ASS is responsible for the third step of the urea cycle and one of the reactions of the citrulline-NO cycle.
Genetic structure
The gene that encodes for this enzyme, ASS, is located on chromosome 9. In humans, ASS is expressed mostly in the cells of liver and kidney.
The expressed ASS gene is at least 65 kb in length, including at least 12 introns.
Enzyme mechanism
In the first step of the catalyzed reaction, citrulline attacks the α-phosphate of ATP to form citrulline adenylate, a reactive intermediate. The attachment of AMP to the ureido (urea-like) group on citrulline activates the carbonyl center for subsequent nucleophilic attack. This activation facilitates the second step, in which the α-amino group of aspartate attacks the ureido group. Attack by aspartate is the rate-limiting step of the reaction. This step produces free AMP and L-argininosuccinate.
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver...
published: 10 Mar 2020
Medical vocabulary: What does Argininosuccinate Synthase mean
What does Argininosuccinate Synthase mean in English?
published: 17 Jan 2016
UREA CYCLE MADE EASY 2020 - METABOLISMS MADE SIMPLE
UREA CYCLE MADE EASY 2020 - METABOLISMS MADE SIMPLE
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism resu...
published: 10 Mar 2020
How to say argininosuccinate synthase ASS in German?
published: 31 May 2017
Upregulation of Argininosuccinate Synthetase and it's Effects on Arginine (Along with NO) production
A video recorded for Biochemistry 4002 class at Memorial University. John Jeddore, Greg Morrow, George Furey, Allison Guzzwell
published: 14 Oct 2010
Gene Music using Protein Sequence of ASS1 "ARGININOSUCCINATE SYNTHASE 1"
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The Urea cycle is a biochemical pathway in which the free ammonia is converted into urea so that it can be easily excreted.
Urea is the major end product of nitrogen metabolism in humans.
Deficiencies of the various enzymes and transporters involved in the urea cycle can cause urea cycle disorders:
N-Acetylglutamate synthase deficiency
Carbamoyl phosphate synthetase deficiency
Ornithine transcarbamoylase deficiency
Citrullinemia (Deficiency of argininosuccinic acid synthase)
Argininosuccinic aciduria (Deficiency of argininosuccinic acid lyase)
Argininemia (Deficiency of arginase)
...
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism results in waste ammonia. All animals need a way to excrete this product. Most aquatic organisms, or ammonotelic organisms, excrete ammonia without converting it.[1] Organisms that cannot easily and safely remove nitrogen as ammonia convert it to a less toxic substance such as urea or uric acid via the urea cycle, which occurs mainly in the liver. Urea produced by the liver is then released into the bloodstream where it travels to the kidneys and is ultimately excreted in urine.
Steps of the urea cycle:
Carbamoyl phosphate is converted to citrulline. With catalysis by ornithine transcarbamoylase, the carbamoyl phosphate group is donated to ornithine and releases a phosphate group.
A condensation reaction occurs between the amino group of aspartate and the carbonyl group of citrulline to form argininosuccinate. This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase.
Argininosuccinate undergoes cleavage by argininosuccinase to form arginine and fumarate.
Arginine is cleaved by arginase to form urea and ornithine. The ornithine is then transported back to the mitochondria to begin the urea cycle again.
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism results in waste ammonia. All animals need a way to excrete this product. Most aquatic organisms, or ammonotelic organisms, excrete ammonia without converting it.[1] Organisms that cannot easily and safely remove nitrogen as ammonia convert it to a less toxic substance such as urea or uric acid via the urea cycle, which occurs mainly in the liver. Urea produced by the liver is then released into the bloodstream where it travels to the kidneys and is ultimately excreted in urine.
Steps of the urea cycle:
Carbamoyl phosphate is converted to citrulline. With catalysis by ornithine transcarbamoylase, the carbamoyl phosphate group is donated to ornithine and releases a phosphate group.
A condensation reaction occurs between the amino group of aspartate and the carbonyl group of citrulline to form argininosuccinate. This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase.
Argininosuccinate undergoes cleavage by argininosuccinase to form arginine and fumarate.
Arginine is cleaved by arginase to form urea and ornithine. The ornithine is then transported back to the mitochondria to begin the urea cycle again.
