VMAC Activators
The volume-regulated anion channel (VMAC) engage a specific cellular signaling pathway that results in the phosphorylation and activation of VMAC. These chemicals can initiate their effects by various mechanisms, yet they converge on a common molecular endpoint. Forskolin, for example, directly stimulates adenylyl cyclase, the enzyme responsible for converting ATP into cyclic AMP (cAMP). The increase in cAMP levels subsequently activates protein kinase A (PKA), which then phosphorylates VMAC, thereby increasing its channel activity. Similarly, isoproterenol, epinephrine, and dobutamine, all beta-adrenergic agonists, bind to their respective receptors on the cell surface. This receptor-ligand interaction triggers a G protein-coupled response that leads to the activation of adenylyl cyclase, resulting in elevated cAMP levels. Once activated, PKA proceeds to phosphorylate VMAC.
Another set of chemicals operates by inhibiting the degradation of cAMP, thereby indirectly raising its intracellular concentration. IBMX, a non-selective inhibitor, along with more selective inhibitors such as rolipram, cilostamide, anagrelide, and milrinone, target various phosphodiesterases (PDEs), which are enzymes that normally break down cAMP. Inhibition of PDEs by these chemicals results in sustained cAMP levels, activating PKA and culminating in VMAC phosphorylation. Glucagon, by binding to its receptor, activates adenylyl cyclase, echoing the cAMP-PKA pathway leading to VMAC activation. Prostaglandin E1 (PGE1) also raises cAMP levels via its own receptor-mediated process, thus promoting PKA activation and subsequent VMAC phosphorylation. Terbutaline, a beta-2 adrenergic agonist, similarly induces adenylyl cyclase activity through its interaction with G protein-coupled receptors, following the same cAMP and PKA-dependent activation of VMAC. Overall, these chemical activators, through their distinct interactions with cellular components, ensure the phosphorylation and activation of VMAC by leveraging the pivotal role of cAMP and PKA within the cell.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Forskolin | 66575-29-9 | sc-3562 sc-3562A sc-3562B sc-3562C sc-3562D | 5 mg 50 mg 1 g 2 g 5 g | $76.00 $150.00 $725.00 $1385.00 $2050.00 | 73 | |
Forskolin activates adenylyl cyclase, leading to an increase in cyclic AMP (cAMP) levels. Elevated cAMP activates PKA (protein kinase A), which can phosphorylate and thereby activate VMAC by increasing its channel activity. | ||||||
Isoproterenol Hydrochloride | 51-30-9 | sc-202188 sc-202188A | 100 mg 500 mg | $27.00 $37.00 | 5 | |
Isoproterenol, a beta-adrenergic agonist, binds to beta-receptors triggering a G protein-coupled response that activates adenylyl cyclase. The subsequent rise in cAMP levels activates PKA, which then phosphorylates and activates VMAC. | ||||||
(−)-Epinephrine | 51-43-4 | sc-205674 sc-205674A sc-205674B sc-205674C sc-205674D | 1 g 5 g 10 g 100 g 1 kg | $40.00 $102.00 $197.00 $1739.00 $16325.00 | ||
Epinephrine engages beta-adrenergic receptors, initiating a signaling cascade that results in cAMP production. The cAMP activates PKA, which can then phosphorylate and enhance VMAC channel activity. | ||||||
IBMX | 28822-58-4 | sc-201188 sc-201188B sc-201188A | 200 mg 500 mg 1 g | $159.00 $315.00 $598.00 | 34 | |
IBMX is a non-selective inhibitor of phosphodiesterases, enzymes that degrade cAMP. By preventing cAMP degradation, IBMX indirectly elevates cAMP levels, which activates PKA, leading to the phosphorylation and activation of VMAC. | ||||||
Rolipram | 61413-54-5 | sc-3563 sc-3563A | 5 mg 50 mg | $75.00 $212.00 | 18 | |
Rolipram selectively inhibits PDE4, a phosphodiesterase that degrades cAMP. The inhibition of PDE4 increases cAMP levels, thereby activating PKA, which in turn can phosphorylate and activate VMAC channels. | ||||||
Cilostamide (OPC 3689) | 68550-75-4 | sc-201180 sc-201180A | 5 mg 25 mg | $90.00 $350.00 | 16 | |
Cilostamide selectively inhibits PDE3, another phosphodiesterase involved in cAMP degradation. By blocking PDE3, cilostamide increases cAMP levels, which activates PKA, leading to phosphorylation and activation of VMAC. | ||||||
Anagrelide | 68475-42-3 | sc-491875 | 25 mg | $147.00 | ||
Anagrelide inhibits PDE3, leading to an accumulation of cAMP. This elevation in cAMP activates PKA, which is known to phosphorylate and thereby activate VMAC. | ||||||
Milrinone | 78415-72-2 | sc-201193 sc-201193A | 10 mg 50 mg | $162.00 $683.00 | 7 | |
Milrinone is a selective PDE3 inhibitor. By inhibiting PDE3, it increases intracellular cAMP levels, resulting in PKA activation. PKA then phosphorylates and activates the VMAC channel. | ||||||
Dobutamine | 34368-04-2 | sc-507555 | 100 mg | $295.00 | ||
Dobutamine, through its agonistic effect on beta-1 adrenergic receptors, leads to adenylyl cyclase activation and increased cAMP. This triggers PKA activation, which can phosphorylate and activate VMAC. | ||||||
PGE1 (Prostaglandin E1) | 745-65-3 | sc-201223 sc-201223A | 1 mg 10 mg | $30.00 $142.00 | 16 | |
PGE1 binds to its E-prostanoid receptor, which can trigger an increase in cAMP levels via adenylyl cyclase activation. The resulting PKA activation leads to phosphorylation and subsequent activation of VMAC. | ||||||