Leonard K. Kaczmarek

Protein kinase modulation of a neuronal cation channel requires protein-protein interactions mediated by an Src homology 3 domain.

Endogenous parathyroid hormone-related protein functions as a neuroprotective agent.

HSV-1 helper virus 5dl1.2 suppresses sodium currents in amplicon-transduced neurons.

Localization of the Slack potassium channel in the rat central nervous system.

Prolonged activation of Ca2+-activated K+ current contributes to the long-lasting refractory period of Aplysia bag cell neurons.

Modulation of the kv3.1b potassium channel isoform adjusts the fidelity of the firing pattern of auditory neurons.

BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development.

Modulation of mitochondrial function by endogenous Zn2+ pools.

Compensatory anion currents in Kv1.3 channel-deficient thymocytes.

Modulation of synaptic transmission by the BCL-2 family protein BCL-xL.

How to make a relationship last: release sites with different levels of commitment.

Functional specialization of male and female vocal motoneurons.

Slick (Slo2.1), a rapidly-gating sodium-activated potassium channel inhibited by ATP.

The voltage-gated potassium channel Kv1.3 regulates peripheral insulin sensitivity.

Loss of Kv3.1 tonotopicity and alterations in cAMP response element-binding protein signaling in central auditory neurons of hearing impaired mice.

Act locally: new ways of regulating voltage-gated ion channels.

Activation of a calcium entry pathway by sodium pyrithione in the bag cell neurons of Aplysia.

Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminals.

The appearance of a protein kinase A-regulated splice isoform of slo is associated with the maturation of neurons that control reproductive behavior.

Aminoglycosides block the Kv3.1 potassium channel and reduce the ability of inferior colliculus neurons to fire at high frequencies.

Exposure to hypoxia rapidly induces mitochondrial channel activity within a living synapse.

Requirement of voltage-gated calcium channel beta4 subunit for T lymphocyte functions.

Localization of the Na+-activated K+ channel Slick in the rat central nervous system.

For K+ channels, Na+ is the new Ca2+.

Regulation of the timing of MNTB neurons by short-term and long-term modulation of potassium channels.

Actions of BAX on mitochondrial channel activity and on synaptic transmission.

Association/dissociation of a channel-kinase complex underlies state-dependent modulation.

Acoustic environment determines phosphorylation state of the Kv3.1 potassium channel in auditory neurons.

Retraction.

Policing the ball: a new potassium channel subunit determines inactivation rate.

Modulation of Kv3.1b potassium channel phosphorylation in auditory neurons by conventional and novel protein kinase C isozymes.

Opposite regulation of Slick and Slack K+ channels by neuromodulators.

Pharmacological activation and inhibition of Slack (Slo2.2) channels.

A store-operated Ca(2+) influx pathway in the bag cell neurons of Aplysia.

Non-conducting functions of voltage-gated ion channels.

Functional analysis of a novel potassium channel (KCNA1) mutation in hereditary myokymia.

Slack and Slick K(Na) channels regulate the accuracy of timing of auditory neurons.

Sodium-dependent potassium channels of a Slack-like subtype contribute to the slow afterhyperpolarization in lamprey spinal neurons.

Comparative effects of sodium pyrithione evoked intracellular calcium elevation in rodent and primate ventral horn motor neurons.

Bcl-xL inhibitor ABT-737 reveals a dual role for Bcl-xL in synaptic transmission.

Repetitive firing triggers clustering of Kv2.1 potassium channels in Aplysia neurons.

PKC-induced intracellular trafficking of Ca(V)2 precedes its rapid recruitment to the plasma membrane.

Protein kinase C modulates inactivation of Kv3.3 channels.

Amino-termini isoforms of the Slack K+ channel, regulated by alternative promoters, differentially modulate rhythmic firing and adaptation.

Na+-mediated coupling between AMPA receptors and KNa channels shapes synaptic transmission.

The N-terminal domain of Slack determines the formation and trafficking of Slick/Slack heteromeric sodium-activated potassium channels.

Use of optical biosensors to detect modulation of Slack potassium channels by G protein-coupled receptors.

Kv1.3 is the exclusive voltage-gated K+ channel of platelets and megakaryocytes: roles in membrane potential, Ca2+ signalling and platelet count.

The slack sodium-activated potassium channel provides a major outward current in olfactory neurons of Kv1.3-/- super-smeller mice.

Controlling auditory excitability: the benefits of a cultured environment.

Fragile X mental retardation protein controls gating of the sodium-activated potassium channel Slack.

Localization of Kv1.3 channels in presynaptic terminals of brainstem auditory neurons.

A less flexible BK channel opens more easily.

Fragile X mental retardation protein is required for rapid experience-dependent regulation of the potassium channel Kv3.1b.

Potassium channel modulation and auditory processing.

Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potential.

Gradients and modulation of K(+) channels optimize temporal accuracy in networks of auditory neurons.

De novo gain-of-function KCNT1 channel mutations cause malignant migrating partial seizures of infancy.

Regulation of neuronal excitability by interaction of fragile X mental retardation protein with slack potassium channels.

An evolutionarily conserved mode of modulation of Shaw-like K⁺ channels.

A sodium-activated potassium channel supports high-frequency firing and reduces energetic costs during rapid modulations of action potential amplitude.

Expression of Kv1.3 potassium channels regulates density of cortical interneurons.

Slack, Slick and Sodium-Activated Potassium Channels.

The contribution of TWIK-1 channels to astrocyte K(+) current is limited by retention in intracellular compartments.

Clinical whole-genome sequencing in severe early-onset epilepsy reveals new genes and improves molecular diagnosis.