Loader

Pathways

PathWhiz ID Pathway Meta Data

PW088320

Pw088320 View Pathway
metabolic

Malate-Aspartate Shuttle

Rattus norvegicus
The malate-aspartate shuttle system, also called the malate shuttle, is an essential system used by mitochondria, that allows electrons to move across the impermeable membrane between the cytosol and the mitochondrial matrix. The electrons are created during glycolysis, and are needed for oxidative phosphorylation. The malate-aspartate shuttle is needed as the inner membrane is not permeable to NADH or NAD+, but is permeable to the ions that attach to malate. When the malate gets inside the membrane,the energy inside of malate is taken out by creating NADH from NAD+, which regenerates oxaloacetate. NADH can then transfer electrons to the electron transport chain.

PW088457

Pw088457 View Pathway
metabolic

Malate-Aspartate Shuttle

Caenorhabditis elegans
The malate-aspartate shuttle system, also called the malate shuttle, is an essential system used by mitochondria, that allows electrons to move across the impermeable membrane between the cytosol and the mitochondrial matrix. The electrons are created during glycolysis, and are needed for oxidative phosphorylation. The malate-aspartate shuttle is needed as the inner membrane is not permeable to NADH or NAD+, but is permeable to the ions that attach to malate. When the malate gets inside the membrane,the energy inside of malate is taken out by creating NADH from NAD+, which regenerates oxaloacetate. NADH can then transfer electrons to the electron transport chain.

PW128301

Pw128301 View Pathway
drug action

Malathion Action Pathway

Homo sapiens
Malathion is a cholinesterase inhibitor used to treat head lice due to its low toxicity to humans. Malathion is an organophosphate which acts to inhibit acetylcholinesterase activity, it acts by binding to cholinesterase stopping the breakdown of acetylcholine to choline and acetic acid. Due to this, the neuron cannot return to a resting state after being activated, this causes the lice to experience muscle spasms and ultimately die. It is administered through a topical application which is readily absorbed by the insects, and only 8% by human skin. It is metabolized into metabolites known as malathion dicarboxylic acid, malathion monocarboxylic acid and malaoxon.

PW144881

Pw144881 View Pathway
drug action

Malathion Drug Metabolism Action Pathway

Homo sapiens

PW176507

Pw176507 View Pathway
metabolic

Malathion Predicted Metabolism Pathway

Homo sapiens
Metabolites of Malathion are predicted with biotransformer.

PW000207

Pw000207 View Pathway
disease

Malonic Aciduria

Homo sapiens
Malonyl-CoA decarboxylase deficiency, also called malonic aciduria, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder caused by a defective MLYCD gene. The MLYCD gene codes for the protein malonyl-CoA decarboxylase which regulates the creation and degradation of fatty acids. This disorder is characterized by a large accumulation of fatty acid byproducts in the tissues. Symptoms of the disorder include delayed development, hypotonia, seizures, vomiting, diarrhea and cardiomyopathy. Treatment with L-carnitine is very effective, as it encourages beta-oxidation of fatty acids. Less than 30 cases globally have ever been reported, making this disorder extremely rare.

PW121993

Pw121993 View Pathway
disease

Malonic Aciduria

Rattus norvegicus
Malonyl-CoA decarboxylase deficiency, also called malonic aciduria, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder caused by a defective MLYCD gene. The MLYCD gene codes for the protein malonyl-CoA decarboxylase which regulates the creation and degradation of fatty acids. This disorder is characterized by a large accumulation of fatty acid byproducts in the tissues. Symptoms of the disorder include delayed development, hypotonia, seizures, vomiting, diarrhea and cardiomyopathy. Treatment with L-carnitine is very effective, as it encourages beta-oxidation of fatty acids. Less than 30 cases globally have ever been reported, making this disorder extremely rare.

PW127183

Pw127183 View Pathway
disease

Malonic Aciduria

Homo sapiens
Malonyl-CoA decarboxylase deficiency, also called malonic aciduria, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder caused by a defective MLYCD gene. The MLYCD gene codes for the protein malonyl-CoA decarboxylase which regulates the creation and degradation of fatty acids. This disorder is characterized by a large accumulation of fatty acid byproducts in the tissues. Symptoms of the disorder include delayed development, hypotonia, seizures, vomiting, diarrhea and cardiomyopathy. Treatment with L-carnitine is very effective, as it encourages beta-oxidation of fatty acids. Less than 30 cases globally have ever been reported, making this disorder extremely rare.

PW121768

Pw121768 View Pathway
disease

Malonic Aciduria

Mus musculus
Malonyl-CoA decarboxylase deficiency, also called malonic aciduria, is a rare inborn error of metabolism (IEM) and autosomal recessive disorder caused by a defective MLYCD gene. The MLYCD gene codes for the protein malonyl-CoA decarboxylase which regulates the creation and degradation of fatty acids. This disorder is characterized by a large accumulation of fatty acid byproducts in the tissues. Symptoms of the disorder include delayed development, hypotonia, seizures, vomiting, diarrhea and cardiomyopathy. Treatment with L-carnitine is very effective, as it encourages beta-oxidation of fatty acids. Less than 30 cases globally have ever been reported, making this disorder extremely rare.

PW127185

Pw127185 View Pathway
disease

Malonyl-CoA Decarboxylase Deficiency

Homo sapiens
Malonyl CoA decarboxylase deficiency, also claled MCD deficiency, is a rare inborn error of fatty acid metabolism and autosomal-recessive metabolic disorder, which is caused by a defective mitochondrial malonyl CoA decarboxylase due to reduced activity. Mitochondrial malonyl CoA decarboxylase catalyzes the conversion of intramitochondrial malonyl CoA to acetyl CoA, which is a key product that involve in many biochemical reactions. This disorder is characterized by a large accumulation of methylmalonic acid in the mitochondrial. Symptoms of the disorder include hypotonia (i.e. weak muscle tone), hypoglycemia (i.e. low blood sugar), diarrhea, seizures and vomiting. The Malonyl CoA decarboxylase deficiency is an extremely rare genetic disease happened in early childhood, which only less than 30 cases have been reported. There is currently no cure for Malonyl CoA decarboxylase deficiency, treatment involves managing the disorder's symptoms.