 4-aminobutyrate transaminase, an enzyme This set ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate transaminase, an ...
... may refer to: 4-aminobutyrate transaminase, an enzyme 4-aminobutyrate-pyruvate transaminase, an enzyme This ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate transaminase, an enzyme ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate ... transaminase, an enzyme This set index page lists enzyme articles associated with the same name. If an internal link led you ...
... may refer to: 4-aminobutyrate transaminase, an enzyme 4-aminobutyrate-pyruvate transaminase, ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate transaminase, an ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate ... transaminase, an enzyme This set index page lists enzyme articles associated with the same name. If an internal link led you ...
... may refer to: 4-aminobutyrate-pyruvate transaminase, an enzyme 4-aminobutyrate ... transaminase, an enzyme This set index page lists enzyme articles associated with the same name. If an internal link led you ...
... glycine transaminase MeSH D08.811.913.477.700.535 - leucine transaminase MeSH D08.811.913.477.700.550 - l-lysine 6-transaminase ... transaminases MeSH D08.811.913.477.700.100 - alanine transaminase MeSH D08.811.913.477.700.120 - 2-aminoadipate transaminase ... beta-alanine-pyruvate transaminase MeSH D08.811.913.477.700.347 - d-alanine transaminase MeSH D08.811.913.477.700.470 - ... tryptophan transaminase MeSH D08.811.913.477.700.900 - tyrosine transaminase MeSH D08.811.913.555.150 - amidinotransferases ...
The carboxylate form of GABA is γ-aminobutyrate. Two general classes of GABA receptor are known: GABAA in which the receptor is ... GABA transaminase enzymes catalyze the conversion of 4-aminobutanoic acid (GABA) and 2-oxoglutarate (α-ketoglutarate) into ... Parviz M, Vogel K, Gibson KM, Pearl PL (2014-11-25). "Disorders of GABA metabolism: SSADH and GABA-transaminase deficiencies". ... GABA reuptake inhibitors: deramciclane, hyperforin, tiagabine.[citation needed] GABA transaminase inhibitors: gabaculine, ...
... a gene related to the enzyme 4-aminobutyrate-pyruvate transaminase Pop 2 (mixtape), a 2017 mixtape by Charli XCX Pop2! The ...
In enzymology, a N6-acetyl-beta-lysine transaminase (EC 2.6.1.65) is an enzyme that catalyzes the chemical reaction 6-acetamido ... This enzyme belongs to the family of transferases, specifically the transaminases, which transfer nitrogenous groups. The ... conversion of 6-N-acetyl-L-beta-lysine to 3-keto-6-acetamidohexanoate and of 4-aminobutyrate to succinic semialdehyde by ... different transaminases". Arch. Biochem. Biophys. 197 (1): 226-35. doi:10.1016/0003-9861(79)90240-6. PMID 44448. Portal: ...
... a new potent inhibitor of gamma-aminobutyrate transaminase, on brain gamma-aminobutyrate content and convulsions in mice". Life ... Rando, Robert; Bangerter, F.W. (May 13, 1977). "The In Vivo Inhibition of GABA-transaminase by Gabaculine". Biochemical and ... gabaculine is extremely potent and toxic when compared to other GABA transaminase inhibitors, with an ED50 of 35 mg/kg and LD50 ... which acts as a potent and irreversible GABA transaminase inhibitor, and also a GABA reuptake inhibitor. Gabaculine is also ...
... aspartate transaminase EC 2.6.1.2: alanine transaminase EC 2.6.1.3: cysteine transaminase EC 2.6.1.4: glycine transaminase EC ... D-amino-acid transaminase EC 2.6.1.11: acetylornithine transaminase EC 2.6.1.12: alanine-oxo-acid transaminase EC 2.6.1.13: ... neamine transaminase EC 2.6.1.94: 2′-deamino-2′-hydroxyneamine transaminase EC 2.6.1.95: neomycin C transaminase EC 2.6.1.96: 4 ... aminobutyrate-pyruvate transaminase EC 2.6.1.97: archaeosine synthase EC 2.6.1.98: UDP-2-acetamido-2-deoxy-ribo-hexuluronate ...