UREA CYCLE MADE EASY 2020 - METABOLISMS MADE SIMPLE
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism results in waste ammonia. All animals need a way to excrete this product. Most aquatic organisms, or ammonotelic organisms, excrete ammonia without converting it.[1] Organisms that cannot easily and safely remove nitrogen as ammonia convert it to a less toxic substance such as urea or uric acid via the urea cycle, which occurs mainly in the liver. Urea produced by the liver is then released into the bloodstream where it travels to the kidneys and is ultimately excreted in urine.
Steps of the urea cycle:
Carbamoyl phosphate is converted to citrulline. With catalysis by ornithine transcarbamoylase, the carbamoyl phosphate group is donated to ornithine and releases a phosphate group.
A condensation reaction occurs between the amino group of aspartate and the carbonyl group of citrulline to form argininosuccinate. This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase.
Argininosuccinate undergoes cleavage by argininosuccinase to form arginine and fumarate.
Arginine is cleaved by arginase to form urea and ornithine. The ornithine is then transported back to the mitochondria to begin the urea cycle again.
Regulation:
N-Acetylglutamic acid(NAG)
The synthesis of carbamoyl phosphate and the urea cycle are dependent on the presence of N-acetylglutamic acid (NAcGlu), which allosterically activates CPS1. NAcGlu is an obligate activator of carbamoyl phosphate synthetase. Synthesis of NAcGlu by N-acetylglutamate synthase (NAGS) is stimulated by both Arg, allosteric stimulator of NAGS, and Glu, a product in the transamination reactions and one of NAGS's substrates, both of which are elevated when free amino acids are elevated. So Glu not only is a substrate for NAGS but also serves as an activator for the urea cycle.
UREA CYCLE MADE EASY 2020 - METABOLISMS MADE SIMPLE
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism results in waste ammonia. All animals need a way to excrete this product. Most aquatic organisms, or ammonotelic organisms, excrete ammonia without converting it.[1] Organisms that cannot easily and safely remove nitrogen as ammonia convert it to a less toxic substance such as urea or uric acid via the urea cycle, which occurs mainly in the liver. Urea produced by the liver is then released into the bloodstream where it travels to the kidneys and is ultimately excreted in urine.
Steps of the urea cycle:
Carbamoyl phosphate is converted to citrulline. With catalysis by ornithine transcarbamoylase, the carbamoyl phosphate group is donated to ornithine and releases a phosphate group.
A condensation reaction occurs between the amino group of aspartate and the carbonyl group of citrulline to form argininosuccinate. This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase.
Argininosuccinate undergoes cleavage by argininosuccinase to form arginine and fumarate.
Arginine is cleaved by arginase to form urea and ornithine. The ornithine is then transported back to the mitochondria to begin the urea cycle again.
Regulation:
N-Acetylglutamic acid(NAG)
The synthesis of carbamoyl phosphate and the urea cycle are dependent on the presence of N-acetylglutamic acid (NAcGlu), which allosterically activates CPS1. NAcGlu is an obligate activator of carbamoyl phosphate synthetase. Synthesis of NAcGlu by N-acetylglutamate synthase (NAGS) is stimulated by both Arg, allosteric stimulator of NAGS, and Glu, a product in the transamination reactions and one of NAGS's substrates, both of which are elevated when free amino acids are elevated. So Glu not only is a substrate for NAGS but also serves as an activator for the urea cycle.
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Gene Music using Protein Sequence of ASS1 'ARGININOSUCCINATE SYNTHASE 1'
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Gene Music using Protein Sequence of ASS1 'ARGININOSUCCINATE SYNTHASE 1'
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The Urea cycle is a biochemical pathway in which the free ammonia is converted into urea so that it can be easily excreted.
Urea is the major end product of nitrogen metabolism in humans.
Deficiencies of the various enzymes and transporters involved in the urea cycle can cause urea cycle disorders:
N-Acetylglutamate synthase deficiency
Carbamoyl phosphate synthetase deficiency
Ornithine transcarbamoylase deficiency
Citrullinemia (Deficiency of argininosuccinic acid synthase)
Argininosuccinic aciduria (Deficiency of argininosuccinic acid lyase)
Argininemia (Deficiency of arginase)
Hyperornithinemia, hyperammonemia, homocitrullinuria syndrome (Deficiency of the mitochondrial ornithine transporter)
Most urea cycle disorders are associated with hyperammonemia, however argininemia and some forms of argininosuccinic aciduria do not present with elevated ammonia.
