calmodulin

Calmodulin-Dependent Protein Kinase II (290-309) is a potent CaMK antagonist with an IC50 of 52 nM for inhibiting Ca2+/calmodulin-dependent protein kinase II.

Calmodulin-Dependent Protein Kinase II 290-309 acetate is an effective antagonist of Ca2+/calmodulin-dependent protein kinase II (IC50 = 52 nM).

Calmodulin Binding Peptide 1, a potent CaM-binding peptide with picomolar (pM) affinity, originates from smooth muscle myosin light-chain kinase (MLCK peptide). It effectively blocks inositol trisphosphate (IP3)-induced calcium (Ca2+) release [1].

Calmodulin-Dependent Protein Kinase II (281-309) is a synthetic peptide phosphorylatable at Thr286 by PKC, inhibiting CaM kinase II with an IC50 of 80 nM.

CALP2 acetate is an antagonist of calmodulin showing high affinity for binding to the CaM EF-hand/Ca2+-binding site with a Kd of 7.9 µM. CALP2 acetate potently inhibits of adhesion and degranulation. CALP2 acetate is also a strong activator of alveolar macrophages. CALP2 acetate inhibits CaM-dependent phosphodiesterase activity and increases intracellular Ca2+ concentrations.

CALP1 acetate is a calmodulin (CaM) agonist (Kd of 88 µM) that binds to the CaM EF-hand/Ca2+-binding site. CALP1 blocks calcium influx and apoptosis (IC50 of 44.78 µM) by inhibiting the open of calcium channel. CALP1 blocks glutamate receptor channels and blocks a store-operated nonselective cation channel. CALP1 activates CaM-dependent phosphodiesterase activity.

Calmodulin-Dependent Protein Kinase II (290-309) acetate is a potent CaMK antagonist with an IC50 of 52 nM for the inhibition of Ca2+/calmodulin-dependent protein kinase II [1].

Calmodulin-Dependent Protein Kinase Substrate Analog, a synthetic peptide substrate, is activated by Ca2+ and calmodulin (CaM). It serves as a substrate for protein kinases, leveraging a dependency on Ca2+ and CaM for its function [1].

Calmodulin Dependent Protein Kinase Substrate is a synthetic peptide that interacts specifically with calmodulin-dependent protein kinases (CaMK) and requires calcium ions (Ca 2+) and calmodulin (CaM) for activation. It is utilized in studies involving protein kinase activity [1].

Myristoylated Calmodulin Kinase IINtide (Myr-CaMKIINtide) serves as a selective and noncompetitive inhibitor of CaMKII [1].

Autocamtide-2-related inhibitory peptide is a potent and highly specific inhibitor of CaMKII, with an IC50 of 40 nM.

Autocamtide 2 TFA is a highly selective peptide substrate of calcium/calmodulin-dependent protein kinase II (CaMKII). Autocamtide 2 TFA can be used in the CaMKII activity assay.

CALP3 acetate is a potent Ca2+ channel blocker that activates EF hand motifs of Ca2+-binding proteins. CALP3 acetate can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin (CaM), Ca2+ channels and pumps.

Camstatin acetate binds calmodulin and inhibits neuronal nitric oxide synthase. Camstatin acetate is a functionally active 25-residue fragment of the single calmodulin-binding IQ motif of PEP-19.

Camstatin TFA, a 25-residue fragment derived from the IQ motif of PEP-19, effectively binds to calmodulin and inhibits neuronal nitric oxide (NO) synthase, demonstrating its functional activity [1].

Syntide 2 (TFA), a substrate peptide for Ca2+- and calmodulin (CaM)-dependent protein kinase II (CaMKII), selectively inhibits the gibberellin (GA) response without affecting constitutive and abscisic acid-regulated events [1].

CALP2 TFA, a potent calmodulin (CaM) antagonist with a dissociation constant (Kd) of 7.9 µM, exhibits high affinity for the CaM EF-hand/Ca2+-binding site. This compound effectively inhibits CaM-dependent phosphodiesterase activity and elevates intracellular Ca2+ concentrations. Furthermore, it significantly hinders adhesion and degranulation, while also acting as a robust activator of alveolar macrophages [1] [2] [3] [4].

CALP1 TFA, a calmodulin (CaM) agonist with a dissociation constant (Kd) of 88 µM, selectively binds to the CaM EF-hand/Ca2+-binding site, inhibiting calcium channel opening. This action blocks calcium influx and apoptosis with an IC50 of 44.78 µM, modulates glutamate receptor channel activity, and impedes a store-operated nonselective cation channel. Additionally, CALP1 TFA enhances CaM-dependent phosphodiesterase activity, denoting its multifaceted role in modulating cellular calcium dynamics [1] [2] [3] [4].

Calcineurin Autoinhibitory Peptide TFA is a selective inhibitor of Ca2+/calmodulin-dependent protein phosphatase (calcineurin), exhibiting an inhibitory concentration (IC50) of approximately 10 μM. This compound has been shown to protect neurons from excitatory neuronal death [1] [2].

Myelin Basic Protein (MHP4-14) TFA, a synthetic peptide comprising residues 4-14 of myelin basic protein, serves as a highly selective substrate for protein kinase C (PKC) with a K_m of 7 μM. It is not phosphorylated by cyclic AMP-dependent protein kinase, casein kinases I and II, Ca^2+/calmodulin-dependent protein kinase II, or phosphorylase kinase, making it an ideal candidate for protein kinase C assays in crude tissue extracts, ensuring minimal background interference [1] [2].

Neurogranin (48-76), mouse, is a peptide comprising residues 48-76 of Neurogranin, a post-synaptically exclusive calmodulin-binding protein that mediates NMDAR-driven synaptic plasticity by regulating the calcium-calmodulin (Ca2+-CaM) pathway [1].

Autocamtide-3, a selective substrate for CaMKII (Ca2+/calmodulin-dependent kinase II) (CaMK), comprises a 13-amino-acid peptide featuring Thr287 [1].

Myristoylated AC3-I is a biologically active peptide and a myristoylated variant of the Autocamtide-3-Derived Inhibitory Peptide (AC3-I). It acts as a highly specific inhibitor of Calmodulin-Dependent Protein Kinase II (CaMKII) with enhanced resistance to proteolysis. This compound is a derivative of Autocamtide-3, where the Thr-9 phosphorylation site is replaced by Ala.

SK-MLCK M13 is a biologically active peptide representing the calmodulin (CaM)-binding domain of CaM target proteins, where CaM is a ubiquitous Ca2+ binding protein.