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Kv channel interacting protein 2

KChIP2, Kv channel-interacting protein 2
This gene encodes a member of the family of voltage-gated potassium (Kv) channel-interacting proteins (KCNIPs), which belongs to the recoverin branch of the EF-hand superfamily. Members of the KCNIP family are small calcium binding proteins. They all have EF-hand-like domains, and differ from each other in the N-terminus. They are integral subunit components of native Kv4 channel complexes. They may regulate A-type currents, and hence neuronal excitability, in response to changes in intracellular calcium. Multiple alternatively spliced transcript variants encoding distinct isoforms have been identified from this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Kv1.4, Kv4.3, Kv4.2, FasT, CAN
Papers on KChIP2
Coexpression of auxiliary subunits KChIP and DPPL in potassium channel Kv4-positive nociceptors and pain-modulating spinal interneurons.
New
Tsaur et al., Taipei, Taiwan. In J Comp Neurol, Apr 2016
In this study we mapped the protein distribution of KChIP1, KChIP2, KChIP3, DPP6, and DPP10 in adult rat dorsal root ganglion (DRG) and spinal cord by immunohistochemistry.
Reductions in the cardiac transient outward K+ current Ito caused by chronic β-adrenergic receptor stimulation are partly rescued by inhibition of nuclear factor kappaB.
New
Backx et al., United States. In J Biol Chem, Feb 2016
Ito,f channels are formed by the co-assembly of the pore-forming α-subunits, Kv4.2 and Kv4.3, together with the accessory β-subunit KChIP2.
Myocardial KChIP2 Expression in Guinea Pig Resolves an Expanded Electrophysiologic Role.
New
Deschênes et al., Cleveland, United States. In Plos One, Dec 2015
Studies have indicated that the K+ channel interacting protein 2 (KChIP2), originally identified as an auxiliary subunit for the channel Kv4, a component of the transient outward K+ channel (Ito), is a Ca2+ binding protein whose regulatory function does not appear restricted to Kv4 modulation.
Preservation of cardiac function by prolonged action potentials in mice deficient of KChIP2.
New
Thomsen et al., Copenhagen, Denmark. In Am J Physiol Heart Circ Physiol, Sep 2015
Potassium channel-interacting protein 2 (KChIP2) is reduced in heart failure and interacts under physiological conditions with both Kv4 to conduct the fast-recovering transient outward K(+) current (Ito,f) and with CaV1.2 to mediate the inward L-type Ca(2+) current (ICa,L).
Two novel Brugada syndrome-associated mutations increase KV4.3 membrane expression and function.
New
Xu et al., Suzhou, China. In Int J Mol Med, Jul 2015
The human cardiac fast transient outward K+ channel is composed of the KV4.3 α subunit encoded by KCND3 and the K+ channel‑interacting protein 2 (KChIP2) β subunit, and determines the early repolarization of the action potential (AP).
Repolarization Alternans and Ventricular Arrhythmia in a Repaired Tetralogy of Fallot Animal Model.
Lin et al., Taipei, Taiwan. In J Am Heart Assoc, 2014
Expressions of Kv4.3 and KChIP2 decreased in the rTOF group.
Kv4.3-Encoded Fast Transient Outward Current Is Presented in Kv4.2 Knockout Mouse Cardiomyocytes.
Backx et al., Toronto, Canada. In Plos One, 2014
Human cardiac Ito,f appears to be encoded by the Kv4.3 pore-forming α-subunit plus the auxiliary KChIP2 β-subunit while mouse cardiac Ito,f requires Kv4.2 and Kv4.3 α-subunits plus KChIP2.
Effects of C-reactive protein on K(+) channel interaction protein 2 in cardiomyocytes.
Chen et al., Guangzhou, China. In Am J Transl Res, 2014
K(+) channel interaction protein 2 (KChIP2) is a necessary subunit for the formation of transient outward potassium current (Ito.f)
Circadian rhythms govern cardiac repolarization and arrhythmogenesis.
