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KCNIP2 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. Additionally we are shipping KCNIP2 Antibodies (107) and many more products for this protein.
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A novel KCNQ1 (show KCNQ1 Proteins)-G229D mutation identified in a juvenile-onset AF patient altered the IKs activity and kinetics, thereby increasing the arrhythmogenicity to AF.
mutations cause a gainoffunction of KV4.3 (show KCND3 Proteins)/KChIP2encoded channels by increasing membrane protein expression and slowing channel inactivation.
The "structurally minimal" isoform KChIP2d modulates recovery of K(v)4.3 (show KCND3 Proteins) N-terminal deletion mutant Delta2-39.
KChIP2 differentially regulates total and cell surface Kv4.2 (show KCND2 Proteins) protein expression and Kv4 (show KCNC1 Proteins) current densities.
The I(to) activator NS5806 modified Kv4.3 (show KCND3 Proteins)/KChIP2 gating in several ways that inhibit current.
The cytoplasmic accessory subunit KChIP2 also assembles with Kv4.2 (show KCND2 Proteins) to increase peak current, shift V1/2 ~5mV, slow time to peak ~10%, slow inactivation ~100%, and speed recovery from inactivation ~250% without overshoot.
N-linked glycosylation of DPP10 plays an important role in modulating Kv4.3 (show KCND3 Proteins) channel/KCHIP2 complex activities.
Down-regulated atrial KChIP2 and Kv4.3 (show KCND3 Proteins) mRNA expressions in rheumatic heart disease patients with chronic atrial fibrillation might be one of the molecular bases responsible for the down-regulation of the I(to) current density of AF.
Regulation of Kv4.3 (show KCND3 Proteins) current by KChIP2 splice variants
Analysis with chimeric proteins between KChIP2 and NCS-1 (show NCS1 Proteins) reveals that the three regions of KChIP2 are necessary and sufficient for its effective binding to Kv4.3 (show KCND3 Proteins) protein
The downregulation of repolarizing currents in heart failure is accentuated in KChIP2(-/-) mice.
Real-time RT-PCR and Western blotting revealed that Kv4.2 (show KCND2 Proteins) expression was downregulated in both BSO-treated groups, whereas KChIP2 expression was downregulated only in the H/M-Sod2 (show SOD2 Proteins)(+/-)+BSO group (P<0.05).
Development of heart failure is independent of K+ channel (show KCNC4 Proteins)-interacting protein 2 expression.
KChIP2 is essential for physiologic somatodendritic potassium current modulation and homeostatic stability.
The combined down-regulation of Kv4.2 (show KCND2 Proteins), Kv1.5 (show KCNA5 Proteins) and KChIP2 prior to the onset of HF may play an important role in the premature sudden death in this DCM model.
KChIP2 has a role in mediating regulation of CaV1.2 (show CACNA1C Proteins)
KChIP2 transcripts were highly expressed in layer IV of the cerebral cortex and in striatum and hippocampus, but expressed at low levels in cerebellum.
KChIP2 contributes to the formation of functional mouse ventricular Kv1.5 (show KCNA5 Proteins) channels
KChIP2 modulates multiple K(V) and Na(V) currents, these results suggest that KChIP2 is a multimodal regulator of cardiac ionic currents.
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.
Kv channel interacting protein 2
, A-type potassium channel modulatory protein 2
, Kv channel-interacting protein 2
, cardiac voltage-gated potassium channel modulatory subunit
, potassium channel-interacting protein 2
, Kv channel-interacting protein
, potassium channel auxiliary subunit KCHIP2