PathWhiz

PathWhiz ID	Pathway	Meta Data
PW176796 View Pathway	drug action Clozapine H1-Antihistamine Immune Response Action Pathway Homo sapiens Clozapine is an H1-antihistamine although it is mostly used as an antipsychotic. 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. H1-antihistamines act on H1 receptors in T-cells to inhibit the immune response, in blood vessels to constrict dilated blood vessels, and in smooth muscles of lungs and intestines to relax those muscles. 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. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Carin Li Created On: December 19, 2023 at 15:07 Last Updated: December 19, 2023 at 15:07
PW126857 View Pathway	drug action Clozapine Serotonin Antagonist Action Pathway Homo sapiens Clozapine is an antipsychotic drug used in treatment resistant schizophrenia and to decrease suicide risk in schizophrenic patients. Clozapine is available as oral tablets. Clozapine is part of a group of drugs known as second-generation antipsychotics or atypical antipsychotics. Antipsychotic drugs are vital in treating the core symptoms of schizophrenia: hallucinations and delusions As an atypical antipsychotic, clozapine acts an antagonist to both dopamine and serotonin receptors. Clozapine's antipsychotic action is likely mediated through a combination of antagonistic effects at D2 receptors in the mesolimbic pathway and 5-HT2A receptors in the frontal cortex. D2 antagonism relieves positive symptoms while 5-HT2A antagonism alleviates negative symptoms. Side effects of clozapine include agranulocytosis, myocarditis, orthostatic hypotension, sedation, tachycardia, sexual dysfunction, urinary retention, constipation. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Karxena Harford Created On: April 20, 2022 at 22:21 Last Updated: April 20, 2022 at 22:21
PW012919 View Pathway	metabolic CMP-3-Deoxy-D-Manno-Octulosonate (CMP-Kdo) Biosynthesis Arabidopsis thaliana CMP-3-deoxy-D-manno-octulosonate (CMP-Kdo) biosynthesis is a pathway that occurs in the cytosol by which D-ribulose 5-phosphate becomes CMP-3-deoxy-D-manno-octulosonate (CMP-Kdo). Kdo is a component in the plant cell wall, specifically of pectic polysaccharide rhamnogalacturonan II. First, arabinose-5-phosphate isomerase catalyzes the conversion of D-ribulose 5-phosphate to D-arabinose 5-phosphate. Second, D-arabinose 5-phosphate is spontaneously converted into D-arabinofuranose 5-phosphate. Third, 3-deoxy-8-phosphooctulonate synthase converts D-arabinofuranose 5-phosphate into 3-deoxy-D-manno-octulosonate 8-phosphate (KDO-8P). This enzme is a homotetramer. Fourth, the predicted enzyme 3-deoxy-manno-octulosonate-8-phosphatase (coloured orange in the image) is theorized to catalyze the conversion of 3-deoxy-D-manno-octulosonate 8-phosphate (KDO-8P) into 3-deoxy-D-manno-2-octulosonate (Kdo). The last reaction is localized to the mitochondria outer membrane whereby 3-deoxy-manno-octulosonate cytidylyltransferase (coloured dark green in the image) catalyzes the conversion of 3-deoxy-D-manno-2-octulosonate (Kdo) into CMP-3-deoxy-D-manno-octulosonate (CMP-Kdo). This enzyme requires a magnesium ion as a cofactor. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Carin Li Created On: February 24, 2017 at 16:00 Last Updated: February 24, 2017 at 16:00
PW000562 View Pathway	protein Coagulation Homo sapiens Blood coagulation can be initiated by either an extrinsic or an intrinsic pathway, resulting in a cascade of serine protease activation that ultimately leads to the formation of thrombin, which converts soluble fibrinogen to an insoluble fibrin clot. The extrinsic, or tissue factor, pathway is initiated upon vascular injury, when the membrane-bound protein tissue factor (TF) comes into contact with factor VII or VIIa in plasma. The TF-VIIa complex is the strongest known activator of the coagulation cascade, and converts factors IX and X to IXa and Xa, respectively. Factors VII, IX, and X are vitamin-K-dependent proteins produced in the liver. In the intrinsic, or contact, pathway, injury exposes collagen to the