PathWhiz

PathWhiz ID	Pathway	Meta Data
PW145649 View Pathway	drug action Apremilast Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 16:18 Last Updated: October 07, 2023 at 16:18
PW145062 View Pathway	drug action Apraclonidine Drug Metabolism Action Pathway Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: October 07, 2023 at 15:00 Last Updated: October 07, 2023 at 15:00
PW121905 View Pathway	disease Apparent Mineralocorticoid Excess Syndrome Mus musculus Apparent mineralocorticoid excess (AME), also known as cortisol 11-beta-ketoreductase deficiency, is an extremely rare inborn error of metabolism (IEM) and autosomal recessive disorder of the steroidogenesis pathway. It is caused by a mutation in the HSD11B2 gene which encodes for corticosteroid 11-beta-dehydrogenase isozyme 2, and enzyme that converts cortisol to cortisone in the cell. Without this enzyme being functional, an accumulation of tetrahydrocortisol builds up, while tetrahydrocortisone levels dissipate. AME is characterized excessive thirst and urination, and along with this, symptoms include low levels of aldosterone, failure to thrive and hypertension. Treatment with corticoids that suppress the secretion of cortisol within the body can affect blood pressure and aldosterone levels. Antihypertensive agents are also effective. It is estimated that AME affects less than 1 in 1,000,000 individuals, with less than 100 reported cases as of 2019. 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
PW122129 View Pathway	disease Apparent Mineralocorticoid Excess Syndrome Rattus norvegicus Apparent mineralocorticoid excess (AME), also known as cortisol 11-beta-ketoreductase deficiency, is an extremely rare inborn error of metabolism (IEM) and autosomal recessive disorder of the steroidogenesis pathway. It is caused by a mutation in the HSD11B2 gene which encodes for corticosteroid 11-beta-dehydrogenase isozyme 2, and enzyme that converts cortisol to cortisone in the cell. Without this enzyme being functional, an accumulation of tetrahydrocortisol builds up, while tetrahydrocortisone levels dissipate. AME is characterized excessive thirst and urination, and along with this, symptoms include low levels of aldosterone, failure to thrive and hypertension. Treatment with corticoids that suppress the secretion of cortisol within the body can affect blood pressure and aldosterone levels. Antihypertensive agents are also effective. It is estimated that AME affects less than 1 in 1,000,000 individuals, with less than 100 reported cases as of 2019. 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
PW127371 View Pathway	disease Apparent Mineralocorticoid Excess Syndrome Homo sapiens Apparent mineralocorticoid excess (AME), also known as cortisol 11-beta-ketoreductase deficiency, is an extremely rare inborn error of metabolism (IEM) and autosomal recessive disorder of the steroidogenesis pathway. It is caused by a mutation in the HSD11B2 gene which encodes for corticosteroid 11-beta-dehydrogenase isozyme 2, and enzyme that converts cortisol to cortisone in the cell. Without this enzyme being functional, an accumulation of tetrahydrocortisol builds up, while tetrahydrocortisone levels dissipate. AME is characterized excessive thirst and urination, and along with this, symptoms include low levels of aldosterone, failure to thrive and hypertension. Treatment with corticoids that suppress the secretion of cortisol within the body can affect blood pressure and aldosterone levels. Antihypertensive agents are also effective. It is estimated that AME affects less than 1 in 1,000,000 individuals, with less than 100 reported cases as of 2019. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ray Kruger Created On: December 19, 2022 at 16:14 Last Updated: December 19, 2022 at 16:14
PW000694 View Pathway	disease Apparent Mineralocorticoid Excess Syndrome Homo sapiens Apparent mineralocorticoid excess (AME), also known as cortisol 11-beta-ketoreductase deficiency, is an extremely rare inborn error of metabolism (IEM) and autosomal recessive disorder of the steroidogenesis pathway. It is caused by a mutation in the HSD11B2 gene which encodes for corticosteroid 11-beta-dehydrogenase isozyme 2, and enzyme that converts cortisol to cortisone in the cell. Without this enzyme being functional, an accumulation of tetrahydrocortisol builds up, while tetrahydrocortisone levels dissipate. AME is characterized excessive thirst and urination, and along with this, symptoms include low levels of aldosterone, failure to thrive and hypertension. Treatment with corticoids that suppress the secretion of cortisol within the body can affect blood pressure and aldosterone levels. Antihypertensive agents are also effective. It is estimated that AME affects less than 1 in 1,000,000 individuals, with less than 100 reported cases as of 2019. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: June 23, 2014 at 01:24 Last Updated: June 23, 2014 at 01:24
PW064764 View Pathway	protein Apoptotic DNA Fragmentation and Tissue Homeostasis Homo sapiens Apoptotic endonucleases degrade chromosomal DNA during programmed cell death. ICAD and CAD exist in the nucleus in normal cells and is a major endonuclease in apoptosis. Its activation is normally caspase dependent. EndoG resides in mitochondria in normal cells and travels to the nucleus, where it fragments chromosomal DNA upon activation of apoptosis. Once released from the mitochondrial intermembrane space, EndoG activity is caspase independent. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Jonas Patron Created On: June 13, 2018 at 15:10 Last Updated: June 13, 2018 at 15:10
PW109198 View Pathway	protein Apoptotic DNA Fragmentation and Tissue Homeostasis Mus musculus Apoptotic endonucleases degrade chromosomal DNA during programmed cell death. ICAD and CAD exist in the nucleus in normal cells and is a major endonuclease in apoptosis. Its activation is normally caspase dependent. EndoG resides in mitochondria in normal cells and travels to the nucleus, where it fragments chromosomal DNA upon activation of apoptosis. Once released from the mitochondrial intermembrane space, EndoG activity is caspase independent. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 31, 2018 at 12:31 Last Updated: August 31, 2018 at 12:31
PW109276 View Pathway	protein Apoptotic DNA Fragmentation and Tissue Homeostasis Rattus norvegicus Apoptotic endonucleases degrade chromosomal DNA during programmed cell death. ICAD and CAD exist in the nucleus in normal cells and is a major endonuclease in apoptosis. Its activation is normally caspase dependent. EndoG resides in mitochondria in normal cells and travels to the nucleus, where it fragments chromosomal DNA upon activation of apoptosis. Once released from the mitochondrial intermembrane space, EndoG activity is caspase independent. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 31, 2018 at 12:48 Last Updated: August 31, 2018 at 12:48
PW109245 View Pathway	protein Apoptotic DNA Fragmentation and Tissue Homeostasis Bos taurus Apoptotic endonucleases degrade chromosomal DNA during programmed cell death. ICAD and CAD exist in the nucleus in normal cells and is a major endonuclease in apoptosis. Its activation is normally caspase dependent. EndoG resides in mitochondria in normal cells and travels to the nucleus, where it fragments chromosomal DNA upon activation of apoptosis. Once released from the mitochondrial intermembrane space, EndoG activity is caspase independent. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: August 31, 2018 at 12:40 Last Updated: August 31, 2018 at 12:40