Andy Hudmon
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View article: K<sup>+</sup> currents in ventricular cardiomyocytes of p.N98S-calmodulin mutant mice
K<sup>+</sup> currents in ventricular cardiomyocytes of p.N98S-calmodulin mutant mice Open
Despite in vitro and in silico evidence implicating cardiac K + channel dysregulation in LQTS associated with missense mutations in genes-encoding calmodulin, their effects on native cardiac K + currents are unknown. Using a knock-in mouse…
View article: Substrate selectivity of the PRDM9 lysine methyltransferase domain
Substrate selectivity of the PRDM9 lysine methyltransferase domain Open
Lysine methylation is a dynamic, post-translational mark that regulates the function of histone and non-histone proteins. Many of the enzymes that mediate lysine methylation, known as lysine methyltransferases (KMTs), were originally ident…
View article: CaMKII Inhibition Attenuates Distinct Gain-of-Function Effects Produced by Mutant Nav1.6 Channels and Reduces Neuronal Excitability
CaMKII Inhibition Attenuates Distinct Gain-of-Function Effects Produced by Mutant Nav1.6 Channels and Reduces Neuronal Excitability Open
Aberrant Nav1.6 activity can induce hyperexcitability associated with epilepsy. Gain-of-function mutations in the SCN8A gene encoding Nav1.6 are linked to epilepsy development; however, the molecular mechanisms mediating these changes are …
View article: Distinctive Properties and Powerful Neuromodulation of Nav1.6 Sodium Channels Regulates Neuronal Excitability
Distinctive Properties and Powerful Neuromodulation of Nav1.6 Sodium Channels Regulates Neuronal Excitability Open
Voltage-gated sodium channels (Navs) are critical determinants of cellular excitability. These ion channels exist as large heteromultimeric structures and their activity is tightly controlled. In neurons, the isoform Nav1.6 is highly enric…
View article: Neurohormonal Regulation of I <sub>Ks</sub> in Heart Failure: Implications for Ventricular Arrhythmogenesis and Sudden Cardiac Death
Neurohormonal Regulation of I <sub>Ks</sub> in Heart Failure: Implications for Ventricular Arrhythmogenesis and Sudden Cardiac Death Open
Heart failure (HF) results in sustained alterations in neurohormonal signaling, including enhanced signaling through the sympathetic nervous system and renin‐angiotensin‐aldosterone system pathways. While enhanced sympathetic nervous syste…
View article: CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability
CaMKII enhances voltage-gated sodium channel Nav1.6 activity and neuronal excitability Open
Nav1.6 is the primary voltage-gated sodium channel isoform expressed in mature axon initial segments and nodes, making it critical for initiation and propagation of neuronal impulses. Thus, Nav1.6 modulation and dysfunction may have profou…
View article: Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na<sub>v</sub>1.5
Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na<sub>v</sub>1.5 Open
The cardiac voltage-gated sodium channel Na v 1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Loss-of-function mutations in its gene SCN5A are linked to cardiac arrhythmias such as Brugada Syndrome (BrS…
View article: CaMKII Nav16 MS Scaffold Files
CaMKII Nav16 MS Scaffold Files Open
This folder contains Scaffold files for each run, which includes all five conditions (a detailed description of each condition can be found below in Methods).The following runs and conditions are labeled accordingly:530181 and 181= Naive53…
View article: CaMKII Nav16 MS Raw Files_Naive
CaMKII Nav16 MS Raw Files_Naive Open
Files in this folder contain raw mass spectrometry data to examine Nav1.6 phosphorylation under naive conditions. A detailed description of methods can be found below.MethodsCaMKII phosphorylation sites on Nav1.6 were examined with mass sp…
View article: CaMKII Nav16 MS Raw Files_CaMKII Inhibition
CaMKII Nav16 MS Raw Files_CaMKII Inhibition Open
Files in this folder contain raw mass spectrometry data to examine Nav1.6 phosphorylation following CaMKII inhibition with the inhibitors KN93 and tatCN21. A detailed description of methods can be found below.MethodsCaMKII phosphorylation …