bloodstream where is binds to factor XII and activates it to XIIa. Factor XIIa converts prekallikrein to kallikrein and factor XI to XIa. Both the extrinsic and intrinsic pathways result in the activation of factor IX to IXa, which forms the 'tenase' complex with factor VIIIa, calcium and phospholipids. This complex converts factor X to Xa and is important in haemostasis. Factor Xa complexes with factor Va (which functions as a non-enzymatic cofactor), calcium and a phospholipid membrane surface to form what is called the prothrombinase complex, which converts prothrombin to thrombin. Thrombin converts soluble fibrinogen to insoluble fibrin polymer, which is stabilized by cross-linking by coagulation factor XIIIa. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: WishartLab Created On: August 30, 2013 at 12:38 Last Updated: August 30, 2013 at 12:38
PW120591 View Pathway	protein Coagulation Mus musculus Blood coagulation can be initiated by either an extrinsic or an intrinsic pathway, resulting in a cascade of serine protease activation that ultimately leads to the formation of thrombin, which converts soluble fibrinogen to an insoluble fibrin clot. The extrinsic, or tissue factor, pathway is initiated upon vascular injury, when the membrane-bound protein tissue factor (TF) comes into contact with factor VII or VIIa in plasma. The TF-VIIa complex is the strongest known activator of the coagulation cascade, and converts factors IX and X to IXa and Xa, respectively. Factors VII, IX, and X are vitamin-K-dependent proteins produced in the liver. In the intrinsic, or contact, pathway, injury exposes collagen to the bloodstream where is binds to factor XII and activates it to XIIa. Factor XIIa converts prekallikrein to kallikrein and factor XI to XIa. Both the extrinsic and intrinsic pathways result in the activation of factor IX to IXa, which forms the 'tenase' complex with factor VIIIa, calcium and phospholipids. This complex converts factor X to Xa and is important in haemostasis. Factor Xa complexes with factor Va (which functions as a non-enzymatic cofactor), calcium and a phospholipid membrane surface to form what is called the prothrombinase complex, which converts prothrombin to thrombin. Thrombin converts soluble fibrinogen to insoluble fibrin polymer, which is stabilized by cross-linking by coagulation factor XIIIa. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 14:03 Last Updated: September 10, 2018 at 14:03
PW120617 View Pathway	protein Coagulation Rattus norvegicus Blood coagulation can be initiated by either an extrinsic or an intrinsic pathway, resulting in a cascade of serine protease activation that ultimately leads to the formation of thrombin, which converts soluble fibrinogen to an insoluble fibrin clot. The extrinsic, or tissue factor, pathway is initiated upon vascular injury, when the membrane-bound protein tissue factor (TF) comes into contact with factor VII or VIIa in plasma. The TF-VIIa complex is the strongest known activator of the coagulation cascade, and converts factors IX and X to IXa and Xa, respectively. Factors VII, IX, and X are vitamin-K-dependent proteins produced in the liver. In the intrinsic, or contact, pathway, injury exposes collagen to the bloodstream where is binds to factor XII and activates it to XIIa. Factor XIIa converts prekallikrein to kallikrein and factor XI to XIa. Both the extrinsic and intrinsic pathways result in the activation of factor IX to IXa, which forms the 'tenase' complex with factor VIIIa, calcium and phospholipids. This complex converts factor X to Xa and is important in haemostasis. Factor Xa complexes with factor Va (which functions as a non-enzymatic cofactor), calcium and a phospholipid membrane surface to form what is called the prothrombinase complex, which converts prothrombin to thrombin. Thrombin converts soluble fibrinogen to insoluble fibrin polymer, which is stabilized by cross-linking by coagulation factor XIIIa. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 14:08 Last Updated: September 10, 2018 at 14:08
