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Pathways

Showing 41 - 50 of 35939 pathways
SMPDB ID Pathway Chemical Compounds Proteins

SMP00168

Pw000082 View Pathway
disease

AICA-Ribosiduria

Homo sapiens
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.

SMP00055

Pw000001 View Pathway
metabolic

Alanine Metabolism

Homo sapiens
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.

SMP00095

Pw000137 View Pathway
drug action

Alendronate Action Pathway

Homo sapiens
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.

SMP00413

Pw000419 View Pathway
drug action

Alfentanil Action Pathway

Homo sapiens
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.

SMP59689

Pw060631 View Pathway
drug action

Alimemazine H1-Antihistamine Action

Homo sapiens
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.

SMP00169

Pw000180 View Pathway
disease

Alkaptonuria

Homo sapiens
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.

SMP00018

Pw000006 View Pathway
metabolic

Alpha Linolenic Acid and Linoleic Acid Metabolism

Homo sapiens
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).

SMP00297

Pw000365 View Pathway
drug action

Alprenolol Action Pathway

Homo sapiens
Alprenolol non-selectively blocks beta-1 adrenergic receptors mainly in the heart, inhibiting the effects of epinephrine and norepinephrine resulting in a decrease in heart rate and blood pressure. By binding beta-2 receptors in the juxtaglomerular apparatus, alprenolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production and therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively.

SMP00280

Pw000302 View Pathway
drug action

Alteplase Action Pathway

Homo sapiens
Alteplase binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin. It also produces limited conversion of plasminogen in the absence of fibrin.

SMP00685

Pw000662 View Pathway
drug action

Alvimopan Action Pathway

Homo sapiens
Alvimopan is a peripherally acting μ opioid antagonist. It competitively binds to mu-opioid receptor in the gastrointestinal tract. Unlike methylnaltrexone (another peripherally acting mu-receptor antagonist) that bears a quaternary amine, alvimopan owes its selectivity for peripheral receptors to its kinetics. Alvimopan binds to peripheral mu-receptors with a Ki of 0.2 ng/mL and dissociates slower than most other ligands.
Showing 41 - 50 of 35939 pathways