PathWhiz

PathWhiz ID	Pathway	Meta Data
PW144280 View Pathway	drug action Cystine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 13:05 Last Updated: October 07, 2023 at 13:05
PW000699 View Pathway	disease Cystinosis, Ocular Nonnephropathic Homo sapiens Ocular non-nephropathic cystinosis, also known as adult-onset cystinosis, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the cysteine metabolism pathway. It is caused by a defect in the CTNS gene, which encodes the protein cystinosin, which acts as a cystine/H+ symporter that transports L-cysteine out of the lysosome. Ocular non-nephropathic cystinosis is characterized by a buildup of cysteine in cells, in the case of this form in the cornea. Symptoms include photophobia and damage to the cornea due to crystals forming from the excess cysteine. However, unlike other forms of cystinosis, no or minimal kidney damage occurs. Treatment with cysteamine, a drug that can convert cysteine into a form that can be secreted by the lysosome, can be effective in all of the forms of cystinosis. It is estimated that ocular non-nephropathic cystinosis affects less than 1 in 100,000 to 200,000 individuals, which is the rate of the more severe nephropathic cystinosis. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: June 23, 2014 at 02:48 Last Updated: June 23, 2014 at 02:48
PW122134 View Pathway	disease Cystinosis, Ocular Nonnephropathic Rattus norvegicus Ocular non-nephropathic cystinosis, also known as adult-onset cystinosis, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the cysteine metabolism pathway. It is caused by a defect in the CTNS gene, which encodes the protein cystinosin, which acts as a cystine/H+ symporter that transports L-cysteine out of the lysosome. Ocular non-nephropathic cystinosis is characterized by a buildup of cysteine in cells, in the case of this form in the cornea. Symptoms include photophobia and damage to the cornea due to crystals forming from the excess cysteine. However, unlike other forms of cystinosis, no or minimal kidney damage occurs. Treatment with cysteamine, a drug that can convert cysteine into a form that can be secreted by the lysosome, can be effective in all of the forms of cystinosis. It is estimated that ocular non-nephropathic cystinosis affects less than 1 in 100,000 to 200,000 individuals, which is the rate of the more severe nephropathic cystinosis. 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
PW121910 View Pathway	disease Cystinosis, Ocular Nonnephropathic Mus musculus Ocular non-nephropathic cystinosis, also known as adult-onset cystinosis, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the cysteine metabolism pathway. It is caused by a defect in the CTNS gene, which encodes the protein cystinosin, which acts as a cystine/H+ symporter that transports L-cysteine out of the lysosome. Ocular non-nephropathic cystinosis is characterized by a buildup of cysteine in cells, in the case of this form in the cornea. Symptoms include photophobia and damage to the cornea due to crystals forming from the excess cysteine. However, unlike other forms of cystinosis, no or minimal kidney damage occurs. Treatment with cysteamine, a drug that can convert cysteine into a form that can be secreted by the lysosome, can be effective in all of the forms of cystinosis. It is estimated that ocular non-nephropathic cystinosis affects less than 1 in 100,000 to 200,000 individuals, which is the rate of the more severe nephropathic cystinosis. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:50 Last Updated: September 10, 2018 at 15:50
PW127177 View Pathway	disease Cystinosis, Ocular Nonnephropathic Homo sapiens Ocular non-nephropathic cystinosis, also known as adult-onset cystinosis, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder of the cysteine metabolism pathway. It is caused by a defect in the CTNS gene, which encodes the protein cystinosin, which acts as a cystine/H+ symporter that transports L-cysteine out of the lysosome. Ocular non-nephropathic cystinosis is characterized by a buildup of cysteine in cells, in the case of this form in the cornea. Symptoms include photophobia and damage to the cornea due to crystals forming from the excess cysteine. However, unlike other forms of cystinosis, no or minimal kidney damage occurs. Treatment with cysteamine, a drug that can convert cysteine into a form that can be secreted by the lysosome, can be effective in all of the forms of cystinosis. It is estimated that ocular non-nephropathic cystinosis affects less than 1 in 100,000 to 200,000 individuals, which is the rate of the more severe nephropathic cystinosis. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: November 02, 2022 at 11:52 Last Updated: November 02, 2022 at 11:52
PW122135 View Pathway	disease Cystinuria Rattus norvegicus Cystinuria is a genetic condition caused by mutations in the SLC7A9 or SLC3A1 gene. These two genes are responsible for creating subunits of a protein that reabsorbs cystine into the blood, located in the kidneys. The mutations cause this process to be compromised and allows the amino acids to build up and have a high concentration in urine. This causes crystals to form and become stones as they grow larger. These stones can become lodged in the bladder or in the kidneys which can cause pain, develop infection and disrupt the passing of urine through the urinary tract if the stones create a blockage there. 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
PW121911 View Pathway	disease Cystinuria Mus musculus Cystinuria is a genetic condition caused by mutations in the SLC7A9 or SLC3A1 gene. These two genes are responsible for creating subunits of a protein that reabsorbs cystine into the blood, located in the kidneys. The mutations cause this process to be compromised and allows the amino acids to build up and have a high concentration in urine. This causes crystals to form and become stones as they grow larger. These stones can become lodged in the bladder or in the kidneys which can cause pain, develop infection and disrupt the passing of urine through the urinary tract if the stones create a blockage there. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 15:50 Last Updated: September 10, 2018 at 15:50
PW000700 View Pathway	disease Cystinuria Homo sapiens Cystinuria is a genetic condition caused by mutations in the SLC7A9 or SLC3A1 gene. These two genes are responsible for creating subunits of a protein that reabsorbs cystine into the blood, located in the kidneys. The mutations cause this process to be compromised and allows the amino acids to build up and have a high concentration in urine. This causes crystals to form and become stones as they grow larger. These stones can become lodged in the bladder or in the kidneys which can cause pain, develop infection and disrupt the passing of urine through the urinary tract if the stones create a blockage there. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: June 23, 2014 at 03:01 Last Updated: June 23, 2014 at 03:01
PW145085 View Pathway	drug action Cytarabine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 15:03 Last Updated: October 07, 2023 at 15:03
PW012920 View Pathway	metabolic Cytokinins Degradation Arabidopsis thaliana Cytokinins (CK) are a class of plant growth substances (phytohormones) that promote cell division, or cytokinesis, in plant roots and shoots. They are involved primarily in cell growth and differentiation, but also affect apical dominance, axillary bud growth, and leaf senescence. . Their regulation can take the form of biosynthesis, import, conjugation, and degradation. Homeostasis regulation by irreversible degradation is carried out by cytokinin oxidases which form adenine-like compounds resulting from the cleavage of the N6-isopentenyl-side chain. The cytokinins degradation pathway consists of five different degradation reactions that can be localized to either the endoplasmic reticulum or the vacuole. Cytokinin oxidase was found to catalyze two such reactions: the conversion of N6-dimethylallyladenine into 3-methyl-2-butenal and adenine and the conversion of trans-zeatin into 3-methyl-4-trans-hydroxy-2-butenal and adenine. It has not yet been determined if cytokinin oxidase also catalyzes the other three reactions in the cytokinins degradation pathway: the conversion of isopentenyl adenosine into adenosine and 3-methyl-2-butenal, the conversion of cis-zeatin into 3-methyl-4-cis-hydroxy-2-butenal and adenine, and the conversion of trans-zeatin riboside into 3-methyl-4-trans-hydroxy-2-butenal and adenosine. As such, the enzyme of these reactions are coloured orange in the image. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Carin Li Created On: February 24, 2017 at 16:01 Last Updated: February 24, 2017 at 16:01