... succinic semialdehyde transaminase gene (gabT) and characterization of the succinic semialdehyde dehydrogenase gene (gabD)". ... 2 H+ This enzyme participates in the degradation of glutamate and 4-aminobutyrate. Bartsch K, von Johnn-Marteville A, Schulz A ...
I. The inhibition of gamma-aminobutyric acid-alpha-ketoglutaric acid transaminase in vitro and in vivo by U-7524 (amino- ... Wolfgang Löscher; Dagmar Hönack; Martina Gramer (1989). "Use of Inhibitors of γ-Aminobutyric Acid (GABA) Transaminase for the ... Aminooxyacetic acid, often abbreviated AOA or AOAA, is a compound that inhibits 4-aminobutyrate aminotransferase (GABA-T) ... At concentrations high enough to fully inhibit 4-aminobutyrate aminotransferase activity, aminooxyacetic acid is indicated as a ...
As a transaminase, GABA-Ts role is to move functional groups from an amino acid and a α-keto acid, and vice versa. In the case ... "GABA-TRANSAMINASE DEFICIENCY". www.omim.org. Retrieved 2020-10-18. Fait A, Fromm H, Walter D, Galili G, Fernie AR (January 2008 ... This means that it is in the transferase class of enzymes, the nitrogenous transferase sub-class and the transaminase sub- ... Parviz M, Vogel K, Gibson KM, Pearl PL (November 2014). "Disorders of GABA metabolism: SSADH and GABA-transaminase deficiencies ...
The ABAT gene provides instructions for making the GABA-transaminase enzyme. Learn about this gene and related health ... GABA-transaminase deficiency. At least 10 mutations in the ABAT gene have been identified in people with GABA-transaminase ... The ABAT gene mutations that cause GABA-transaminase deficiency lead to a shortage (deficiency) of functional GABA-transaminase ... The ABAT gene provides instructions for making the GABA-transaminase enzyme. This enzyme helps break down a brain chemical ( ...
GABA-transaminase) deficiency. J Inherit Metab Dis. 1999;22:414-27. ... 4-Hydroxybutyric acid and the clinical phenotype of succinic semialdehyde dehydrogenase deficiency, an inborn error of GABA ... 4-Hydroxybutyric acid and the clinical phenotype of succinic semialdehyde dehydrogenase deficiency, an inborn error of GABA ... Note: As mentioned above, increased concentrations of 4-HBA may also be detected in plasma and cerebrospinal fluid. In addition ...
Dive into the research topics of Effects of high-dose γ-vinyl GABA (vigabatrin) administration on visual and somatosensory evoked potentials in dogs. Together they form a unique fingerprint. ...
The Arabidopsis POP2 gene encodes a transaminase that degrades GABA and contributes to the formation of a gradient leading up ... 4-Aminobutyrate Transaminase. abstract. During angiosperm reproduction, pollen grains form a tube that navigates through female ...
Differences in the kinetic properties of brain gamma-aminobutyrate aminotransferase (GABA-transaminase; GABA-T) in different ... Studies on gamma-aminobutyrate aminotransferase (GABA-T) activities in human and rodent brain homogenates. ...
ID: GO:0009330 Type: http://bio2vec.net/ontology/gene_function Label: DNA topoisomerase complex (ATP-hydrolyzing) Synonyms: DNA topoisomerase complex (ATP-hydrolyzing) Alternative IDs: als API: GO SPARQL: GO ...
free K63-linked pUb:activated TAK1 complex:pUbtraf6:ticam1:activated TLR3/TLR4 complex (human) ...
Involved in transaminase activity. Specific function:. Can metabolize asymmetric dimethylarginine (ADMA) via transamination to ... Catalyzes the conversion of gamma-aminobutyrate and L-beta-aminoisobutyrate to succinate semialdehyde and methylmalonate ... 1. 4-aminobutyrate aminotransferase, mitochondrial. General function:. Involved in 4-aminobutyrate transaminase activity. ...
