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Showing 41 - 50 of 48688 pathways
SMPDB ID Pathway Chemical Compounds Proteins

SMP0000516

Pw000492 View Pathway
Disease

Adrenoleukodystrophy, X-Linked

X-linked adrenoleukodystrophy is a genetic disorder that occurs primarily in males. It mainly affects the nervous system and the adrenal glands, which are small glands located on top of each kidney. In this disorder, the fatty covering (myelin) that insulates nerves in the brain and spinal cord is prone to deterioration (demyelination), which reduces the ability of the nerves to relay information to the brain. In addition, damage to the outer layer of the adrenal glands (adrenal cortex) causes a shortage of certain hormones (adrenocortical insufficiency). Adrenocortical insufficiency may cause weakness, weight loss, skin changes, vomiting, and coma. There are three distinct types of X-linked adrenoleukodystrophy: a childhood cerebral form, an adrenomyeloneuropathy type, and a form called Addison disease only.

SMP0063771

Pw064763 View Pathway
Protein

Ahr Signal Transduction Pathway

The AhR signal transduction pathway is present in a diverse range of species, tissues, and cell types, and to date, the majority of genes which respond to AhR ligands have been shown to utilize the AHR-DRE-dependent mechanism of action. The aryl hydrocarbon receptor (AHR) is a soluble, ligand-dependent transcription factor that mediates many of the biological and toxicological actions of a structurally diverse group of natural and synthetic hydrophobic chemicals, including the environmental contaminant 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD). Following ligand binding, the cytosolic ligand-AHR complex undergoes transformation during which it translocates into the nucleus and dissociates from two molecules of HSP90 (a heat shock protein of 90 kDa) and XAP2. Following its association with at least one nuclear factor, the AHR nuclear translocator (ARNT) protein, the AHR complex is converted into its high affinity DNA-binding form. The binding of the transformed heteromeric ligand-AHR-ARNT complex to its specific DNA recognition site, the dioxin responsive element (DRE), leads to chromatin and nucleosome disruption, increased promoter accessibility, and increased rates of transcription of an adjacent gene.
  • 2,3,7,8-tetrachlorodibenzo-p-dioxin

SMP0000168

Pw000082 View Pathway
Disease

AICA-Ribosiduria

AICA-ribosiduria is a metabolic disease caused by a defect in final steps of purine de novo biosynthesis. This defect is caused by a mutation in the ATIC which codes for bifunctional purine biosynthesis protein PURH. A deficiency in this enzyme results in accumulation of 5-aminoimidazole-4-carboxamide in urine. Symptoms include mental retardation, epilepsy, dysmorphic features, and congenital blindness.

SMP0000055

Pw000001 View Pathway
Metabolic

Alanine Metabolism

Alanine is most commonly produced by the reductive amination of pyruvate via alanine transaminase. This reversible reaction involves the interconversion of alanine and pyruvate, coupled to the interconversion of alpha-ketoglutarate (2-oxoglutarate) and glutamate. Because transamination reactions are readily reversible and pyruvate is widespread, alanine can be easily formed in most tissues. Another route to the production of alanine is through the enzyme called alanine-glyoxylate transaminase. This reaction involves the interconversion of alanine and pyruvate, coupled to the interconversion of glyoxylate and glycine. Once synthesized, alanine can be coupled to alanyl tRNA via alanyl-tRNA synthetase and used by the body in protein synthesis. Alanine constitutes about 8% of human proteins. Under fasting conditions, alanine, derived from protein breakdown, can be converted to pyruvate and used to synthesize glucose via gluconeogenesis in the liver. Alternately, alanine, after conversion to pyruvate, can be fully oxidized via the TCA cycle in other tissues.

SMP0062881

Pw063838 View Pathway
Drug Action

Alcaftadine H1-Antihistamine Action

Alcaftadine is a second-generation piperidine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.