Organisms that cannot easily and quickly remove ammonia usually have to convert it to some other substance, like urea or uric acid, which are much less toxic. Insufficiency of the urea cycle occurs in some genetic disorders (inborn errors of metabolism), and in liver failure. The result of liver failure is accumulation of nitrogenous waste, mainly ammonia, which leads to hepatic encephalopathy.
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The Urea cycle is a biochemical pathway in which the free ammonia is converted into urea so that it can be easily excreted.
Urea is the major end product of nitrogen metabolism in humans.
Deficiencies of the various enzymes and transporters involved in the urea cycle can cause urea cycle disorders:
N-Acetylglutamate synthase deficiency
Carbamoyl phosphate synthetase deficiency
Ornithine transcarbamoylase deficiency
Citrullinemia (Deficiency of argininosuccinic acid synthase)
Argininosuccinic aciduria (Deficiency of argininosuccinic acid lyase)
Argininemia (Deficiency of arginase)
Hyperornithinemia, hyperammonemia, homocitrullinuria syndrome (Deficiency of the mitochondrial ornithine transporter)
Most urea cycle disorders are associated with hyperammonemia, however argininemia and some forms of argininosuccinic aciduria do not present with elevated ammonia.
Organisms that cannot easily and quickly remove ammonia usually have to convert it to some other substance, like urea or uric acid, which are much less toxic. Insufficiency of the urea cycle occurs in some genetic disorders (inborn errors of metabolism), and in liver failure. The result of liver failure is accumulation of nitrogenous waste, mainly ammonia, which leads to hepatic encephalopathy.
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism results in waste ammonia. All animals need a way to excrete this product. Most aquatic organisms, or ammonotelic organisms, excrete ammonia without converting it.[1] Organisms that cannot easily and safely remove nitrogen as ammonia convert it to a less toxic substance such as urea or uric acid via the urea cycle, which occurs mainly in the liver. Urea produced by the liver is then released into the bloodstream where it travels to the kidneys and is ultimately excreted in urine.
Steps of the urea cycle:
Carbamoyl phosphate is converted to citrulline. With catalysis by ornithine transcarbamoylase, the carbamoyl phosphate group is donated to ornithine and releases a phosphate group.
A condensation reaction occurs between the amino group of aspartate and the carbonyl group of citrulline to form argininosuccinate. This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase.
Argininosuccinate undergoes cleavage by argininosuccinase to form arginine and fumarate.
Arginine is cleaved by arginase to form urea and ornithine. The ornithine is then transported back to the mitochondria to begin the urea cycle again.
UREA CYCLE MADE EASY 2020 - METABOLISMS MADE SIMPLE
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The urea cycle (also known as the ornithine cycle) is a cycle of biochemical reactions that produces urea from ammonia. This cycle occurs in ureotelic organisms. The urea cycle converts highly toxic ammonia to urea for excretion. This cycle was the first metabolic cycle to be discovered (Hans Krebs and Kurt Henseleit, 1932), five years before the discovery of the TCA cycle. This cycle was described in more detail later on by Ratner and Cohen. The urea cycle takes place primarily in the liver and, to a lesser extent, in the kidneys.
Amino acid catabolism results in waste ammonia. All animals need a way to excrete this product. Most aquatic organisms, or ammonotelic organisms, excrete ammonia without converting it.[1] Organisms that cannot easily and safely remove nitrogen as ammonia convert it to a less toxic substance such as urea or uric acid via the urea cycle, which occurs mainly in the liver. Urea produced by the liver is then released into the bloodstream where it travels to the kidneys and is ultimately excreted in urine.
Steps of the urea cycle:
Carbamoyl phosphate is converted to citrulline. With catalysis by ornithine transcarbamoylase, the carbamoyl phosphate group is donated to ornithine and releases a phosphate group.
A condensation reaction occurs between the amino group of aspartate and the carbonyl group of citrulline to form argininosuccinate. This reaction is ATP dependent and is catalyzed by argininosuccinate synthetase.
Argininosuccinate undergoes cleavage by argininosuccinase to form arginine and fumarate.
Arginine is cleaved by arginase to form urea and ornithine. The ornithine is then transported back to the mitochondria to begin the urea cycle again.
