PathWhiz ID | Pathway | Meta Data |
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PW058500View Pathway |
drug action
Brompheniramine H1-Antihistamine ActionHomo sapiens
Brompheniramine is a first-generation alkylamine 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.
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Creator: Carin Li Created On: September 15, 2017 at 11:13 Last Updated: September 15, 2017 at 11:13 |
PW176677View Pathway |
drug action
Brompheniramine H1-Antihistamine Blood Vessel Constriction Action PathwayHomo sapiens
Brompheniramine is an 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. 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.
Allergies causes blood vessel dilation which causes swelling (edema) and fluid leakage. Brompheniramine inhibits the H1 histamine receptor on blood vessel endothelial cells. This normally activates the Gq signalling cascade which activates phospholipase C which catalyzes the production of Inositol 1,4,5-trisphosphate (IP3) and Diacylglycerol (DAG). Because of the inhibition, IP3 doesn't activate the release of calcium from the sarcoplasmic reticulum, and DAG doesn't activate the release of calcium into the cytosol of the endothelial cell. This causes a low concentration of calcium in the cytosol, and it, therefore, cannot bind to calmodulin. Calcium bound calmodulin is required for the activation of the calmodulin-binding domain of nitric oxide synthase. The inhibition of nitric oxide synthesis prevents the activation of myosin light chain phosphatase. This causes an accumulation of myosin light chain-phosphate which causes the muscle to contract and the blood vessel to constrict, decreasing the swelling and fluid leakage from the blood vessels caused by allergens.
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Creator: Ray Kruger Created On: December 19, 2023 at 13:46 Last Updated: December 19, 2023 at 13:46 |
PW176769View Pathway |
drug action
Brompheniramine H1-Antihistamine Immune Response Action PathwayHomo sapiens
Brompheniramine is an 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. 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.
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Creator: Carin Li Created On: December 19, 2023 at 15:01 Last Updated: December 19, 2023 at 15:01 |
PW146715View Pathway |
drug action
Bronopol Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 18:52 Last Updated: October 07, 2023 at 18:52 |
PW146851View Pathway |
drug action
Brown iron oxide Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 19:11 Last Updated: October 07, 2023 at 19:11 |
PW109277View Pathway |
protein
BTG Family Proteins and Cell Cycle RegulationRattus norvegicus
BTG Family Member-2 (BTG2) is endowed with antiproliferative activity. The expression of BTG2 in cycling cells induces accumulation of hypophosphorylated, growth-inhibitory forms of Retinoblastoma protein(Rb) and lead to G1 arrest through impairment of DNA synthesis. Rb is a nuclear phosphoprotein whose phosphorylation state oscillates regularly during the cell cycle. Hypophosphorylated Rb associates with members of the E2F family of transcription factors, impairing their activity and leading to a cell cycle block in G1. Conversely, the phosphorylation of Rb inactivates its growth suppression activity by freeing E2F molecules, thus enabling them to transactivate genes required for the progression of the cell into S phase and the remainder of the cell cycle. Cyclin-dependent kinases (CDKs) are the molecules responsible for Rb phosphorylation and its consequent inactivation.
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Creator: Ana Marcu Created On: August 31, 2018 at 12:48 Last Updated: August 31, 2018 at 12:48 |
PW109247View Pathway |
protein
BTG Family Proteins and Cell Cycle RegulationBos taurus
BTG Family Member-2 (BTG2) is endowed with antiproliferative activity. The expression of BTG2 in cycling cells induces accumulation of hypophosphorylated, growth-inhibitory forms of Retinoblastoma protein(Rb) and lead to G1 arrest through impairment of DNA synthesis. Rb is a nuclear phosphoprotein whose phosphorylation state oscillates regularly during the cell cycle. Hypophosphorylated Rb associates with members of the E2F family of transcription factors, impairing their activity and leading to a cell cycle block in G1. Conversely, the phosphorylation of Rb inactivates its growth suppression activity by freeing E2F molecules, thus enabling them to transactivate genes required for the progression of the cell into S phase and the remainder of the cell cycle. Cyclin-dependent kinases (CDKs) are the molecules responsible for Rb phosphorylation and its consequent inactivation.
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Creator: Ana Marcu Created On: August 31, 2018 at 12:40 Last Updated: August 31, 2018 at 12:40 |
PW064765View Pathway |
protein
BTG Family Proteins and Cell Cycle RegulationHomo sapiens
BTG Family Member-2 (BTG2) is endowed with antiproliferative activity. The expression of BTG2 in cycling cells induces accumulation of hypophosphorylated, growth-inhibitory forms of Retinoblastoma protein(Rb) and lead to G1 arrest through impairment of DNA synthesis. Rb is a nuclear phosphoprotein whose phosphorylation state oscillates regularly during the cell cycle. Hypophosphorylated Rb associates with members of the E2F family of transcription factors, impairing their activity and leading to a cell cycle block in G1. Conversely, the phosphorylation of Rb inactivates its growth suppression activity by freeing E2F molecules, thus enabling them to transactivate genes required for the progression of the cell into S phase and the remainder of the cell cycle. Cyclin-dependent kinases (CDKs) are the molecules responsible for Rb phosphorylation and its consequent inactivation.
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Creator: Jonas Patron Created On: June 14, 2018 at 09:52 Last Updated: June 14, 2018 at 09:52 |
PW109199View Pathway |
protein
BTG Family Proteins and Cell Cycle RegulationMus musculus
BTG Family Member-2 (BTG2) is endowed with antiproliferative activity. The expression of BTG2 in cycling cells induces accumulation of hypophosphorylated, growth-inhibitory forms of Retinoblastoma protein(Rb) and lead to G1 arrest through impairment of DNA synthesis. Rb is a nuclear phosphoprotein whose phosphorylation state oscillates regularly during the cell cycle. Hypophosphorylated Rb associates with members of the E2F family of transcription factors, impairing their activity and leading to a cell cycle block in G1. Conversely, the phosphorylation of Rb inactivates its growth suppression activity by freeing E2F molecules, thus enabling them to transactivate genes required for the progression of the cell into S phase and the remainder of the cell cycle. Cyclin-dependent kinases (CDKs) are the molecules responsible for Rb phosphorylation and its consequent inactivation.
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Creator: Ana Marcu Created On: August 31, 2018 at 12:31 Last Updated: August 31, 2018 at 12:31 |
PW146636View Pathway |
drug action
Bucetin Drug Metabolism Action PathwayHomo sapiens
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Creator: Ray Kruger Created On: October 07, 2023 at 18:41 Last Updated: October 07, 2023 at 18:41 |