4: Calforex montreal taux de change SNMPSweep. If a pressure increase is applied at t 0 to the plate at the origin, there are ... 00 4. 1 Centre of mass of a semi-circular lamina Find the position of the centre of mass of a uniform semi-circular lamina. Two ... 4 and given by Eq. Patterns for the exercise of the combinatorial logic could be generated by truth table or by random ... 4693 4. Class_eval is ideal for adding methods to a class dynamically: class Person end CHAPTER 11 ADVANCED RUBY FEATURES 311 ...
acetylornithine transaminase. Succinylornithine transaminase (EC 2.6.1.81) (characterized). 46%. 96%. 334.7. acetylornithine/N- ... succinylornithine transaminase (EC 2.6.1.81) (characterized). 31%. 96%. 177.2. 4-aminobutyrate-2-oxoglutarate transaminase (EC ... succinylornithine transaminase (EC 2.6.1.81) (characterized). 44%. 94%. 339.7. acetylornithine/N-succinyldiaminopimelate ... 4-aminobutyrate-pyruvate transaminase (EC 2.6.1.96). 50%. 451.1. Confidence: high confidence medium confidence low confidence. ...
ornithine--oxo-acid transaminase (TIGR01885; EC 2.6.1.13; HMM-score: 155.8) Metabolism Energy metabolism Amino acids and amines ... L-lysine 6-transaminase (TIGR03251; EC 2.6.1.36; HMM-score: 64.9) Metabolism Central intermediary metabolism Other 4- ... aminobutyrate aminotransferase (TIGR00699; EC 2.6.1.19; HMM-score: 43.5) *TheSEED: see SACOL1922 ... transaminase, acetylornithine/succinylornithine family (TIGR00707; HMM-score: 175.2) Metabolism Central intermediary metabolism ...
TRANSAMINASE FOLD TYPE I 1m32:E (ASP32) to (ASP129) CRYSTAL STRUCTURE OF 2-AMINOETHYLPHOSPHONATE TRANSAMINASE , PLP-DEPENDENT ... COLI GAMMA-AMINOBUTYRATE AMINOTRANSFERASE , AMINOTRANSFERASE, TRANSFERASE 2vyc:A (GLY205) to (SER302) CRYSTAL STRUCTURE OF ACID ... MYCOBATERIUM TUBERCULOSIS TRANSAMINASE BIOA COMPLEXED WITH 2- HYDRAZINYLBENZO[D]THIAZOLE , PLP, TRANSAMINASE, TRANSFERASE 2j5v: ... INHIBITOR COMPLEX TRANSAMINASE PLP, TRANSFERASE-TRANSFERASE INHIBITOR COMPLEX 2bhd:A (ALA98) to (LEU174) MG SUBSTITUTED E. COLI ...
Table 4 Association between the abundance of indoor microbial species and wheeze, rhinitis and rhinoconjunctivitis in high ... 4. LEfSe analysis for characteristic KEGG functional pathways in urban and rural dust samples in Shanxi, China. The second- ... 4. A higher abundance of genes related to human disease and the immune system was detected in urban schools, including "Human ... Each classroom was vacuumed for 4 min, vacuumed for 2 min on the floor and vacuumed for 2 min on the upper surfaces of desks, ...
Align candidate Ac3H11_4179 (Gamma-aminobutyrate:alpha-ketoglutarate aminotransferase (EC 2.6.1.19)) to HMM TIGR00700 (gabT: 4- ... aminobutyrate transaminase (EC 2.6.1.19)). # hmmsearch :: search profile(s) against a sequence database # HMMER 3.3.1 (Jul 2020 ... to candidate Ac3H11_4179 Gamma-aminobutyrate:alpha-ketoglutarate aminotransferase (EC 2.6.1.19) ... 4179 Gamma-aminobutyrate:alpha-ketoglutarate aminotransferase (EC 2.6.1.1 # score bias c-Evalue i-Evalue hmmfrom hmm to alifrom ...
... aminobutyrate transaminase. 4‐Aminobutanoate (GABA) plays a significant role in micro‐organisms in the cytosolic regulation of ... or γ-aminobutyrate) for another amino acid substrate [63]. As the LA stress time increased, the levels increased by 0.79 times ... 4. Patterns of gene expression across two treatments (0 (CK), 30, and 60 min) inferred by STEM analysis; in each frame, the ... L. m QZ1178 was inoculated into liquid MRS medium at 30 °C for 24 h. Cultures were centrifuged at 6,000 rpm (4 °C) for 10 min, ...
Metabolite 4abut_c in iNJ661. 4-Aminobutanoate.
