PathWhiz

PathWhiz ID	Pathway	Meta Data
PW686803 View Pathway	metabolic Adenine and Adenosine Salvage III Prevotella intermedia ATCC 25611 = DSM 20706 Adenosine is first incorporated into the cytosol through either a nupG or a nupC transporter. Once in the cytosol, adenosine is degraded into adenine by reacting with a water and a adenosine nucleosidase, releasing a D-ribofuranose and a adenine. The adenine then reacts with a PRPP through a adenine phosphoribosyltransferase resulting in the release of a pyrophosphate and an AMP . The AMP in turn reacts with a water molecule through a AMP nucleosidase resulting in the release of a D-ribofuranose 5-phosphate and a adenine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: February 27, 2025 at 16:18 Last Updated: February 27, 2025 at 16:18
PW548768 View Pathway	metabolic Adenine and Adenosine Salvage III Prevotella shahii DSM 15611 = JCM 12083 Adenosine is first incorporated into the cytosol through either a nupG or a nupC transporter. Once in the cytosol, adenosine is degraded into adenine by reacting with a water and a adenosine nucleosidase, releasing a D-ribofuranose and a adenine. The adenine then reacts with a PRPP through a adenine phosphoribosyltransferase resulting in the release of a pyrophosphate and an AMP . The AMP in turn reacts with a water molecule through a AMP nucleosidase resulting in the release of a D-ribofuranose 5-phosphate and a adenine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: February 27, 2025 at 16:26 Last Updated: February 27, 2025 at 16:26
PW686805 View Pathway	metabolic Adenine and Adenosine Salvage III Prevotella salivae DSM 15606 Adenosine is first incorporated into the cytosol through either a nupG or a nupC transporter. Once in the cytosol, adenosine is degraded into adenine by reacting with a water and a adenosine nucleosidase, releasing a D-ribofuranose and a adenine. The adenine then reacts with a PRPP through a adenine phosphoribosyltransferase resulting in the release of a pyrophosphate and an AMP . The AMP in turn reacts with a water molecule through a AMP nucleosidase resulting in the release of a D-ribofuranose 5-phosphate and a adenine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: February 27, 2025 at 16:26 Last Updated: February 27, 2025 at 16:26
PW686832 View Pathway	metabolic Adenine and Adenosine Salvage III Tatumella ptyseos ATCC 33301 Adenosine is first incorporated into the cytosol through either a nupG or a nupC transporter. Once in the cytosol, adenosine is degraded into adenine by reacting with a water and a adenosine nucleosidase, releasing a D-ribofuranose and a adenine. The adenine then reacts with a PRPP through a adenine phosphoribosyltransferase resulting in the release of a pyrophosphate and an AMP . The AMP in turn reacts with a water molecule through a AMP nucleosidase resulting in the release of a D-ribofuranose 5-phosphate and a adenine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: February 27, 2025 at 18:19 Last Updated: February 27, 2025 at 18:19
PW549071 View Pathway	metabolic Adenine and Adenosine Salvage III Yersinia frederiksenii ATCC 33641 Adenosine is first incorporated into the cytosol through either a nupG or a nupC transporter. Once in the cytosol, adenosine is degraded into adenine by reacting with a water and a adenosine nucleosidase, releasing a D-ribofuranose and a adenine. The adenine then reacts with a PRPP through a adenine phosphoribosyltransferase resulting in the release of a pyrophosphate and an AMP . The AMP in turn reacts with a water molecule through a AMP nucleosidase resulting in the release of a D-ribofuranose 5-phosphate and a adenine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: February 27, 2025 at 18:34 Last Updated: February 27, 2025 at 18:34
PW561804 View Pathway	metabolic Adenine and Adenosine Salvage III Bacteroides massiliensis Adenosine is first incorporated into the cytosol through either a nupG or a nupC transporter. Once in the cytosol, adenosine is degraded into adenine by reacting with a water and a adenosine nucleosidase, releasing a D-ribofuranose and a adenine. The adenine then reacts with a PRPP through a adenine phosphoribosyltransferase resulting in the release of a pyrophosphate and an AMP . The AMP in turn reacts with a water molecule through a AMP nucleosidase resulting in the release of a D-ribofuranose 5-phosphate and a adenine. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: March 09, 2025 at 03:25 Last Updated: March 09, 2025 at 03:25
PW144304 View Pathway	drug action Adenine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 13:21 Last Updated: October 07, 2023 at 13:21
