Pathways

Rac1 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.

Rac1 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.

Rac1 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.

Racepinephrine is a bronchodilator used to treat asthma. It can be found under the brand name Asthmanefrin and is orally inhaled to act on both alpha and beta adrenergic receptors. This drug has a rapid onset and short duration and acts as a smooth muscle relaxant and constrictor in different tissues. It is a beta-2 adrenergic receptor agonist which allows for the activation of adenylyl cyclase to relax the smooth muscle of the lungs, and it is also an alpha-1 adrenergic receptor agonist which causes smooth muscle constriction of arterioles. Constricting the pre capillary arterioles reduces the hydrostatic pressure and consequently bronchial mucosal edema. Racepinephrine is a racemic mixture consisting of d-Epinephrine and l-Epinephrine enantiomers. Epinephrine is a non-selective α- and β-adrenergic receptor agonist. Epinephrine also activates alpha 1A adrenergic receptors in blood vessels. Alpha 1A adrenergic receptor is coupled to Gq signaling pathway, therefore, activation of alpha 1A receptors leads to activation of protein kinase C and opening of IP3 receptors on the endoplasmic reticulum which increases intracellular calcium. Calcium is necessary for muscle contraction; thus, administration of epinephrine minimizes the vasodilation and increased the vascular permeability that occurs during anaphylaxis. Side effects of using racepinephrine may include blurred vision, chest pain, and difficulty speaking.

Racepinephrine is a bronchodilator used to treat asthma. It can be found under the brand name Asthmanefrin and is orally inhaled to act on both alpha and beta adrenergic receptors. This drug has a rapid onset and short duration and acts as a smooth muscle relaxant and constrictor in different tissues. It is a beta-2 adrenergic receptor agonist which allows for the activation of adenylyl cyclase to relax the smooth muscle of the lungs, and it is also an alpha-1 adrenergic receptor agonist which causes smooth muscle constriction of arterioles. Constricting the pre capillary arterioles reduces the hydrostatic pressure and consequently bronchial mucosal edema. Racepinephrine is a racemic mixture consisting of d-Epinephrine and l-Epinephrine enantiomers. Epinephrine is a non-selective α- and β-adrenergic receptor agonist. It is a bronchodilator used in the temporary relief of mild symptoms of intermittent asthma including wheezing, tightness of chest and shortness of breath. It is an active ingredient in oral inhalation over-the-counter products as racepinephrine hydrochloride. Once racepinephrine is administered and it binds to the beta-2 adrenergic receptor, the G protein signalling cascade begins. The alpha and beta/gamma subunits of the G protein separate and GDP is replaced with GTP on the alpha subunit. This alpha subunit then activates adenylyl cyclase which converts ATP to cAMP. cAMP then activates protein kinase A (PKA) which in turn phosphorylates targets and inhibits MLCK through decreased calcium levels causing muscle relaxation. PKA can phosphorylate certain Gq-coupled receptors as well as phospholipase C (PLC) and thereby inhibit G protein-coupled receptor (GPCR) -PLC-mediated phosphoinositide (PI) generation, and thus calcium flux. PKA phosphorylates the inositol 1,4,5-trisphosphate (IP3) receptor to reduce its affinity for IP3 and further limit calcium mobilization. PKA phosphorylates myosin light chain kinase (MLCK) and decreases its affinity to calcium calmodulin, thus reducing activity and myosin light chain (MLC) phosphorylation. PKA also phosphorylates KCa++ channels in ASM, increasing their open-state probability (and therefore K+ efflux) and promoting hyperpolarization. Since myosine light chain kinase is not activated, Serine/threonine-protein phosphatase continues to dephosphorylate myosin LC-P, and more cannot be synthesized so myosin remains unbound from actin causing muscle relaxation. This relaxation of the smooth muscles in the lungs causes the bronchial airways to relax which causes bronchodialation, making it easier to breathe. Side effects of using racepinephrine may include blurred vision, chest pain, and difficulty speaking.