Figures & data
Corticosteroids cross the cell membrane and bind to receptors that are stabilized by regulatory proteins. The glucocorticoid receptor (GR) then crosses the nuclear membrane, binds to a response element and modulates transcription. β2-adrenergic receptor agonists bind to the β2-adrenergic receptor and mediate smooth muscle relaxation via PKA and regulate various genes via the transcription factor CREB. The cysteinyl leukotrienes in LTC4, LTD4 and LTE4,and dihydroxy leukotriene LTB4 are synthesized from arachidonic acid in a series of steps via an enzymatic cascade as depicted. Following translocation into the extracellular space, cysteinyl leukotrienes activate their cognate GPCRs (including CYSLTR1) and mediate a variety of effects such as smooth muscle contraction.
AC: Adenylcyclase; ALOX5: Arachidonate 5-lipoxygenase; β2AR: β2-adrenergic receptor; cAMP: Cyclic adenosine monophosphate; cysLTR: Cysteinyl Leukotriene receptor; CREB: Cyclic AMP response element-binding; DAG: Diacyl glycerol; GC: Glucocorticoid; GPCR: G-protein-coupled receptor; GR: Glucocorticoid receptor; IP3: Inositol-triphosphate; LTA4: Leukotriene A4; LTB4: Leukotriene B4; LTC4: Leukotriene C4; LTD4: Leukotriene D4; LTE4: Leukotriene E4; LTC4S: Leukotriene C4 synthase; LTA4H: Leukotriene A4 hydrolase; LTSI: Leukotriene synthesis inhibitor; LTRA: Leukotriene receptor antagonist; PKA: Cyclic-AMP dependent protein kinase; PKC: Protein kinase C; PLC: Phospholipase C.
![Figure 1. Targets of current asthma medication.Corticosteroids cross the cell membrane and bind to receptors that are stabilized by regulatory proteins. The glucocorticoid receptor (GR) then crosses the nuclear membrane, binds to a response element and modulates transcription. β2-adrenergic receptor agonists bind to the β2-adrenergic receptor and mediate smooth muscle relaxation via PKA and regulate various genes via the transcription factor CREB. The cysteinyl leukotrienes in Figure 1 LTC4, LTD4 and LTE4,and dihydroxy leukotriene LTB4 are synthesized from arachidonic acid in a series of steps via an enzymatic cascade as depicted. Following translocation into the extracellular space, cysteinyl leukotrienes activate their cognate GPCRs (including CYSLTR1) and mediate a variety of effects such as smooth muscle contraction.AC: Adenylcyclase; ALOX5: Arachidonate 5-lipoxygenase; β2AR: β2-adrenergic receptor; cAMP: Cyclic adenosine monophosphate; cysLTR: Cysteinyl Leukotriene receptor; CREB: Cyclic AMP response element-binding; DAG: Diacyl glycerol; GC: Glucocorticoid; GPCR: G-protein-coupled receptor; GR: Glucocorticoid receptor; IP3: Inositol-triphosphate; LTA4: Leukotriene A4; LTB4: Leukotriene B4; LTC4: Leukotriene C4; LTD4: Leukotriene D4; LTE4: Leukotriene E4; LTC4S: Leukotriene C4 synthase; LTA4H: Leukotriene A4 hydrolase; LTSI: Leukotriene synthesis inhibitor; LTRA: Leukotriene receptor antagonist; PKA: Cyclic-AMP dependent protein kinase; PKC: Protein kinase C; PLC: Phospholipase C.](/cms/asset/b0d1aed3-819e-432f-b0bd-f74c0852c677/ierx_a_11219267_f0001_b.jpg)