
PathWhiz ID | Pathway | Meta Data |
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PW495609 |
Allantoin Degradation (Anaerobic)Escherichia coli (strain SMS-3-5 / SECEC)
Allantoin can be degraded in anaerobic conditions. The first step involves allantoin being degraded by an allantoinase resulting in an allantoate. This compound in turn is metabolized by reacting with water and 2 hydrogen ions through an allantoate amidohydrolase resulting in the release of a carbon dioxide, ammonium and an S-ureidoglycine. The latter compund is further degrades through a S-ureidoglycine aminohydrolase resulting in the release of an ammonium and an S-ureidoglycolate.
S-ureidoglycolate can be metabolized into oxalurate by two different reactions. The first reactions involves a NAD driven ureidoglycolate dehydrogenase resulting in the release of a hydrogen ion , an NADH and a oxalurate. On the other hand S-ureidoglycolate can react with NADP resulting in the release of an NADPH, a hydroge ion and an oxalurate.
It is hypothesized that oxalurate can interact with a phosphate and release a a carbamoyl phosphate and an oxamate.
The carbamoyl phosphate can be further degraded by reacting with an ADP, and a hydrogen ion through a carbamate kinase resulting in the release of an ammonium , ATP and carbon dioxide
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Creator: Julia Wakoli Created On: February 03, 2025 at 12:32 Last Updated: February 03, 2025 at 12:32 |
PW686083 |
Allantoin Degradation (Anaerobic)Campylobacter jejuni RM1221
Allantoin can be degraded in anaerobic conditions. The first step involves allantoin being degraded by an allantoinase resulting in an allantoate. This compound in turn is metabolized by reacting with water and 2 hydrogen ions through an allantoate amidohydrolase resulting in the release of a carbon dioxide, ammonium and an S-ureidoglycine. The latter compund is further degrades through a S-ureidoglycine aminohydrolase resulting in the release of an ammonium and an S-ureidoglycolate.
S-ureidoglycolate can be metabolized into oxalurate by two different reactions. The first reactions involves a NAD driven ureidoglycolate dehydrogenase resulting in the release of a hydrogen ion , an NADH and a oxalurate. On the other hand S-ureidoglycolate can react with NADP resulting in the release of an NADPH, a hydroge ion and an oxalurate.
It is hypothesized that oxalurate can interact with a phosphate and release a a carbamoyl phosphate and an oxamate.
The carbamoyl phosphate can be further degraded by reacting with an ADP, and a hydrogen ion through a carbamate kinase resulting in the release of an ammonium , ATP and carbon dioxide
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Creator: Julia Wakoli Created On: February 04, 2025 at 09:28 Last Updated: February 04, 2025 at 09:28 |
PW686100 |
Allantoin Degradation (Anaerobic)Bacteroides oleiciplenus YIT 12058
Allantoin can be degraded in anaerobic conditions. The first step involves allantoin being degraded by an allantoinase resulting in an allantoate. This compound in turn is metabolized by reacting with water and 2 hydrogen ions through an allantoate amidohydrolase resulting in the release of a carbon dioxide, ammonium and an S-ureidoglycine. The latter compund is further degrades through a S-ureidoglycine aminohydrolase resulting in the release of an ammonium and an S-ureidoglycolate.
S-ureidoglycolate can be metabolized into oxalurate by two different reactions. The first reactions involves a NAD driven ureidoglycolate dehydrogenase resulting in the release of a hydrogen ion , an NADH and a oxalurate. On the other hand S-ureidoglycolate can react with NADP resulting in the release of an NADPH, a hydroge ion and an oxalurate.
It is hypothesized that oxalurate can interact with a phosphate and release a a carbamoyl phosphate and an oxamate.
The carbamoyl phosphate can be further degraded by reacting with an ADP, and a hydrogen ion through a carbamate kinase resulting in the release of an ammonium , ATP and carbon dioxide
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Creator: Julia Wakoli Created On: February 04, 2025 at 16:01 Last Updated: February 04, 2025 at 16:01 |
PW147005 |
all-trans-Retinoic acid Drug Metabolism PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 10, 2023 at 13:37 Last Updated: October 10, 2023 at 13:37 |
PW121930 |
disease
AlkaptonuriaRattus norvegicus
Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase. A mutation in this enzyme results in accumulation of homogentisic acid in urine. Symptoms, which present in adulthood, include arthritis, black or brown urine, and urolithiasis. Treatment includes a low-protein diet with vitamin C.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51 |
PW121704 |
disease
AlkaptonuriaMus musculus
Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase. A mutation in this enzyme results in accumulation of homogentisic acid in urine. Symptoms, which present in adulthood, include arthritis, black or brown urine, and urolithiasis. Treatment includes a low-protein diet with vitamin C.
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Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49 |
PW000180 |
disease
AlkaptonuriaHomo sapiens
Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase. A mutation in this enzyme results in accumulation of homogentisic acid in urine. Symptoms, which present in adulthood, include arthritis, black or brown urine, and urolithiasis. Treatment includes a low-protein diet with vitamin C.
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Creator: WishartLab Created On: August 19, 2013 at 12:05 Last Updated: August 19, 2013 at 12:05 |
PW127153 |
disease
AlkaptonuriaHomo sapiens
Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase. A mutation in this enzyme results in accumulation of homogentisic acid in urine. Symptoms, which present in adulthood, include arthritis, vulvular heart disease, black or brown urine, black and brown eyes, ears, and skin, and urolithiasis. Treatment includes a low-protein diet with vitamin C.
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Creator: Ray Kruger Created On: October 26, 2022 at 12:31 Last Updated: October 26, 2022 at 12:31 |
PW145925 |
drug action
Aliskiren Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 16:59 Last Updated: October 07, 2023 at 16:59 |
PW126854 |
drug action
Alirocumab Action Pathway (New)Homo sapiens
Alirocumab is a PCSK9 inhibitor used as an adjunct to manage heterozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients who require additional lowering of LDL-cholesterol (LDL-C).
Alirocumab is an antibody eliciting proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor activity that is indicated for: (i) use in reducing the risk of myocardial infarction, stroke, and unstable angina requiring hospitalization in adults with established cardiovascular disease 4, and/or (ii) use as an adjunct to diet or use alone or in combination with other lipid-lowering therapies (statins, ezetimibe, for example) for the treatment of adults with primary hyperlipidemia (including heterozygous familial hypercholesterolemia) to reduce low-density lipoprotein cholesterol (LDL-C) levels in the body.
PCSK9 is secreted by the liver and typically binds to the LDL receptors in serum and marks them for lysosomal degradation. In result, the LDL receptors are not able to recycle to the plasma membrane, reducing their binding to LDL-C and therefore reducing the clearance of LDL-C from plasma. Therefore by inhibiting PCSK9's actions, alirocumab allows for more LDL-C reuptake by the liver and facilitates a higher rate of clearance. Lower LDL cholesterol concentrations are associated with a reduced risk of coronary heart disease.
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Creator: Karxena Harford Created On: April 19, 2022 at 22:54 Last Updated: April 19, 2022 at 22:54 |