Pathways

PathWhiz ID Pathway Meta Data

PW122258

Pw122258 View Pathway
metabolic

Secondary metabolites pathways

Bacteria

PW122253

Pw122253 View Pathway
metabolic

TPN B biosynthesis

Bacteria
Terpenoids, also known as isoprenoids, are a large class of natural products consisting of isoprene (C5) units. There are two biosynthetic pathways, the mevalonate pathway and the non-mevalonate pathway or the MEP/DOXP pathway, for the terpenoid building blocks: isopentenyl diphosphate (IPP) and dimethylallyl diphosphate (DMAPP). The action of prenyltransferases then generates higher-order building blocks: geranyl diphosphate (GPP), farsenyl diphosphate (FPP), and geranylgeranyl diphosphate (GGPP), which are the precursors of monoterpenoids (C10), sesquiterpenoids (C15), and diterpenoids (C20), respectively. Condensation of these building blocks gives rise to the precursors of sterols (C30) and carotenoids (C40). The MEP/DOXP pathway is absent in higher animals and fungi, but in green plants, the MEP/DOXP and mevalonate pathways co-exist in separate cellular compartments. The MEP/DOXP pathway, operating in the plastids, is responsible for the formation of essential oil monoterpenes and linalyl acetate, some sesquiterpenes, diterpenes, and carotenoids and phytol. However, the mevalonate pathway is absent in this organism.

PW122252

Pw122252 View Pathway
drug action

Piroxicam Action Action Pathway

Homo sapiens
Piroxicam is a nonsteroidal oxicam derivative with anti-inflammatory, antipyretic and analgesic properties. As a non-selective, nonsteroidal anti-inflammatory drug (NSAID), piroxicam binds and chelates both isoforms of cyclooxygenases (COX1 and COX2), thereby stalling phospholipase A2 activity and conversion of arachidonic acid into prostaglandin precursors at the rate limiting cyclooxygenase enzyme step. This results in inhibition of prostaglandin biosynthesis. As a second, independent effect, piroxicam inhibits the activation of neutrophils thereby contributing to its overall anti-inflammatory effects. Piroxicam will be transported via Solute carrier family 22 member 6, Solute carrier family 22 member 8, Solute carrier family 22 member 11 and Solute carrier organic anion transporter family member 2B1 into cell. After get into cell, piroxicam will inhibit the Prostaglandin G/H synthase 2 and Prostaglandin G/H synthase 1's function; so that Prostaglandin G2 couldn't be transferred into Prostaglandin H2.

PW122243

Pw122243 View Pathway
disease

Aspartylglucosaminuria

Homo sapiens
Aspartylglucosaminuria (AGU) is an inherited disease that is characterized by a decline in mental functioning, accompanied by an increase in skin, bone and joint issues. The disease is caused by a defect in an enzyme known as aspartylglucosaminidase (normally present in the liver and brain as well as other tissues). This enzyme plays a significant role in our bodies because it aids in breaking down certain sugars (for example, oligosaccharides) that are attached to specific proteins (for example, glycoproteins). Aspartylglucosaminuria itself is characterized as a lysosomal disease because it does deal with inadequate activity in an enzyme's function. Aspartylglucosaminidase functions to break down glycoproteins. These proteins are most abundant in the tissues of the body and in the surfaces of major organs, such as the liver, spleen, thyroid and nerves. When glycoproteins are not broken down, aspartylglucosaminidase backs up in the lysosomes along with other substances. This backup causes progressive damage to the tissues and organs. Aspartylglucosaminuria is a genetic condition that is inherited from both parents. The AGU patient is born with two copies of the mutated AGA gene. One copy comes from the mother’s egg and the other copy comes from the father’s sperm. In order to develop aspartylglucosaminuria, the individual must inherit changes in both of his AGU genes (autonomic recessive inheritance). When a person receives one changed form of the gene AGU from one of the parents, the individual is then classified as a carrier [Wikipedia].

