Browsing Pathways
Showing 171 -
180 of 605359 pathways
SMPDB ID | Pathway Name and Description | Pathway Class | Chemical Compounds | Proteins |
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SMP0063795View Pathway |
Rac 1 Cell Motility Signaling PathwayRac1 is signaling protein part of the Rho GTPase family it is involved in cell motility, cell growth and cytoskeletal reorganization. Rac1 activity is regulated by guanine nucleotide exchange factors (GEFs). GEFs cause the release of GDP, allowing GDP to bind and Rac1 to become activated. GTPase-activated proteins (GAPs) down regulate the activity of GEFs be stimulating the inactivation via binding of GDP to Rac1. Active Rac1 stimulates proteins (ie. Wiskott–Aldrich syndrome) leading to actin polymerization. Actin polymerization is also regulated by cofilin. PAK proteins are critical effectors to cytoskeleton reorganization. PAK1 phosphorylates and activates LIM kinase. LIM kinase then phosphorylates cofilin, inactivating it leading to reduced actin filament severing and depolymerization, therby increasing polymerized actin. Rac1 stimulates lamellipodia and filopodia formation which are involved in cell movement and sensing the environment. It is proposed that PAK1 is involved in the phosphorylation of myosin light chain affecting myosin light chain phosphorylation.
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SMP0063783View Pathway |
Phospholipase C Signaling PathwayPhospholipase C pathways is one of the major intracellular signalling pathways regulating hormones. It functions to activate inositol lipid signalling pathways causing the hydrolysis of PIP2 by PLC to IP3 and diacylglycerol to activate protein kinase C. IP3 releases calcium from the endoplasmic reticulum. PIP3 is an important regulator of AKT signaling and downstream pathways.
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SMP0000301View Pathway |
Esmolol Action PathwayEsmolol, sold as Brevibloc, is a cardioselective beta-1 receptor blocker drug. As a beta-blocker, esmolol blocks the agonistic effect of the sympathetic neurotransmitters by competing for receptor binding sites, and as it is cardioselective, it binds primarily to those in the heart. Esmolol is injected intravenously, and when it enters the heart, it binds to the beta-1 adrenergic receptor, preventing signalling. Normally, epinephrine and norepinephrine bind to the beta-1 adrenergic receptor with equal affinity and trigger a G-protein signalling cascade that result in the heart muscle contracting. When esmolol binds, it causes the rate and force of these heart contractions to be decreased, in order to help treat supraventricular tachycardia. Esmolol is rapidly metabolized in red blood cells, and once metabolized it is inactivated, giving it a short time of activity within the body.
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Drug Action
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SMP0000636View Pathway |
Venlafaxine Metabolism PathwayVenlafaxine (also named as Effexor or Elafax) is an antidepressant medication, which belongs to the class of serotonin-norepinephrine reuptake inhibitor (SNRI). Venlafaxine is well absorbed into the circulation system. Venlafaxine is also metabolized to N-desmethylvenlafaxine. The N-demethylation is catalyzed by CYP3A4 and CYP2C19. N-desmethylvenlafaxine is a weaker serotonin and norepinephrine reuptake inhibitor. Both O-desmethylvenlafaxine (as potent a serotonin-norepinephrine reuptake inhibitor) and N-desmethylvenlafaxine are further metabolized by CYP2C19, CYP2D6 and/or CYP3A4 to a minor metabolite N,O-didesmethylvenlafaxine that is further metabolized into N,N,O-tridesmethylvenlafaxine or excreted as N,O-didesmethylvenlafaxine gucuronide. Later on, O-desmethylvenlafaxine is exported without any change in chemical structure. Venlafaxine is exported via two transporters: Multidrug resistance protein 1 and ATP-binding cassette sub-family G member 2.
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SMP0000641View Pathway |
Doxepin Metabolism PathwayDoxepin is a tricyclic antidepressant (TCA) that can be used for treating major depressive disorder and sleep maintenance. Doxepin is metabolized by cytochrome P450 2C19, 1A2, 2C9, 3A4 to form N-desmethyldoxepin, and form (E)-2-hydroxydoxepin by solely cytochrome P450 2D6 in ER of liver.
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SMP0000154View Pathway |
Ramipril Action PathwayRamipril (trade name: Altace) belongs to the class of drugs known as angiotensin-converting enzyme (ACE) inhibitors and is used primarily to lower high blood pressure (hypertension). This drug can also be used in the treatment of congestive heart failure and type II diabetes. Ramipril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form ramiprilat via cleavage of its ester group by the liver. Angiotensin-converting enzyme (ACE) is a component of the body's renin–angiotensin–aldosterone system (RAAS) and cleaves inactive angiotensin I into the active vasoconstrictor angiotensin II. ACE (or kininase II) also degrades the potent vasodilator bradykinin. Consequently, ACE inhibitors decrease angiotensin II concentrations and increase bradykinin concentrations resulting in blood vessel dilation and thereby lowering blood pressure.
