Loader

Pathways

PathWhiz ID Pathway Meta Data

PW132444

Pw132444 View Pathway
metabolic

Upadacitinib Drug Metabolism

Homo sapiens
Upadacitinib is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Upadacitinib passes through the liver and is then excreted from the body mainly through the kidney.

PW146906

Pw146906 View Pathway
drug action

Upadacitinib Drug Metabolism Action Pathway

Homo sapiens

PW123957

Pw123957 View Pathway
signaling

UPR

Mus musculus
UPR

PW002026

Pw002026 View Pathway
metabolic

Uracil Degradation III

Escherichia coli
Uracil is a pyrimidine nucleobase found in RNA, and can be used as a source of nitrogen for E. coli. There are at least three pathways through which uracil is degraded. This one begins with uracil, which originates from purine degradation. The putative monooxygenase enzyme rutA catalyzes the breakdown of uracil into peroxyaminoacrylate, using FMNH2 as a cofactor. Peroxyaminoacrylate is then broken down into both carbamic acid and 3-aminoacrylate following the addition of a water molecule by the putative isochorismatase family protein rutB. Carbamic acid can then spontaneously, with the addition of a hydrogen ion, split into an ammonium ion and a molecule of carbon dioxide. 3-aminoacrylate, on the other hand, is catalyzed by the UPF0076 protein rutC to form 2-aminoacrylic acid. This compound enters into a reaction catalyzed by protein rutD, which adds a water molecule and hydrogen ion and forms malonic semialdehyde with ammonium being a byproduct. Finally, the putative NADH dehydrogenase/NAD(P)H nitroreductase rutE complex converts malonic semialdehyde into hydroxypropionic acid, which is then used to form other necessary chemicals. The ammonium ions produced will be the important source of nitrogen for the bacteria.

PW123529

Pw123529 View Pathway
metabolic

Uracil Degradation III

Pseudomonas aeruginosa
Uracil is a pyrimidine nucleobase found in RNA, and can be used as a source of nitrogen for E. coli. There are at least three pathways through which uracil is degraded. This one begins with uracil, which originates from purine degradation. The putative monooxygenase enzyme rutA catalyzes the breakdown of uracil into peroxyaminoacrylate, using FMNH2 as a cofactor. Peroxyaminoacrylate is then broken down into both carbamic acid and 3-aminoacrylate following the addition of a water molecule by the putative isochorismatase family protein rutB. Carbamic acid can then spontaneously, with the addition of a hydrogen ion, split into an ammonium ion and a molecule of carbon dioxide. 3-aminoacrylate, on the other hand, is catalyzed by the UPF0076 protein rutC to form 2-aminoacrylic acid. This compound enters into a reaction catalyzed by protein rutD, which adds a water molecule and hydrogen ion and forms malonic semialdehyde with ammonium being a byproduct. Finally, the putative NADH dehydrogenase/NAD(P)H nitroreductase rutE complex converts malonic semialdehyde into hydroxypropionic acid, which is then used to form other necessary chemicals. The ammonium ions produced will be the important source of nitrogen for the bacteria.

PW144898

Pw144898 View Pathway
drug action

Uracil mustard Drug Metabolism Action Pathway

Homo sapiens

PW012928

Pw012928 View Pathway
metabolic

Urate Degradation to Glyoxylate

Arabidopsis thaliana
Purine nucleotides are eventually degraded to ammonia and carbon dioxide. This pathway begins in the peroxisome and follows the degradation a urate intermediate to glyoxylate. The last three steps take place in the endoplasmic reticulum. First, uricase converts urate into 5-hydroxyisourate. Steps two and three are catalyzed by the bifunctional enzyme S-allantoin synthase: the conversion of 5-hydroxyisourate into 5-hydroxy-2-oxo-4-ureido-2,5-dihydro-1H-imidazole-5-carboxylate (OHCU) and the conversion of OHCU into S-allantoin. Fourth, allantoinase requires zinc ion as a cofactor to catalyze the conversion of S-allantoin into allantoate. Next allantoate must be transported out of the peroxisome and into the endoplasmic reticulum. Fifth, allantoate amidohydrolase catalyzes the conversion of allantoate into S-ureidoglycine. This enzyme is a homodimer and requires manganese ion as a cofactor. Sixth, ureidoglycine aminohydrolase requires a manganese ion as a cofactor to catalyze the conversion of S-ureidoglycine into S-ureidoglycolate. Seventh, ureidoglycolate amidohydrolase catalyzes the conversion of S-ureidoglycolate into glyoxylate.

PW012915

Pw012915 View Pathway
metabolic

Urate Degradation to Ureidoglycolate

Arabidopsis thaliana
Purine nucleotides are eventually degraded to ammonia and carbon dioxide. This pathway begins in the peroxisome and follows the degradation a urate intermediate to S-ureidoglycolate. The last two steps take place in the endoplasmic reticulum. First, uricase converts urate into 5-hydroxyisourate. Steps two and three are catalyzed by the bifunctional enzyme S-allantoin synthase: the conversion of 5-hydroxyisourate into 5-hydroxy-2-oxo-4-ureido-2,5-dihydro-1H-imidazole-5-carboxylate (OHCU) and the conversion of OHCU into S-allantoin. Fourth, allantoinase requires zinc ion as a cofactor to catalyze the conversion of S-allantoin into allantoate. Next allantoate must be transported out of the peroxisome and into the endoplasmic reticulum. Fifth, allantoate amidohydrolase catalyzes the conversion of allantoate into S-ureidoglycine. This enzyme is a homodimer and requires manganese ion as a cofactor. Sixth, ureidoglycine aminohydrolase requires a manganese ion as a cofactor to catalyze the conversion of S-ureidoglycine into S-ureidoglycolate.

PW132171

Pw132171 View Pathway
metabolic

Urea C-13 Drug Metabolism

Homo sapiens
Urea C-13 is a drug that is not metabolized by the human body as determined by current research and biotransformer analysis. Urea C-13 passes through the liver and is then excreted from the body mainly through the kidney.

PW146180

Pw146180 View Pathway
drug action

Urea C-13 Drug Metabolism Action Pathway

Homo sapiens