Loader

Pathways

PathWhiz ID Pathway Meta Data

PW495609

Pw495609 View Pathway
metabolic

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

PW686083

Pw686083 View Pathway
metabolic

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

PW686100

Pw686100 View Pathway
metabolic

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

PW147005

Pw147005 View Pathway
metabolic

all-trans-Retinoic acid Drug Metabolism Pathway

Homo sapiens

PW121930

Pw121930 View Pathway
disease

Alkaptonuria

Rattus 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.

PW121704

Pw121704 View Pathway
disease

Alkaptonuria

Mus 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.

PW000180

Pw000180 View Pathway
disease

Alkaptonuria

Homo 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.

PW127153

Pw127153 View Pathway
disease

Alkaptonuria

Homo 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.

PW145925

Pw145925 View Pathway
drug action

Aliskiren Drug Metabolism Action Pathway

Homo sapiens

PW126854

Pw126854 View Pathway
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.