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SMP0000597View Pathway |
Ramipril Metabolism PathwayRamipril (trade name: Altace) belongs to the class of drugs known as angiotensin-converting enzyme (ACE) inhibitors and is used primarily to lower high blood pressure (hypertension). This drug can also be used in the treatment of congestive heart failure and type II diabetes. Ramipril is a prodrug which, following oral administration, undergoes biotransformation in vivo into its active form ramiprilat via cleavage of its ester group by the liver. Angiotensin-converting enzyme (ACE) is a component of the body's renin–angiotensin–aldosterone system (RAAS) and cleaves inactive angiotensin I into the active vasoconstrictor angiotensin II. ACE (or kininase II) also degrades the potent vasodilator bradykinin. Consequently, ACE inhibitors decrease angiotensin II concentrations and increase bradykinin concentrations resulting in blood vessel dilation and thereby lowering blood pressure.
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SMP0000616View Pathway |
Rabeprazole Metabolism PathwayRabeprazole is a drug that belongs to the anti secretory drug class. It is used as an anti-ulcer medication, and helps relieve gastric acid reflux, gastric irritation and gastric pain. It inhibits the proton pump action of ATPase, which blocks the final step of gastric acid secretion. The pathway begins in the parietal cell in the stomach, where rabeprazole and a hydrogen ion use the active metabolite in rabeprazole —rabeprazole thioether — to inhibit potassium-transporting ATPase at the secretory surface of the gastric parietal cell. Now in the gastric endothelial cell, these secretory surfaces are inhibited by rabeprazole and by G-Protein signalling cascade through somatostatin receptor type 4, which is activated by somatostatin. At the same time, potassium-transporting ATPase is activated by the G-protein signalling cascade, through histamine H2 receptor, gastrin/cholecystokinin type B receptor, and muscarinic acetylcholine receptor M3 which are activated by histamine, gastrin and acetylcholine, respectively. The potassium transporting ATPase also converts water and ATP to a phosphate molecule and ADP. Alongside the transporters, potassium is brought into the cell. Carbonic anhydrase 1 uses water and carbon dioxide to create hydrogen carbonate and a hydrogen ion, which are both transported out of the endothelial cell, into the gastric lumen. A chloride ion is transported into the gastric endothelial cell through a chloride anion exchanger and is transported out of the cell through a chloride intracellular channel protein 2, back into the gastric lumen.
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SMP0090032View Pathway |
Ion Channel and Phorbal Esters Signaling PathwayIonomycin is an ionophore, a compound that binds calcium ions reversibly, and is used to transport calcium ions across the cell’s plasma membrane, increasing cellular calcium concentration. This increased concentration activates the protein-tyrosine kinase 2-beta, which is responsible for regulation of actin in the cell’s cytoskeleton, as well as cell movement, polarization, adhesion and spreading. It is also important for B-cells and T-cells to migrate and spread.
When the P2Y purinoceptor 2 is activated on the cell surface, it activates 1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase gamma-1 (PLCG1), an enzyme that is responsible for regulating the conversion of phosphatidylinositol (PIP2) into inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DG). IP3 then activates an IP3 sensitive calcium channel, increasing the concentration of intracellular calcium. The calcium can activate protein-tyrosine kinase 2-beta, and can also activate protein kinase C. DG also works to activate protein kinase C in the cell.
Phorbal esters are compounds found in certain families of plants, and are found to promote tumor growth. As such, they are commonly used in research. In this pathway, they are shown to activate protein kinase C in the same way as calcium does, as well as mimicking the action of DG.
Phorbal esters, in conjunction with ionomycin, are used in this case to study the cellular response to DAG and calcium signalling without needing the cells to undergo other stimulation, mimicking things like T-cell activation easily.
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SMP0000261View Pathway |
Ticlopidine Action PathwayTiclopidine, marketed as Ticlid, is an antiplatelet drug that targets the P2Y12 receptor of platelets. Ticlopidine is taken orally and is a prodrug that must be metabolically activated before it can be effective. It first enters the liver and enters the endoplasmic reticulum where it is metabolized to form the active metabolite. First, it is catalyzed by cytochromes P450 2C19, 2B6 and 1A2 into 2-oxoclopidogrel. Secondly, it is processed by cytochromes P450 2B6, 2C9, 2C19, 3A4, 3A5, and serum paraoxonase/arylesterase 1 into the active metabolite of clopidogrel. The active metabolite of clopidogrel then enters the blood stream, where it binds irreversibly to the P2Y purinoreceptor 12 on the surface of platelet cells, preventing ADP from binding to and activating it. Clopidogrel prevents the activation of the Gi protein associated with the P2Y12 receptor from inactivating adenylate cyclase in the platelet, leading to a buildup of cAMP. This cAMP then activates calcium efflux pumps, preventing calcium buildup in the platelet, which would cause activation, and later, aggregation.
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Showing 171 -
180 of 65006 pathways