Loader

Pathways

PathWhiz ID Pathway Meta Data

PW127615

Pw127615 View Pathway
drug action

Zanamivir Action Pathway

Homo sapiens
Zanamivir, also known as Relenza, is an inhibitor of the viral neuraminidase protein. This antiviral is used to treat and prevent influenza A and B infections. By interacting with the neuraminidase, Zabamivir renders the influenza virus unable to escape its host cell. Neuraminidases are essential for the cleaving of the terminal sialic acids on the glycosylated HA during the virus budding to facilitate its release. In consequence, the virus will not be able to infect other cells. This molecule is available as an intravenous solution or as a powder for inhalation.

PW144675

Pw144675 View Pathway
drug action

Zanamivir Drug Metabolism Action Pathway

Homo sapiens

PW132540

Pw132540 View Pathway
metabolic

Zanubrutinib Drug Metabolism

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

PW146905

Pw146905 View Pathway
drug action

Zanubrutinib Drug Metabolism Action Pathway

Homo sapiens

PW124096

Pw124096 View Pathway
metabolic

Zeatin Biosynthesis

Arabidopsis thaliana
Zeatin encourages lateral bud growth, resulting in bushier plants. It stimulates cell division when sprayed on meristems. Terpenoid backbone biosynthesis produces dimethylallyl diphosphate which, with different reactants, can result in different products with a byproduct of diphosphate. When reacted with tRNA adenine via tRNA dimethylallyltransferase, it results in the formation of tRNA containing 6-isopentenyl adenosine. When reacted via adenylate isopentenyltransferase 1, chloroplastic with either ATP, ADP, or AMP, it results in the formation of the corresponding isopentenyl, which in turn reacts with oxygen and reduced NADPH hemoprotein reductase via cytokinin hydroxylase, resulting in the formation of trans-zeatin riboside with the corresponding phosphates and byproducts of water and oxidized NADPH hemoprotein reductase.

PW012895

Pw012895 View Pathway
metabolic

Zeaxanthin Biosynthesis

Arabidopsis thaliana
Zeaxanthin biosynthesis is a pathway that occurs in the chloroplast by which lycopene becomes zeaxanthin, one of the most common carotenoid alcohols found in nature . The first two reactions are catalyzed by lycopene beta cyclase which uses NAD(P)H as a cofactor to convert lycopene into gamma-carotene and gamma-carotene into beta-carotene. The last two reactions are catalyzed by beta-carotene 3-hydroxylase which uses ferredoxin and Fe2+ as cofactors to convert beta-carotene into beta-cryptoxanthin and beta-cryptoxanthin into zeaxanthin.

PW132554

Pw132554 View Pathway
metabolic

Zeaxanthin Drug Metabolism

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

PW146281

Pw146281 View Pathway
drug action

Zeaxanthin Drug Metabolism Action Pathway

Homo sapiens

PW127262

Pw127262 View Pathway
disease

Zellweger Syndrome

Homo sapiens
Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.

PW121974

Pw121974 View Pathway
disease

Zellweger Syndrome

Rattus norvegicus
Zellweger syndrome, also known as cerebrohepatorenal syndrome, is an autosomal recessive peroxisome biogenesis disorder that is part of the family of Zellweger spectrum disorders. It is caused by a defect in one of 12 or more of the PEX genes (PEX1, 2, 3, 5, 6, 10, 12, 13, 14, 16, 19 and 26) that produce proteins called peroxins. Peroxins are used in the formation of peroxisomes, and can be involved in recognition of proteins targeted for the peroxisome, as well as their transport into the peroxisome. Peroxisomes typically break down both very long chain and branched fatty acids, but if they aren't present, these fatty acids build up in the blood and body, harming organs such as the brain and liver. Additionally, due to the fact that some processes, such as plasmalogen biosynthesis, occur in or using peroxisomes, and can lead to deficiencies in plasmalogens. These are important in brain and lung function, leading to other symptoms. Zellweger syndrome is characterized by an increase in levels of very long chain fatty acids in the blood plasma, as well as more visible physical symptoms, such as an abnormally large or small head at birth, characteristic facial features and poor muscle tone, which can lead to an inability of infants to feed. Other symptoms include an enlarged liver, skeletal abnormalities and low CNS function. Infants very rarely live longer than one year, and the only treatment is for symptoms the patient is experiencing, not for the syndrome itself.