Regulation:
N-Acetylglutamic acid(NAG)
The synthesis of carbamoyl phosphate and the urea cycle are dependent on the presence of N-acetylglutamic acid (NAcGlu), which allosterically activates CPS1. NAcGlu is an obligate activator of carbamoyl phosphate synthetase. Synthesis of NAcGlu by N-acetylglutamate synthase (NAGS) is stimulated by both Arg, allosteric stimulator of NAGS, and Glu, a product in the transamination reactions and one of NAGS's substrates, both of which are elevated when free amino acids are elevated. So Glu not only is a substrate for NAGS but also serves as an activator for the urea cycle.
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Gene Music using Protein Sequence of ASS1 'ARGININOSUCCINATE SYNTHASE 1'
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The Urea cycle is a biochemical pathway in which the free ammonia is converted into urea so that it can be easily excreted.
Urea is the major end product of nitrogen metabolism in humans.
Deficiencies of the various enzymes and transporters involved in the urea cycle can cause urea cycle disorders:
N-Acetylglutamate synthase deficiency
Carbamoyl phosphate synthetase deficiency
Ornithine transcarbamoylase deficiency
Citrullinemia (Deficiency of argininosuccinic acid synthase)
Argininosuccinic aciduria (Deficiency of argininosuccinic acid lyase)
Argininemia (Deficiency of arginase)
Hyperornithinemia, hyperammonemia, homocitrullinuria syndrome (Deficiency of the mitochondrial ornithine transporter)
Most urea cycle disorders are associated with hyperammonemia, however argininemia and some forms of argininosuccinic aciduria do not present with elevated ammonia.
Organisms that cannot easily and quickly remove ammonia usually have to convert it to some other substance, like urea or uric acid, which are much less toxic. Insufficiency of the urea cycle occurs in some genetic disorders (inborn errors of metabolism), and in liver failure. The result of liver failure is accumulation of nitrogenous waste, mainly ammonia, which leads to hepatic encephalopathy.
Subscribe : https://www.youtube.com/channel/UCOmrniWfKi-uCD6Oh6fqhgw
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CHECK OUT NEWEST VIDEO: "Nucleic acids - DNA and RNA structure "
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-~-~~-~~~-~~-~-
... chronic management of adult and pediatric patients with UCDs, involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC) or argininosuccinic acid synthetase (AS).
... the chronic management of adult and pediatric patients with UCDs involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC) or argininosuccinate synthetase (AS).
... chronic management of adult and pediatric patients with UCDs, involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC) or argininosuccinic acid synthetase (AS).
... of adult and pediatric patients with urea cycle disorders (UCDs) involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC) or argininosuccinate synthetase (AS).
In the U.S., OLPRUVA™ (sodium phenylbutyrate) is approved for the treatment of urea cycle disorders (UCDs) involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS).
In the U.S., OLPRUVA™ (sodium phenylbutyrate) is approved for the treatment of urea cycle disorders (UCDs) involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS).
... synthetase (CPS), ornithine transcarbamylase (OTC) or argininosuccinic acid synthetase (AS).[2] Please see Important SafetyInformation and full Prescribing Information, including Patient Information.
... of certain patients living with urea cycle disorders (UCDs) involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC) or argininosuccinic acid synthetase (AS).
... synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS).5Please see Important SafetyInformation and full Prescribing Information, including Patient Information.
... of Olpruva sodium phenylbutyrate for the treatment of urea cycle disorders involving deficiencies of carbamylphosphate synthetase, ornithine transcarbamylase, or argininosuccinic acid synthetase.
... of Olpruva sodium phenylbutyrate for the treatment of urea cycle disorders involving deficiencies of carbamylphosphate synthetase, ornithine transcarbamylase, or argininosuccinic acid synthetase.
In the U.S., OLPRUVA™ (sodium phenylbutyrate) is approved for the treatment of urea cycle disorders (UCDs) involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS).
In the U.S., OLPRUVA™ (sodium phenylbutyrate) is approved for the treatment of urea cycle disorders (UCDs) involving deficiencies of carbamylphosphate synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS).
... synthetase (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase (AS).4 Please see Important SafetyInformation and full Prescribing Information, including Patient Information.
Victoria Advocate
23 Jan 2024
Victoria Advocate
23 Jan 2024