The class of chemicals known as NF-M activators consists of compounds that influence the protein through pathways involving cyclic adenosine monophosphate (cAMP) or cyclic guanosine monophosphate (cGMP). Notable activators in this class include Forskolin, Rolipram, and others, which target these cyclic nucleotide pathways, leading to the activation of protein kinase A (PKA) or protein kinase G (PKG). The activation of these kinases can result in the phosphorylation of NF-M, thereby influencing its function. Understanding how these chemicals modulate NF-M provides valuable insights into potential strategies for enhancing cellular processes dependent on proper cytoskeletal organization and dynamics. Forskolin, a diterpene found in the Indian coleus plant, activates adenylyl cyclase, leading to an increase in intracellular cAMP levels. Elevated cAMP levels, in turn, activate PKA. Activated PKA can phosphorylate NF-M, influencing its interactions within the cytoskeleton and impacting cellular processes dependent on NF-M function.
Rolipram, a phosphodiesterase 4 (PDE4) inhibitor, increases intracellular cAMP levels by preventing its degradation. Similar to Forskolin, the elevated cAMP activates PKA, leading to the phosphorylation of NF-M. The modulation of NF-M through the cAMP-PKA pathway showcases the intricate ways in which these activators can influence cytoskeletal dynamics. Other activators within this class likely follow similar pathways involving cAMP or cGMP to influence NF-M. By understanding the mechanisms through which these chemicals activate NF-M, researchers gain valuable insights into potential strategies for enhancing cellular processes that rely on proper cytoskeletal organization. In summary, the class of NF-M activators, including Forskolin, Rolipram, and others, operates through pathways involving cAMP or cGMP, ultimately leading to the activation of PKA or PKG and subsequent phosphorylation of NF-M. These activators provide valuable tools for researchers seeking to modulate cytoskeletal dynamics and enhance cellular processes dependent on proper NF-M function. The insights gained from studying the impact of these chemicals contribute to a deeper understanding of the regulatory mechanisms governing the cytoskeleton and its role in cellular function.
| 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 | $78.00 $153.00 $740.00 $1413.00 $2091.00 | 73 | |
Forskolin activates NF-M by increasing intracellular cAMP levels. Acting through adenylate cyclase, forskolin stimulates cAMP production, leading to the activation of PKA. PKA, in turn, modulates NF-M through phosphorylation events, promoting its involvement in cellular processes dependent on cytoskeletal organization and dynamics. | ||||||
Rolipram | 61413-54-5 | sc-3563 sc-3563A | 5 mg 50 mg | $77.00 $216.00 | 18 | |
Rolipram activates NF-M by inhibiting phosphodiesterase 4 (PDE4). PDE4 normally degrades cAMP, and by blocking its activity, rolipram enhances cAMP levels. Elevated cAMP activates PKA, which can phosphorylate NF-M, promoting its engagement in cellular processes related to cytoskeletal organization and dynamics. | ||||||
Sp-cAMPS | 93602-66-5 | sc-201571 | 1 mg | $97.00 | 3 | |
Sp-cAMPS activates NF-M by serving as a cell-permeable cAMP analog. It directly elevates intracellular cAMP levels, leading to the activation of PKA. PKA, in turn, phosphorylates NF-M, modulating its function in cellular processes dependent on cytoskeletal organization and dynamics. The direct mimicry of cAMP by Sp-cAMPS provides a targeted approach for NF-M activation. | ||||||
Milrinone | 78415-72-2 | sc-201193 sc-201193A | 10 mg 50 mg | $165.00 $697.00 | 7 | |
Milrinone activates NF-M by inhibiting phosphodiesterase 3 (PDE3). PDE3 normally degrades cAMP, and by blocking its activity, milrinone enhances cAMP levels. Elevated cAMP activates PKA, which can phosphorylate NF-M, promoting its engagement in cellular processes related to cytoskeletal organization and dynamics. | ||||||
Cilostazol | 73963-72-1 | sc-201182 sc-201182A | 10 mg 50 mg | $109.00 $322.00 | 3 | |
Cilostazol activates NF-M by inhibiting phosphodiesterase 3 (PDE3). PDE3 normally degrades cAMP, and by blocking its activity, cilostazol enhances cAMP levels. Elevated cAMP activates PKA, which can phosphorylate NF-M, promoting its engagement in cellular processes related to cytoskeletal organization and dynamics. | ||||||
8-Bromo-cAMP | 76939-46-3 | sc-201564 sc-201564A | 10 mg 50 mg | $126.00 $328.00 | 30 | |
8-Bromo-cAMP activates NF-M by serving as a cell-permeable cAMP analog. It directly elevates intracellular cAMP levels, leading to the activation of PKA. PKA, in turn, phosphorylates NF-M, modulating its function in cellular processes dependent on cytoskeletal organization and dynamics. The direct mimicry of cAMP by 8-Bromo-cAMP provides a targeted approach for NF-M activation. | ||||||
Zaprinast (M&B 22948) | 37762-06-4 | sc-201206 sc-201206A | 25 mg 100 mg | $105.00 $250.00 | 8 | |
Zaprinast activates NF-M by inhibiting phosphodiesterase 5 (PDE5). PDE5 normally degrades cGMP, and by blocking its activity, zaprinast enhances cGMP levels. Elevated cGMP activates PKG, which can phosphorylate NF-M, promoting its engagement in cellular processes related to cytoskeletal organization and dynamics. | ||||||
IBMX | 28822-58-4 | sc-201188 sc-201188B sc-201188A | 200 mg 500 mg 1 g | $260.00 $350.00 $500.00 | 34 | |
IBMX activates NF-M by inhibiting various phosphodiesterases, leading to increased cAMP and cGMP levels. The elevated levels of both cAMP and cGMP activate PKA and PKG, respectively, which can phosphorylate NF-M. This dual activation provides a synergistic approach to modulating NF-M and influencing cellular processes dependent on cytoskeletal organization and dynamics. | ||||||