Impact
Jain et al., Cleveland, United States. In Nature, 2012
Klf15 transcriptionally controls rhythmic expression of Kv channel-interacting protein 2 (KChIP2), a critical subunit required for generating the transient outward potassium current.
Multistep ion channel remodeling and lethal arrhythmia precede heart failure in a mouse model of inherited dilated cardiomyopathy.
GeneRIF
Kurebayashi et al., Tokyo, Japan. In Plos One, 2011
The combined down-regulation of Kv4.2, Kv1.5 and KChIP2 prior to the onset of HF may play an important role in the premature sudden death in this DCM model.
The "structurally minimal" isoform KChIP2d modulates recovery of K(v)4.3 N-terminal deletion mutant Δ2-39.
Review
GeneRIF
Campbell et al., Buffalo, United States. In Channels (austin), 2011
The "structurally minimal" isoform KChIP2d modulates recovery of K(v)4.3 N-terminal deletion mutant Delta2-39.
Nuclear factor kappaB downregulates the transient outward potassium current I(to,f) through control of KChIP2 expression.
GeneRIF
Backx et al., Toronto, Canada. In Circ Res, 2011
Nuclear factor kappaB downregulates the transient outward potassium current I(to,f) through control of KChIP2 expression.
Co-assembly of Kv4 {alpha} subunits with K+ channel-interacting protein 2 stabilizes protein expression and promotes surface retention of channel complexes.
GeneRIF
Nerbonne et al., Saint Louis, United States. In J Biol Chem, 2010
KChIP2 differentially regulates total and cell surface Kv4.2 protein expression and Kv4 current densities.
Effect of the I(to) activator NS5806 on cloned K(V)4 channels depends on the accessory protein KChIP2.
GeneRIF
Calloe et al., Copenhagen, Denmark. In Br J Pharmacol, 2010
The I(to) activator NS5806 modified Kv4.3/KChIP2 gating in several ways that inhibit current.
Impact of ancillary subunits on ventricular repolarization.
Review
Roepke et al., New York City, United States. In J Electrocardiol, 2007
Some ancillary subunits may exhibit varied expression to shape spatial Kv current variation, for example, KChIP2 and the epicardial-endocardial I(to) current density gradient.
Transient outward potassium current, 'Ito', phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms.
Review
Campbell et al., New York City, United States. In J Physiol, 2005
We also review the possible functional implications of (i) ancillary subunits that regulate Kv1.4 and Kv4.2/4.3 (Kvbeta subunits, DPPs), (ii) KChIP2 isoforms, (iii) spider toxin-mediated block of Kv4.2/4.3 (Heteropoda toxins, phrixotoxins), and (iv) potential mechanisms of modulation of I(to,fast) and I(to,slow) by cellular redox state, [Ca(2)(+)](i) and kinase-mediated phosphorylation.
A role for calsenilin and related proteins in multiple aspects of neuronal function.
Review
Buxbaum, New York City, United States. In Biochem Biophys Res Commun, 2004
For example, KChIP1, KChIP2, and CALP can all bind presenilins and can all modulate A-type potassium channels.
The long QT interval is not only inherited but is also linked to cardiac hypertrophy.
Review
Milliez et al., Paris, France. In J Mol Med (berl), 2003
Such an altered current density is caused by a diminished expression of the genes encoding either the ion channel subunits or regulatory proteins, such as KChIP2.
A defect in the Kv channel-interacting protein 2 (KChIP2) gene leads to a complete loss of I(to) and confers susceptibility to ventricular tachycardia.
Impact
Chien et al., San Diego, United States. In Cell, 2002
KChIP2, a gene encoding three auxiliary subunits of Kv4.2 and Kv4.3, is preferentially expressed in the adult heart, and its expression is downregulated in cardiac hypertrophy.
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