Pathways

PathWhiz ID Pathway Meta Data

PW000270

Pw000270 View Pathway
drug action

Zoledronate Action Pathway

Homo sapiens
Zoledronate (also named zoledronic acid, Zometa or Reclast) is a type of medication that used to treat numbers of bone diseases because of its affinity for hydroxyapatite. Zoledronate targets farnesyl pyrophosphate (FPP) synthase by inhibiting the function of this enzyme in the mevalonate pathway, which prevent the biosynthesis of Geranyl-PP and farnesyl pyrophosphate. Geranyl-PP and farnesyl pyrophosphate are important for geranylgeranylation and farnesylation of GTPase signalling proteins. Lack of Geranyl-PP and farnesyl pyrophosphate will result in decreased rate of bond resorption and turnover as well as block the osteoclast activity, which lead to an increasing mass gain in bone (i.e. 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
Escherichia coli can utilize D-xylose as the sole source of carbon and energy for the cell. A low-affinity proton motive force or a high-affinity ATP-driven (ABC) transport system brings unphosphorylated D-xylose into the cell. Following entry, D-xylose is converted to D-xylulose by an isomerase and then converted to the pentose phosphate pathway intermediate, D-xylulose 5-phosphate via a kinase. D-xylulose 5-phosphate can then enter pathways of metabolism to meet the cells needs.

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