Leucine transaminase (irreversible). OHPBAT. O-Phospho-4-hydroxy-L-threonine:2-oxoglutarate aminotransferase ...
... 提供 transaminase 相关产品,包含各种抑制剂、激动剂和化合物库, ... GABA transaminase) 抑制剂。 Vigabatrin hydrochloride 是一种抗癫痫剂,通过抑制 GABA transaminase 对 GABA 的分解代谢来增加脑中 GABA 的水平。 ... GABA transaminase) 抑制剂。 Vigabatrin hydrochloride 是一种抗癫痫剂,通过抑制 GABA transaminase 对 GABA
Ketol-Isomerase, 2-Amino-2-Deoxy-D-Glucose-6-Phosphate use Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing) ... Kaposis Sarcoma Fibroblast Growth Factor use Fibroblast Growth Factor 4 Kaposis Sarcoma-Associated Herpesvirus use ... Killer Cell Lectin Like Receptor Subfamily C, Member 4 use NK Cell Lectin-Like Receptor Subfamily C ... Killer Cell Lectin-Like Receptor Subfamily C, Member 4 use NK Cell Lectin-Like Receptor Subfamily C ...
GABA Transaminase use 4-Aminobutyrate Transaminase GABA Transporter 1 use GABA Plasma Membrane Transport Proteins ... GABA alpha Ketoglutarate Aminotransferase use 4-Aminobutyrate Transaminase GABA Aminotransferase use 4-Aminobutyrate ... G Protein Coupled Inwardly Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ... G Protein-Coupled Inwardly-Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ...
GABA Transaminase use 4-Aminobutyrate Transaminase GABA Transporter 1 use GABA Plasma Membrane Transport Proteins ... GABA alpha Ketoglutarate Aminotransferase use 4-Aminobutyrate Transaminase GABA Aminotransferase use 4-Aminobutyrate ... G Protein Coupled Inwardly Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ... G Protein-Coupled Inwardly-Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ...
GABA Transaminase use 4-Aminobutyrate Transaminase GABA Transporter 1 use GABA Plasma Membrane Transport Proteins ... GABA alpha Ketoglutarate Aminotransferase use 4-Aminobutyrate Transaminase GABA Aminotransferase use 4-Aminobutyrate ... G Protein Coupled Inwardly Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ... G Protein-Coupled Inwardly-Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ...
GABA Transaminase use 4-Aminobutyrate Transaminase GABA Transporter 1 use GABA Plasma Membrane Transport Proteins ... GABA alpha Ketoglutarate Aminotransferase use 4-Aminobutyrate Transaminase GABA Aminotransferase use 4-Aminobutyrate ... G Protein Coupled Inwardly Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ... G Protein-Coupled Inwardly-Rectifying Potassium Channel 4 use G Protein-Coupled Inwardly-Rectifying Potassium Channels ...
B enzm: 1.1/2/3/4/5/6/7/8/10/11/13/14/15-18, 2.1/2/3/4/5/6/7/8, 2.7.10, 2.7.11-12, 3.1/2/3/4/5/6/7, 3.1.3.48, 3.4.21/22/23/24, ... ISBN 1-60831-270-4. *^ Golan, David E.; Armen H. Tashjian Jr.. Principles of pharmacology (3rd ed. ed.). Philadelphia: Wolters ... Figure 11-4 in: Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. (2007). Rang & Dales pharmacology. Edinburgh: ... ISBN 1-60831-270-4. *^ Stein MB, Fallin MD, Schork NJ, Gelernter J (November 2005). "COMT polymorphisms and anxiety-related ...
GOT: glutamic-oxaloacetic transaminase. GLUD: glutamate dehydrogenase. HK: hexokinase. PK: pyruvate kinase. LDH: lactate ... 1.0; group 4; lactate. <.001)] was an independent predictor for EAD. Belonging to group 1 at 6 h was associated with worse ... ABAT: 4-aminobutyrate aminotransferase. ALDH5A1: aldehyde dehydrogenase 5 family member A1. ASS: argininosuccinate synthase. ... We describe the diagnostic odyssey of a 4-year-old female patient with profound global developmental delays, microcephaly, ...
