IndraLab

Statements


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"Gene deletion of Kv4.2 (Kcnd2) in mice eliminates most of the A-type K+ current in hippocampal and cortical neurons [XREF_BIBR - XREF_BIBR], and increases back propagation of the action potential from the axon to the somatodendritic region [XREF_BIBR]."

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"Kv4.2 could mediate somatodendritic A-type potassium currents, played a vital role in the regulation of neuronal excitability and dendritic signal integration in the hippocampus ( Chen et al., 2006 )."

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"Kv4.2 mediates the majority of A-type potassium currents in dorsal horn and an increase in A-type currents would be predicted to reduce overall neuronal excitability (Hu et al., 2006)."

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"QT prolongation in Nfx mice was explained by a significant decrease in the fast transient outward potassium (K + ) current (I tof ), caused by the downregulation of K + channel 4.2 subunit (Kv4.2) expression."

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"Kv4.2 channel contributes to the cardiac transient outward potassium current (Ito1) being the major contributor in repolarizing the cardiac action potential; in neurons, Kv4.2 is abundant in dendrites[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"The TRPV4 activity-mediated elevation of Kv4.2 and KCHIP is thought to lead to an increase in the rapidly inactivating potassium current in hippocampal pyramidal neurons, which likely contributes to hyperexcitability during the early stage of epileptogenesis (Xu, et al., 2022)."

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"We reported recently that the K+ channel Kv4.2 subunit underlies A-type K+ currents in the spinal cord dorsal horn and is modulated by the ERK signaling pathway."