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Pathways

PathWhiz ID Pathway Meta Data

PW127294

Pw127294 View Pathway
disease

Xanthinuria Type I

Homo sapiens
Xanthinuria Type I (Xanthine Dehydrogenase Deficiency) is a condition caused by an autosomal recessive mutation. The condition was discovered (though not diagnosed) in 1817, when stones formed of almost pure xanthine were first identified by Marcet. The symptoms arise because of a malfunction in the production of xanthine oxidase. It is a rare . It is characterized by a loss of oxidase such as in serum and the uric acid found in the urine. This enzyme deficiency causes the accumulation of xanthine in the plasma, hypoxanthine in the serum, and xanthine in the urine. They will be found in the latter and former in increased quantities. Although the condition can cause a wide range of symptoms including renal xanthine stones, what occurs most of the time is that xanthinuria is asymptomatic and diagnosis is product of chance. The disorder has symptoms including arthralgia, hematuria, mental retardation, stomatisis, and urolithiasis.

PW000489

Pw000489 View Pathway
disease

Xanthinuria Type II

Homo sapiens
Xanthinuria Type II is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective xanthine dehydrogenase. Xanthine dehydrogenase catalyzes the conversion of hypoxanthine into xanthine and conversion of xanthine into uric acid. This disorder is characterized by a large accumulation of xanthine and hypoxanthine; as well as dissipation of uric acid. Symptoms of the disorder include blood in the urine, recurrent urinary tract infections and abdominal pain. It is estimated that xanthinuria types I and II affects 1 in 69,000 individuals.

PW122058

Pw122058 View Pathway
disease

Xanthinuria Type II

Rattus norvegicus
Xanthinuria Type II is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective xanthine dehydrogenase. Xanthine dehydrogenase catalyzes the conversion of hypoxanthine into xanthine and conversion of xanthine into uric acid. This disorder is characterized by a large accumulation of xanthine and hypoxanthine; as well as dissipation of uric acid. Symptoms of the disorder include blood in the urine, recurrent urinary tract infections and abdominal pain. It is estimated that xanthinuria types I and II affects 1 in 69,000 individuals.

PW121834

Pw121834 View Pathway
disease

Xanthinuria Type II

Mus musculus
Xanthinuria Type II is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective xanthine dehydrogenase. Xanthine dehydrogenase catalyzes the conversion of hypoxanthine into xanthine and conversion of xanthine into uric acid. This disorder is characterized by a large accumulation of xanthine and hypoxanthine; as well as dissipation of uric acid. Symptoms of the disorder include blood in the urine, recurrent urinary tract infections and abdominal pain. It is estimated that xanthinuria types I and II affects 1 in 69,000 individuals.

PW127298

Pw127298 View Pathway
disease

Xanthinuria Type II

Homo sapiens
Xanthinuria Type II (Xanthine Dehydrogenase Deficiency) is a rare inborn error of metabolism (IEM) and autosomal recessive disorder and caused by a defective xanthine dehydrogenase. Xanthine dehydrogenase catalyzes the conversion of hypoxanthine into xanthine and conversion of xanthine into uric acid. This disorder is characterized by a large accumulation of xanthine and hypoxanthine; as well as dissipation of uric acid. Symptoms of the disorder include blood in the urine, recurrent urinary tract infections and abdominal pain. It is estimated that xanthinuria types I and II affects 1 in 69,000 individuals.

PW012896

Pw012896 View Pathway
metabolic

Xanthophyll Cycle

Arabidopsis thaliana
Xanthophyll cycle is a pathway that transforms zeaxanthin to violaxanthin and antheraxanthin through enzymes. Xanthophyll cycle mainly takes place in diatoms and dinoflagellates of plants in high-light condition. Zeaxanthin is obatined from zeaxanthin biosynthesis that transforms lycopene to zeaxanthin (indirectly). Zeaxanthin is catalyzed into antheraxanthin and antheraxanthin catalyzed into violaxanthin both by the enzyme, zeaxanthin epoxidase with cofactor FAD. Violaxanthin deepoxidase/antheraxanthin deepoxidase can reverse the above reactions (i.e. violaxanthin to antheraxanthin and antheraxanthin to zeaxanthin).

PW012937

Pw012937 View Pathway
metabolic

xcaazzz

Homo sapiens

PW146158

Pw146158 View Pathway
drug action

Xenon Xe-127 Drug Metabolism Action Pathway

Homo sapiens

PW146082

Pw146082 View Pathway
drug action

Xenon-133 Drug Metabolism Action Pathway

Homo sapiens

PW122448

Pw122448 View Pathway
drug action

Ximelagatran Action

Homo sapiens
Ximelagatran is a prodrug that is converted to melagatran. This drug is a direct thrombin inhibitor that binds directly to the active site of thrombin, preventing coagulation and formation of blood clots due to the inactivation of the enzyme that catalyzes activation of coagulation factors V, XIII and fibrinogen. Ximelagatran is the first direct thrombin inhibitor that could be taken orally, and was thought to be a replacement for warfarin, due to not having as many dietary restrictions involved. However, it was withdrawn from testing and distribution following evidence of liver damage. After oral administration, ximelagatran is absorbed and converted to melagatran through an unknown series of reactions. From there, melagatran directly binds to thrombin, preventing its use as an enzyme. This prevents catalyzation of factor V to factor Va, which would form the prothrombinase complex and create more thrombin. It also prevents the catalysis fibrinogen or factor I to fibrin, which then polymerizes to form the blood clot. The lack of useable thrombin also prevents the catalysis of factor XIII to factor XIIIa, which is necessary to crosslink the polymerized fibrin to form a water insoluble clot.