PW000511 View Pathway	disease Adenine Phosphoribosyltransferase Deficiency (APRT) Homo sapiens Adenine phosphoribosyltransferase deficiency, which is also known as APRTD or APRT deficiency, is a rare inherited inborn error of metabolism (IEM) leading to the recurrent formation of kidney stones. It is an autosomal recessive disorder associated with a mutation in the enzyme adenine phosphoribosyltransferase (APRT). APRT is involved in the nucleotide salvage pathway, which provides an alternative, and energetically more efficient route to nucleotide biosynthesis in humans and most other animals. A defect in this enzyme can lead to the accumulation of the insoluble purine known as 2,8-dihydroxyadenine. In particular, when APRT has reduced or nonexistent activity, adenine accumulates which is then degraded by xanthine dehydrogenase to 2,8-dihydroxyadenine (DHA). 2,8-Dihydroxyadenine is a derivative of adenine which accumulates in 2,8 dihydroxyadenine urolithiasis (kidney stones). Kidney and urinary tract stones can obstruct the urinary tract, resulting in pain and difficulty urinating. If left untreated, the condition can eventually produce kidney failure. APRTD was first diagnosed in 1976. There are two categories of APRTD: type I involves a complete loss of the APRT function while type II involves a partial loss and is mostly found in Japan. APRT deficiency is estimated to affect 1 in 27 000 people in Japan. APRTD is rarer in Europe, where it affects 1 in 50 000 to 100 000 people. A diagnosis of APRTD can be made by analyzing kidney stones or measuring DHA concentrations in urine. APRTD is treatable with regular doses of allopurinol, which inhibits xanthine dehydrogenase activity. APRTD can also be treated with a low-purine diet and a high fluid intake. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 29, 2013 at 10:39 Last Updated: August 29, 2013 at 10:39
PW122080 View Pathway	disease Adenine Phosphoribosyltransferase Deficiency (APRT) Rattus norvegicus Adenine phosphoribosyltransferase deficiency, which is also known as APRTD or APRT deficiency, is a rare inherited inborn error of metabolism (IEM) leading to the recurrent formation of kidney stones. It is an autosomal recessive disorder associated with a mutation in the enzyme adenine phosphoribosyltransferase (APRT). APRT is involved in the nucleotide salvage pathway, which provides an alternative, and energetically more efficient route to nucleotide biosynthesis in humans and most other animals. A defect in this enzyme can lead to the accumulation of the insoluble purine known as 2,8-dihydroxyadenine. In particular, when APRT has reduced or nonexistent activity, adenine accumulates which is then degraded by xanthine dehydrogenase to 2,8-dihydroxyadenine (DHA). 2,8-Dihydroxyadenine is a derivative of adenine which accumulates in 2,8 dihydroxyadenine urolithiasis (kidney stones). Kidney and urinary tract stones can obstruct the urinary tract, resulting in pain and difficulty urinating. If left untreated, the condition can eventually produce kidney failure. APRTD was first diagnosed in 1976. There are two categories of APRTD: type I involves a complete loss of the APRT function while type II involves a partial loss and is mostly found in Japan. APRT deficiency is estimated to affect 1 in 27 000 people in Japan. APRTD is rarer in Europe, where it affects 1 in 50 000 to 100 000 people. A diagnosis of APRTD can be made by analyzing kidney stones or measuring DHA concentrations in urine. APRTD is treatable with regular doses of allopurinol, which inhibits xanthine dehydrogenase activity. APRTD can also be treated with a low-purine diet and a high fluid intake. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:52 Last Updated: September 10, 2018 at 15:52
PW127299 View Pathway	disease Adenine Phosphoribosyltransferase Deficiency (APRT) Homo sapiens Adenine phosphoribosyltransferase deficiency, which is also known as APRTD or APRT deficiency, is a rare inherited inborn error of metabolism (IEM) leading to the recurrent formation of kidney stones. It is an autosomal recessive disorder associated with a mutation in the enzyme adenine phosphoribosyltransferase (APRT). APRT is involved in the nucleotide salvage pathway, which provides an alternative, and energetically more efficient route to nucleotide biosynthesis in humans and most other animals. A defect in this enzyme can lead to the accumulation of the insoluble purine known as 2,8-dihydroxyadenine. In particular, when APRT has reduced or nonexistent activity, adenine accumulates which is then degraded by xanthine dehydrogenase to 2,8-dihydroxyadenine (DHA). 2,8-Dihydroxyadenine is a derivative of adenine which accumulates in 2,8 dihydroxyadenine urolithiasis (kidney stones). Kidney and urinary tract stones can obstruct the urinary tract, resulting in pain and difficulty urinating. If left untreated, the condition can eventually produce kidney failure. APRTD was first diagnosed in 1976. There are two categories of APRTD: type I involves a complete loss of the APRT function while type II involves a partial loss and is mostly found in Japan. APRT deficiency is estimated to affect 1 in 27 000 people in Japan. APRTD is rarer in Europe, where it affects 1 in 50 000 to 100 000 people. A diagnosis of APRTD can be made by analyzing kidney stones or measuring DHA concentrations in urine. APRTD is treatable with regular doses of allopurinol, which inhibits xanthine dehydrogenase activity. APRTD can also be treated with a low-purine diet and a high fluid intake. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: December 04, 2022 at 00:15 Last Updated: December 04, 2022 at 00:15