A study on the involvement of GABA-transaminase in MCT induced pulmonary hypertension.. ... A study on the involvement of GABA-transaminase in MCT induced pulmonary hypertension.. ... 4-Aminobutyrate Transaminase, Animals, Enzyme Inhibitors, gamma-Aminobutyric Acid, Hypertension, Pulmonary, Hypertrophy, Right ...
"L-Lysine 6-Transaminase" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... This graph shows the total number of publications written about "L-Lysine 6-Transaminase" by people in this website by year, ... Below are the most recent publications written about "L-Lysine 6-Transaminase" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "L-Lysine 6-Transaminase". ...
2-Aminoadipate Transaminase 2-Aminoadipic Acid 2-Aminoethanol use Ethanolamine 2-Aminoethylisothiuronium Bromide use beta- ... 4 Hydroxyphenylpyruvate Dioxygenase Deficiency Disease use Tyrosinemias 4-Nitrophenol-2-Hydroxylase use Cytochrome P-450 CYP2E1 ... 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ... 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- ...
Transaminase. 4-Aminobutyric Acid use gamma-Aminobutyric Acid. 4-Aminohippuric Acid use p-Aminohippuric Acid ... 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ... 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- ... 3-Keto-5-alpha-Steroid delta-4-Dehydrogenase use Testosterone 5-alpha-Reductase ...
  • In enzymology, 4-aminobutyrate transaminase (EC 2.6.1.19), also called GABA transaminase or 4-aminobutyrate aminotransferase, or GABA-T, is an enzyme that catalyzes the chemical reaction: 4-aminobutanoate + 2-oxoglutarate ⇌ {\displaystyle \rightleftharpoons } succinate semialdehyde + L-glutamate Thus, the two substrates of this enzyme are 4-aminobutanoate (GABA) and 2-oxoglutarate. (wikipedia.org)
  • The systematic name of this enzyme class is 4-aminobutanoate:2-oxoglutarate aminotransferase. (wikipedia.org)
  • 4-Aminobutyrate aminotransferase (GABA-transaminase) deficiency. (medlineplus.gov)
  • Hypersomnolence-hyperkinetic movement disorder in a child with compound heterozygous mutation in 4-aminobutyrate aminotransferase (ABAT) gene. (medlineplus.gov)
  • The aminotransferase catalyzes the reversible transfer of an amino group to α-keto butyrate to form α-aminobutyrate. (springeropen.com)
  • Serum aminotransferases such as aspartate aminotransferase, AST and alanine transaminase, ALT have been used as clinical markers of tissue damage, with increasing serum levels indicating an increased extent of damage. (medmuv.com)
  • As a transaminase, GABA-T's role is to move functional groups from an amino acid and a α-keto acid, and vice versa. (wikipedia.org)
  • catalyzed by the enzyme 4-aminobutyrate-pyruvate transaminase: (1) 4-aminobutanoate (GABA) + pyruvate ⇌ succinate semialdehyde + L-alanine (2) 4-aminobutanoate (GABA) + glyoxylate ⇌ succinate semialdehyde + glycine The primary role of GABA-T is to break down GABA as part of the GABA-Shunt. (wikipedia.org)
  • The ABAT gene provides instructions for making the GABA-transaminase enzyme. (medlineplus.gov)
  • At least 10 mutations in the ABAT gene have been identified in people with GABA-transaminase deficiency, which is a brain disease (encephalopathy) that begins in infancy. (medlineplus.gov)
  • The ABAT gene mutations that cause GABA-transaminase deficiency lead to a shortage (deficiency) of functional GABA-transaminase enzyme. (medlineplus.gov)
  • This accumulation alters the balance of neurotransmitters in the brain, leading to the neurological problems characteristic of GABA-transaminase deficiency. (medlineplus.gov)
  • The Arabidopsis POP2 gene encodes a transaminase that degrades GABA and contributes to the formation of a gradient leading up to the micropyle. (unipr.it)
  • A study on the involvement of GABA-transaminase in MCT induced pulmonary hypertension. (cornell.edu)
  • Recently, it was shown that Pediococcus acidilactici FAM18098 catabolized serine and threonine and formed α-aminobutyrate (AABA) and alanine in vitro and in cheese (Irmler et al. (springeropen.com)