SMP0000095

Pw000137 View Pathway
Drug Action

Alendronate Action Pathway

Nitrogen-containing bisphosphonates (such as pamidronate, alendronate, risedronate, ibandronate and zoledronate) appear to act as analogues of isoprenoid diphosphate lipids, thereby inhibiting FPP synthase, an enzyme in the mevalonate pathway. Inhibition of this enzyme in osteoclasts prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are essential for the post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins. This activity inhibits osteoclast activity and reduces bone resorption and turnover. In postmenopausal women, it reduces the elevated rate of bone turnover, leading to, on average, a net gain in bone mass.

SMP0000413

Pw000419 View Pathway
Drug Action

Alfentanil Action Pathway

Alfentanil exerts its analgesic by acting on the mu-opioid receptor of sensory neurons. Binding to the mu-opioid receptor activates associated G(i) proteins. These subsequently act to inhibit adenylate cyclase, reducing the level of intracellular cAMP. G(i) also activates potassium channels and inactivates calcium channels causing the neuron to hyperpolarize. The end result is decreased nerve conduction and reduced neurotransmitter release, which blocks the perception of pain signals.

SMP0059689

Pw060631 View Pathway
Drug Action

Alimemazine H1-Antihistamine Action

Alimemazine (trimeprazine) is a first-generation phenothiazine H1-antihistamine. H1-antihistamines interfere with the agonist action of histamine at the H1 receptor and are administered to attenuate inflammatory process in order to treat conditions such as allergic rhinitis, allergic conjunctivitis, and urticaria. Reducing the activity of the NF-κB immune response transcription factor through the phospholipase C and the phosphatidylinositol (PIP2) signalling pathways also decreases antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Furthermore, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release. First-generation antihistamines readily cross the blood-brain barrier and cause sedation and other adverse central nervous system (CNS) effects (e.g. nervousness and insomnia). Second-generation antihistamines are more selective for H1-receptors of the peripheral nervous system (PNS) and do not cross the blood-brain barrier. Consequently, these newer drugs elicit fewer adverse drug reactions.

SMP0000169

Pw000180 View Pathway
Disease

Alkaptonuria

Alkaptonuria (Homogentisic acid oxidase deficiency) is an autosomal recessive disease caused by a mutation in the HGD gene which codes for homogentisate 1,2-dioxygenase. A mutation in this enzyme results in accumulation of homogentisic acid in urine. Symptoms, which present in adulthood, include arthritis, black or brown urine, and urolithiasis. Treatment includes a low-protein diet with vitamin C.

SMP0000018

Pw000006 View Pathway
Metabolic

Alpha Linolenic Acid and Linoleic Acid Metabolism

Linoleic acid is a member of essential fatty acids called omega-6 fatty acids. It is an essential dietary requirement for all mammals. The other group of essential fatty acids is the omega-3 fatty acids (i.e. alpha-linolenic acid). The first step in the metabolism of linoleic acid (LA) is performed by Δ-6-desaturase, which converts LA into gamma-linolenic acid (GLA). GLA is converted to dihomo-gamma-linolenic acid (DGLA), which in turn is converted to arachidonic acid (AA). One of the possible fates of AA is to be transformed into a group of metabolites called eicosanoids. There are three types of eicosanoids are prostaglandins, thromboxanes, and leukotrienes. α-Linolenic acid (ALA), is an essential 18:3n or omega-3 fatty acid. It is considered essential because it cannot be produced entirely within the body and must be acquired through diet. Once acquired, α-Linolenic acid can be “regenerated” endogenously by the cleavage of phospholipids into their constituent fatty acids by phospholipase A2. The resulting fatty acid can then be converted to stearidonic acid through the action of fatty acid desaturase 2. α-Linolenic acid is primarily used by the body in the synthesis of Eicosapentaenoic acid (EPA; 20:5, n−3) and docosahexaenoic acid (DHA; 22:6, n−3), two fatty acids that play a vital role in many metabolic and cell signaling processes. These fatty acids are synthesized via fatty acid desaturase 2, fatty acid desaturase 1 and several elongase enzymes (Q9GZR5) in the liver. α-Linolenic acid is also in the regulation of lipid metabolism by activation of the peroxisome proliferators-activated receptor alpha (PPARa).
Showing 41 - 50 of 48688 pathways