PathWhiz

PathWhiz ID	Pathway	Meta Data
PW144274 View Pathway	drug action Adenosine phosphate Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 13:04 Last Updated: October 07, 2023 at 13:04
PW002091 View Pathway	metabolic Adenosine Nucleotides Degradation Escherichia coli The degradation of of adenosine nucleotides starts with AMP reacting with water through a nucleoside monophosphate phosphatase results in the release of phosphate and a adenosine. Adenosine reacts with water and hydrogen ion through an adenosine deaminase resulting in the release of ammonium and a inosine. Inosine reacts with phosphate through a inosine phosphorylase resulting in the release of an alpha-D-ribose-1-phosphate and an hypoxanthine. Hypoxanthine reacts with a water molecule and a NAD molecule through an hypoxanthine hydroxylase resulting in the release of an hydrogen ion, an NADH and a xanthine. Xanthine in turn is degraded by reacting with a water molecule and a NAD through xanthine NAD oxidoreductase resulting in the release of NADH, a hydrogen ion and urate. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: miguel ramirez Created On: October 13, 2015 at 15:56 Last Updated: October 13, 2015 at 15:56
PW144753 View Pathway	drug action Adenosine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 14:21 Last Updated: October 07, 2023 at 14:21
PW121699 View Pathway	disease Adenosine Deaminase Deficiency Mus musculus Adenosine deaminiase deficiency (immunodeficiency) is an autosomal recessive disease caused by a muation in the ADA gene which codes for adenosine deaminase. A deficiency in this enzyme results in immunodeficiency and a decreased concentration of lymphocytes in blood. Symptoms include diarrhea, severe or recurrent infections, vomiting and early onset in children, infants and newborns. Treatment includes bone-marrow transplants and enzyme replacement therapy. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:49 Last Updated: September 10, 2018 at 15:49
PW000075 View Pathway	disease Adenosine Deaminase Deficiency Homo sapiens Adenosine deaminiase deficiency (immunodeficiency) is an autosomal recessive disease caused by a muation in the ADA gene which codes for adenosine deaminase. A deficiency in this enzyme results in immunodeficiency and a decreased concentration of lymphocytes in blood. Symptoms include diarrhea, severe or recurrent infections, vomiting and early onset in children, infants and newborns. Treatment includes bone-marrow transplants and enzyme replacement therapy. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 01, 2013 at 15:52 Last Updated: August 01, 2013 at 15:52
PW121925 View Pathway	disease Adenosine Deaminase Deficiency Rattus norvegicus Adenosine deaminiase deficiency (immunodeficiency) is an autosomal recessive disease caused by a muation in the ADA gene which codes for adenosine deaminase. A deficiency in this enzyme results in immunodeficiency and a decreased concentration of lymphocytes in blood. Symptoms include diarrhea, severe or recurrent infections, vomiting and early onset in children, infants and newborns. Treatment includes bone-marrow transplants and enzyme replacement therapy. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:51 Last Updated: September 10, 2018 at 15:51
PW127288 View Pathway	disease Adenosine Deaminase Deficiency Homo sapiens Adenosine deaminiase deficiency (immunodeficiency) is an autosomal recessive disease caused by a muation in the ADA gene which codes for adenosine deaminase. A deficiency in this enzyme results in immunodeficiency and a decreased concentration of lymphocytes in blood. Symptoms include diarrhea, severe or recurrent infections, vomiting and early onset in children, infants and newborns. Treatment includes bone-marrow transplants and enzyme replacement therapy. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: December 01, 2022 at 10:12 Last Updated: December 01, 2022 at 10:12
PW398412 View Pathway	metabolic Adenine ribonucleotide biosynthesis Escherichia coli str. K-12 substr. MG1655 Adenine ribonucleotide biosynthesis is an essential pathway in bacteria for producing adenine-containing nucleotides, which are vital for DNA, RNA, and energy metabolism. This process originates from the de novo purine biosynthesis pathway, where inosine monophosphate (IMP) serves as the central precursor for adenine nucleotide formation. To produce adenine ribonucleotides, IMP undergoes a two-step conversion. First, IMP is aminated by adenylosuccinate synthetase, using aspartate and GTP as substrates, to form adenylosuccinate. In the second step, adenylosuccinate lyase cleaves adenylosuccinate to yield AMP (adenosine monophosphate) and fumarate as a byproduct. AMP can subsequently be phosphorylated by kinases to produce ADP and ATP, which are essential for cellular energy transfer and signaling processes. ATP also serves as a cofactor in numerous enzymatic reactions and as a building block for RNA synthesis. This pathway is tightly regulated to maintain adenine nucleotide homeostasis, ensuring bacterial growth, replication, and survival under varying metabolic conditions. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Julia Wakoli Created On: December 17, 2024 at 13:27 Last Updated: December 17, 2024 at 13:27
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