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Pathways

Showing 1 - 10 of 48619 pathways
SMPDB ID Pathway Chemical Compounds Proteins

SMP00107

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.

SMP00747

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.

SMP00316

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.

SMP00746

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.

SMP00279

Pw000301 View Pathway
drug action

Ximelagatran Action Pathway

Homo sapiens
Ximelagatran was the first member of the drug class of direct thrombin inhibitors that can be taken orally. It acts solely by inhibiting the actions of thrombin. Ximelagatran is a prodrug, being converted in vivo to the active agent melagatran.

SMP00513

Pw000489 View Pathway
disease

Xanthinuria type II

Homo sapiens
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase. Classic xanthinuria is a rare metabolic defect concerning the final reactions of purine catabolism. There are two types of the disorder: type I results from xanthine dehydrogenase (XDH) deficiency, while type II is characterized by lack of both XDH and aldehyde oxidase activity. Both types are clinically similar and are characterized by elevated xanthine concentration in body fluids that can lead to xanthine crystallisation. The most common manifestation of the disease is urolithiasis, but in most cases xanthinuria remains asymptomatic and the diagnosis is accidental.

SMP00512

Pw000488 View Pathway
disease

Xanthinuria type I

Homo sapiens
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase. Classic xanthinuria is a rare metabolic defect concerning the final reactions of purine catabolism. There are two types of the disorder: type I results from xanthine dehydrogenase (XDH) deficiency, while type II is characterized by lack of both XDH and aldehyde oxidase activity. Both types are clinically similar and are characterized by elevated xanthine concentration in body fluids that can lead to xanthine crystallisation. The most common manifestation of the disease is urolithiasis, but in most cases xanthinuria remains asymptomatic and the diagnosis is accidental.

SMP00220

Pw000080 View Pathway
disease

Xanthine Dehydrogenase Deficiency (Xanthinuria)

Homo sapiens
Xanthinuria, also known as xanthine oxidase deficiency, is a rare genetic disorder causing the accumulation of xanthine. It is caused by a deficiency of the enzyme xanthine oxidase, which causes accumulation of xanthine in plasma; uric acid in serum; and hypoxanthine, uric acid and xanthine in urine. Symptoms include arthralgia, hematuria, mental retardation, stomatisis, and urolithiasis.

SMP00511

Pw000487 View Pathway
disease

Wolman disease

Homo sapiens
Wolman disease (also known as Wolman’s Disease, early onset LAL Deficiency, and Lysosomal acid lipase deficiency) is a rare inherited condition involving the breakdown and use of fats and cholesterol in the body (lipid metabolism). In affected individuals, harmful amounts of lipids accumulate in the spleen, liver, bone marrow, small intestine, small hormone-producing glands on top of each kidney (adrenal glands), and lymph nodes. In addition to fat deposits, calcium deposits in the adrenal glands are also seen. Infants with Wolman disease are healthy and active at birth but soon develop signs and symptoms of the disorder. These may include an enlarged liver and spleen (hepatosplenomegaly), poor weight gain, low muscle tone, a yellow tint to the skin and the whites of the eyes (jaundice), vomiting, diarrhea, developmental delay, low amounts of iron in the blood (anemia), and poor absorption of nutrients from food. Children affected by this condition develop severe malnutrition and generally do not survive past early childhood.

SMP00268

Pw000311 View Pathway
drug action

Warfarin Action Pathway

Homo sapiens
Warfarin is an anticoagulant that inhibits the liver enzyme vitamin K reductase. This leads to the depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulation factors (II, VII, IX, and X), this ultimately results in reduced cleavage of fibrinogen into fibrin and decreased coagulability of the blood.
Showing 1 - 10 of 48619 pathways