PW120600 View Pathway	protein Coagulation Bos taurus Blood coagulation can be initiated by either an extrinsic or an intrinsic pathway, resulting in a cascade of serine protease activation that ultimately leads to the formation of thrombin, which converts soluble fibrinogen to an insoluble fibrin clot. The extrinsic, or tissue factor, pathway is initiated upon vascular injury, when the membrane-bound protein tissue factor (TF) comes into contact with factor VII or VIIa in plasma. The TF-VIIa complex is the strongest known activator of the coagulation cascade, and converts factors IX and X to IXa and Xa, respectively. Factors VII, IX, and X are vitamin-K-dependent proteins produced in the liver. In the intrinsic, or contact, pathway, injury exposes collagen to the bloodstream where is binds to factor XII and activates it to XIIa. Factor XIIa converts prekallikrein to kallikrein and factor XI to XIa. Both the extrinsic and intrinsic pathways result in the activation of factor IX to IXa, which forms the 'tenase' complex with factor VIIIa, calcium and phospholipids. This complex converts factor X to Xa and is important in haemostasis. Factor Xa complexes with factor Va (which functions as a non-enzymatic cofactor), calcium and a phospholipid membrane surface to form what is called the prothrombinase complex, which converts prothrombin to thrombin. Thrombin converts soluble fibrinogen to insoluble fibrin polymer, which is stabilized by cross-linking by coagulation factor XIIIa. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Ana Marcu Created On: September 10, 2018 at 14:05 Last Updated: September 10, 2018 at 14:05
PW124002 View Pathway	physiological Coagulation (New) Homo sapiens Coagulation of the blood can be initiation from two different pathways that both result in formation of thrombin which converts blood soluble fibrinogen into the insoluble fibrin clot at the site of injury. The intrinsic pathway is activated by trauma inside vasculature and is activated by platelets, exposed endothelium and collagen. In the liver the coagulation factors VII, IX, and X are produced there as they are vitamin K-dependent proteins. Exposed collagen from broken vessels binds to factor XII activating it to XIIa which converts prekallikrein and factor XI to kallikrein and factor XIa respectively. The extrinsic pathway is activated by the external trauma of blood escaping the vasculature system as the membrane-bound protein tissue factor (TF) is exposed to factors VII or VIIa in the plasma forming a strong activator complex. This activator complex of VIIa and TF converts factor X to the activated form. Both the intrinsic and extrinsic pathways lead to the prothrombinase complex as both pathways activate factor X, an important player in the complex. The prothrombinase complex converts prothrombin to thrombin further allowing the conversion of insoluble fibrinogen into fibrin. Fibrin at first is loose and unstable and is stabilized by coagulation factor XIIIa which cross-links them to form the fibrin clot/mesh that stops blood leaking from the vasculature system. The activated proteins are colored orange. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Kristen Yee Created On: July 20, 2020 at 17:20 Last Updated: July 20, 2020 at 17:20
PW064727 View Pathway	physiological Coagulation Cascade Homo sapiens BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Guest: Anonymous Created On: April 24, 2018 at 07:23 Last Updated: April 24, 2018 at 07:23
PW128444 View Pathway	drug action Coagulation Factor VII Human Action Pathway Homo sapiens Coagulation factor VII human is a coagulation factor also known as Balfaxar, Beriplex, Kcentra and Octaplex to treat hemophilia and Glanzmann's thrombasthenia. It is administered intravenously it acts in combination with tissue factor activating coagulation factor VIIa, which goes on to subsequently activate coagulation factor X and IX leading to blood clotting formation. It is broken down via catabolism in the body. BioPAX SVG SBGN SBML PWML All files (.zip)	Creator: Selena Created On: August 29, 2023 at 08:59 Last Updated: August 29, 2023 at 08:59