Pathways

PathWhiz ID Pathway Meta Data

PW000270

Pw000270 View Pathway
drug action

Zoledronate Action Pathway

Homo sapiens
The action of zoledronate on bone tissue is based partly on its affinity for hydroxyapatite, which is part of the mineral matrix of bone. Zoledronate also targets farnesyl pyrophosphate (FPP) synthase. Nitrogen-containing bisphosphonates such as zoledronate appear to act as analogues of isoprenoid diphosphate lipids, thereby inhibiting FPP synthase, an enzyme in the mevalonate pathway. Inhibition of this enzyme in osteoclasts prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are essential for the post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins. This activity inhibits osteoclast activity and reduces bone resorption and turnover. In postmenopausal women, it reduces the elevated rate of bone turnover, leading to, on average, a net gain in bone mass.

PW000724

Pw000724 View Pathway
drug action

Zidovudine Action Pathway

Homo sapiens
Zidovudine, a structural analog of thymidine, is a prodrug that must be phosphorylated to its active 5′-triphosphate metabolite, zidovudine triphosphate (ZDV-TP). It inhibits the activity of HIV-1 reverse transcriptase (RT) via DNA chain termination after incorporation of the nucleotide analogue. It competes with the natural substrate dGTP and incorporates itself into viral DNA.

PW121974

Pw121974 View Pathway
disease

Zellweger Syndrome

Rattus norvegicus
Zellweger syndrome (Cerebrohepatorenal syndrome; Cerebro-hepato-renal syndrome) phenotype is caused by mutations in any of several different genes involved in peroxisome biogenesis, Peroxins (PEX proteins, peroxisomal transport proteins) proteins 1,2,3,5,6,12,14, and 26. Peroxin proteins serve several functions including the recognition of cytoplasmic proteins that contain peroxisomal targeting signals (PTS) that tag them for transport by peroxismnal proteins to the peroxisome. Zellweger syndrome is characterized by accumulation of cholesterol in plasma, tissues and cerebrospinal fluid, decreased chenodeoxycholic acid and increased concentration of bile alcohols and their glyconjugates. Increased concentrations of cholestanol and apolipoprotein B are also observed in spinal fluid. Symptoms include dementia, psychiatric disturbances, pyramidal and/or cerebellar signs, and seizures.

PW000195

Pw000195 View Pathway
disease

Zellweger Syndrome

Homo sapiens
Zellweger syndrome (Cerebrohepatorenal syndrome; Cerebro-hepato-renal syndrome) phenotype is caused by mutations in any of several different genes involved in peroxisome biogenesis, Peroxins (PEX proteins, peroxisomal transport proteins) proteins 1,2,3,5,6,12,14, and 26. Peroxin proteins serve several functions including the recognition of cytoplasmic proteins that contain peroxisomal targeting signals (PTS) that tag them for transport by peroxismnal proteins to the peroxisome. Zellweger syndrome is characterized by accumulation of cholesterol in plasma, tissues and cerebrospinal fluid, decreased chenodeoxycholic acid and increased concentration of bile alcohols and their glyconjugates. Increased concentrations of cholestanol and apolipoprotein B are also observed in spinal fluid. Symptoms include dementia, psychiatric disturbances, pyramidal and/or cerebellar signs, and seizures.

PW121749

Pw121749 View Pathway
disease

Zellweger Syndrome

Mus musculus
Zellweger syndrome (Cerebrohepatorenal syndrome; Cerebro-hepato-renal syndrome) phenotype is caused by mutations in any of several different genes involved in peroxisome biogenesis, Peroxins (PEX proteins, peroxisomal transport proteins) proteins 1,2,3,5,6,12,14, and 26. Peroxin proteins serve several functions including the recognition of cytoplasmic proteins that contain peroxisomal targeting signals (PTS) that tag them for transport by peroxismnal proteins to the peroxisome. Zellweger syndrome is characterized by accumulation of cholesterol in plasma, tissues and cerebrospinal fluid, decreased chenodeoxycholic acid and increased concentration of bile alcohols and their glyconjugates. Increased concentrations of cholestanol and apolipoprotein B are also observed in spinal fluid. Symptoms include dementia, psychiatric disturbances, pyramidal and/or cerebellar signs, and seizures.

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 (Wikipedia). 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.

PW000723

Pw000723 View Pathway
drug action

Zalcitabine Action Pathway

Homo sapiens
Zalcitabine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Within cells, zalcitabine is converted to its active metabolite, dideoxycytidine 5'-triphosphate (ddCTP), by the sequential action of cellular enzymes. ddCTP interferes with viral RNA-directed DNA polymerase (reverse transcriptase) by competing for utilization of the natural substrate deoxycytidine 5'-triphosphate (dCTP), as well as incorpating into viral DNA.

PW002105

Pw002105 View Pathway
metabolic

Xylose Degradation I

Escherichia coli
D-xylose, which can serve as a total source of carbon and energy for Escherichia coli K-12 substr. MG1655, enters the cell either through a low-affinity, proton-motive force-driven or a high-affinity, ATP-driven (ABC) transport system, so it is not phosphorylated during entry. Once inside the cell, an isomerase converts it to D-xylulose and subsequently a kinase converts it to D-xylulose 5-phosphate, an intermediate of the pentose phosphate pathway. Hence it flows through the pathways of central metabolism to satisfy the cell's need for precursor metabolites, reducing power, and metabolic energy. (EcoCyc)

PW002433

Pw002433 View Pathway
metabolic

Xylitol Degradation

Saccharomyces cerevisiae
The degradation of xylose begins with NADP dependent trifunctional aldehyde reductase/xylose reductase/glucose 1-dehydrogenase resulting in the release of a NADPH, hydrogen ion and Xylitol. Xylitol reacts with a NAD D-xylulose reductase resulting in the release of NADH, a hydrogen ion and D-xylulose. Xylulose reacts with ATP through a xylulose kinase resulting in a release of ADP, hydrogen ion and xylulose 5-phosphate. The latter compound, xylulose 5-phosphate through a Ribulose-phosphate 3-epimerase resulting in the release of D-ribulose 5-phosphate. D-ribulose 5-phosphate and xylulose 5-phosphate react with a transketolase resulting in the release of D-glyceraldehyde 3-phosphate and D-sedoheptulose 7-phosphate. These two compounds react through a transaldolase resulting in the release of a D-erythrose 4-phosphate and Beta-D-fructofuranose 6-phosphate. D-erythrose 4-phosphate reacts with a xylulose 5-phosphate through a transketolase resulting in the release of Beta-D-fructofuranose 6-phosphate and D-glyceraldehyde 3-phosphate

PW000911

Pw000911 View Pathway
disease

xx

Homo sapiens