  • Alanine transaminase has an important function in the delivery of skeletal muscle carbon and nitrogen (in the form of alanine) to the liver. (medmuv.com)
  • In the liver, alanine transaminase transfers the ammonia to α-KG and regenerates pyruvate. (medmuv.com)
  • This reaction is catalyzed by alanine transaminase, ALT. (medmuv.com)
  • This means that it is in the transferase class of enzymes, the nitrogenous transferase sub-class and the transaminase sub-subclass. (wikipedia.org)
  • This enzyme belongs to the family of transferases, specifically the transaminases, which transfer nitrogenous groups. (wikipedia.org)
  • Amino acid residues found in the active site of 4-aminobutyrate transaminase include Lys-329, which are found on each of the two subunits of the enzyme. (wikipedia.org)
  • These reaction steps are similar to the ones used in the engineered bacteria, where either a transaminase or a dehydrogenase catalyzes the final step of AABA synthesis (Fotheringham et al. (springeropen.com)
  • During cheese ripening, the bacterial strain Pediococcus acidilactici FAM18098 produces the non-proteinogenic amino acid, α-aminobutyrate (AABA). (springeropen.com)
  • SSADH deficiency leads to abnormal accumulation of the compound succinic semialdehyde, which is reduced or converted to 4-hydroxybutyric acid, also known as GHB (gamma-hydroxybutyric acid). (rarediseases.org)
  • Nicotianamine synthase (NAS) catalyzes the biosynthesis of the low-molecular-mass metal chelator nicotianamine (NA) from the 2-aminobutyrate moieties of three SAM molecules. (bvsalud.org)
  • At least 4 such structures have been solved using pig enzymes: 1OHV, 1OHW, 1OHY, 1SF2, and at least 4 such structures have been solved in Escherichia coli: 1SFF, 1SZK, 1SZS, 1SZU. (wikipedia.org)
  • This graph shows the total number of publications written about "L-Lysine 6-Transaminase" by people in this website by year, and whether "L-Lysine 6-Transaminase" was a major or minor topic of these publications. (ouhsc.edu)
  • Below are the most recent publications written about "L-Lysine 6-Transaminase" by people in Profiles. (ouhsc.edu)
  • We describe the diagnostic odyssey of a 4-year-old female patient with profound global developmental delays, microcephaly, severe hypotonia, retinal dystrophy, seizures, and progressive cerebellar atrophy. (bvsalud.org)
  • In addition, the levels of glial fibrillary acidic protein, ubiquitin carboxyl terminal hydrolase isozyme-L1, glutamic pyruvic transaminase-2, lactate, and glucose were elevated in newborns diagnosed with hypoxic-ischemic encephalopathy. (bvsalud.org)
  • In order to increase GABA contents in rice grains, we constructed a RNA interference (RNAi) vector suppressing the expression of GABA transaminase 1 gene ( OsGABA - T1 ). (chinacrops.org)
  • Choose from 1 of 42 ABAT antibodies, which have been validated in experiments with 4 publications and 160 images featured in our data gallery. (thermofisher.com)
  • This summary NTP report on the metabolism, disposition, and toxicity studies of 1,4-butanediol is based partially on studies that took place from December 1988 through February 1989. (nih.gov)
  • The draft summary report on the metabolism, disposition, and toxicity of 1,4-butanediol was evaluated by the reviewers listed below. (nih.gov)
  • After its discovery in the late 1960s, K. phaffii was first used for biomass and single-cell protein production from methanol [ 3 , 4 ]. (biomedcentral.com)
  • Catalyzes the reversible conversion of 3- phosphohydroxypyruvate to phosphoserine and of 3-hydroxy-2-oxo-4- phosphonooxybutanoate to phosphohydroxythreonine. (string-db.org)
  • At least 4 such structures have been solved using pig enzymes: 1OHV, 1OHW, 1OHY, 1SF2, and at least 4 such structures have been solved in Escherichia coli: 1SFF, 1SZK, 1SZS, 1SZU. (wikipedia.org)
  • National Cancer Institute 1 Introduction 1 Clinical investigations 3 Origins of the cancerous state 4 Development of clinical cancer 5 Autonomy 5 Spread of cancer 6 Wound washings 6 Cancer cells in circulating blood 7 Spread of tumor in animal models. (nih.gov)