View article: CaMKII Nav16 MS Raw Files_Inhibitor Controls
CaMKII Nav16 MS Raw Files_Inhibitor Controls Open
Files in this folder contain raw mass spectrometry data to examine Nav1.6 phosphorylation following treatment with CaMKII inhibitor controls KN92 and tatCN21Ala. A detailed description of methods can be found below.MethodsCaMKII phosphoryl…
View article: CaMKII Nav16 MS Raw Files_Ionomycin
CaMKII Nav16 MS Raw Files_Ionomycin Open
Files in this folder contain raw mass spectrometry data to examine Nav1.6 phosphorylation following ionomycin treatment to promote Ca2+-dependent activation of endogenous CaMKII. A detailed description of methods can be found below.Methods…
View article: Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na<sub>v</sub>1.5
Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na<sub>v</sub>1.5 Open
The cardiac voltage-gated sodium channel Nav1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Loss-of-function mutations in its gene SCN5A are linked to cardiac arrhythmias such as Brugada Syndrome (BrS).…
View article: CaMKII Nav16 MS Raw Files_Preautophosphorylated aCaMKII
CaMKII Nav16 MS Raw Files_Preautophosphorylated aCaMKII Open
Files in this folder contain raw mass spectrometry data to examine Nav1.6 phosphorylation following treatment with recombinant autophosphorylated aCaMKII in vitro. A detailed description of methods can be found below.MethodsCaMKII phosphor…
View article: Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na <sub>v</sub> 1.5
Calmodulin binds to the N-terminal domain of the cardiac sodium channel Na <sub>v</sub> 1.5 Open
The cardiac voltage-gated sodium channel Nav1.5 conducts the rapid inward sodium current crucial for cardiomyocyte excitability. Loss-of-function mutations in its gene SCN5A are linked to cardiac arrhythmias such as Brugada Syndrome (BrS).…
View article: Assemblies of calcium/calmodulin-dependent kinase II with actin and their dynamic regulation by calmodulin in dendritic spines
Assemblies of calcium/calmodulin-dependent kinase II with actin and their dynamic regulation by calmodulin in dendritic spines Open
Significance The structural dynamics of the dendritic synapse, arising from the remodeling of actin cytoskeletons, has been widely associated with memory and cognition. The remodeling is regulated by intracellular Ca 2+ levels. Under low C…
View article: Disruption of nNOS–NOS1AP protein–protein interactions suppresses neuropathic pain in mice
Disruption of nNOS–NOS1AP protein–protein interactions suppresses neuropathic pain in mice Open
Elevated N -methyl- d -aspartate receptor (NMDAR) activity is linked to central sensitization and chronic pain. However, NMDAR antagonists display limited therapeutic potential because of their adverse side effects. Novel approaches target…
View article: Structure‐Based Target‐Specific Screening Leads to Small‐Molecule CaMKII Inhibitors
Structure‐Based Target‐Specific Screening Leads to Small‐Molecule CaMKII Inhibitors Open
Target‐specific scoring methods are more commonly used to identify small‐molecule inhibitors among compounds docked to a target of interest. Top candidates that emerge from these methods have rarely been tested for activity and specificity…
View article: Activation State-Dependent Substrate Gating in Ca<sup>2+</sup>/Calmodulin-Dependent Protein Kinase II
Activation State-Dependent Substrate Gating in Ca<sup>2+</sup>/Calmodulin-Dependent Protein Kinase II Open
Calcium/calmodulin-dependent protein kinase II (CaMKII) is highly concentrated in the brain where its activation by the Ca 2+ sensor CaM, multivalent structure, and complex autoregulatory features make it an ideal translator of Ca 2+ signa…
View article: Constitutive regulation of the glutamate/aspartate transporter <scp>EAAT</scp>1 by Calcium‐Calmodulin‐Dependent Protein Kinase II
Constitutive regulation of the glutamate/aspartate transporter <span>EAAT</span>1 by Calcium‐Calmodulin‐Dependent Protein Kinase II Open
Glutamate clearance by astrocytes is an essential part of normal excitatory neurotransmission. Failure to adapt or maintain low levels of glutamate in the central nervous system is associated with multiple acute and chronic neurodegenerati…