PW122242

Pw122242 View Pathway
disease

Sialidosis Type I

Homo sapiens
Sialidosis is a severe inherited disorder that affects many organs and tissues, including the nervous system. This disorder is divided into two types, which are distinguished by the age at which symptoms appear and the severity of features. Sialidosis type I is the less severe form of this condition. People with this condition typically develop signs and symptoms of sialidosis in their teens or twenties. Characteristic features may include sudden involuntary muscle contractions (myoclonus), distinctive red spots (cherry-red macules) in the eyes, and sometimes additional neurological findings. Sialidosis type I is caused by mutations in the NEU1 gene. Individuals with sialidosis type I have mutations that result in some functional NEU1 enzyme. The condition is inherited in an autosomal recessive pattern. It does not affect intelligence or life expectancy. There is no specific treatment for sialidosis. Management should be multidisciplinary and directed at supportive care and symptomatic relief. Overall health maintenance should be a priority, with seizure control as necessary. Myoclonic seizures often respond poorly to treatment with anticonvulsant medications

PW122234

Pw122234 View Pathway
metabolic

Reaction Enzyme and Element Collection Test

Homo sapiens
Any protein multimer that is not the default errors. Element collections displayed as labels will error.

PW122233

Pw122233 View Pathway
protein

LPS and Citrate Signaling and Inflammation

Rattus norvegicus
Citrate is an important substrate in cellular energy metabolism, which is produced by mitochondria and used in Krebs cycle or released into cytoplasm through a specific mitochondrial carrier, CIC. In the cytosol, citrate and its derivatives, acetyl-CoA and oxaloacetate, are used in normal and pathological processes. Apart from the classical role as metabolic regulator, citrate is also involved in inflammation, cancer, insulin secretion, histone acetylation, neurological disorders and non-alcoholic fatty lever disease.

PW122232

Pw122232 View Pathway
protein

Ion Channel and Phorbal Esters Signaling Pathway

Rattus norvegicus
Molecules transmitting signals into cells often act through receptors in the plasma membrane that stimulate production of second messengers. When activated by a plasma membrane receptor, the enzyme phospholipase C (PLCg) hydrolyzes the membrane lipid phosphatidylinositol (PIP2) into the second messengers diacylglycerol (DAG) and IP3. IP3 releases calcium from intracellular stores into the cytoplasm where calcium alters many cellular activities, including activating protein kinase C. DAG also activates protein kinase C. Biologists often study signaling by artificially manipulating pathways using molecules like ionomycin and phorbol esters as research tools. Ionomycin is a molecule that carries calcium through the plasma membrane to increase the calcium concentration in the cytoplasm and activate protein kinase C without activating phospholipase C. Phorbol esters are molecules that mimic the action of DAG in the activation of protein kinase C, and were originally identified as tumor-promoting agents. The combination of ionomycin and phorbol esters is often used experimentally to study the effect of calcium and DAG signaling in cellular responses like T cell activation.

PW122231

Pw122231 View Pathway
protein

g-Secretase Mediated ErbB4 Signalling Pathway

Rattus norvegicus
The HER4/erbB4 receptor tyrosine kinase is a member of the EGF1 receptor family. HER4 is a receptor for the neuregulins (NRGs), a family of growth and differentiation factors. HER4 can also bind and be activated by heparin-binding EGF growth factor, betacellulin, and epiregulin, members of the EGF family which, unlike the NRGs, are also ligands for the EGF receptor. HER4 mRNA is expressed in several tissues such as heart, brain, kidney, and skeletal muscle, suggesting that this receptor is involved in the development and maintenance of a variety of organs and cell types. It is likely that the control of expression and function of HER4 is important in normal development as well as in disease.

PW122230

Pw122230 View Pathway
protein

G-Protein Signaling Through Tubby Proteins

Rattus norvegicus
The Tubby protein has been implicated as a transcription regulator. Tubby functions in signal transduction from heterotrimeric GTP-binding protein through GPCR (G-Protein Coupled Receptors). Tubby is transported from the plasma membrane to the nucleus through G-AlphaQ activation. Tubby localizes to the plasma membrane by binding PIP2 (Phosphatidylinositol-4, 5-Bisphosphate), a phospholipid that is highly enriched in the plasma membrane, through its carboxyl terminal “Tubby domain". Receptor-mediated activation of G-AlphaQ releases Tubby from the plasma membrane through the action of PLC-Beta (Phospholipase-C-Beta), triggering translocation of Tubby to the cell nucleus and with the release of second messenger IP3 (Inositol 1,4,5-Trisphosphate). In the nucleus, it binds to DNA and regulates transcription.