Ask about this productRelated genes to: KCNIP2 Blocking Peptide
- Gene:
- KCNIP2 NIH gene
- Name:
- potassium voltage-gated channel interacting protein 2
- Previous symbol:
- -
- Synonyms:
- KCHIP2
- Chromosome:
- 10q24.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-05-23
- Date modifiied:
- 2016-02-04
Related products to: KCNIP2 Blocking Peptide
Related articles to: KCNIP2 Blocking Peptide
- Hypertension is highly prevalent in Asian populations and represents a major cardiovascular risk factor. However, most genome-wide association studies (GWASs) and transcriptome-wide association studies (TWASs) have focused primarily on Caucasian cohorts. This study aimed to identify genetic loci and gene expression signatures associated with hypertension in an Asian population. - Source: PubMed
Publication date: 2026/07/24
Chang Sheng-NanLee Guan-WeiChen Jien-JiunWang Chih-HsienChiu Fu-ChunHuang Pang-ShuoChuang Eric YTsai Chia-Ti - This study aims to explore the molecular association between di(2-ethylhexyl)phthalate (DEHP) and dilated cardiomyopathy (DCM) through interpretable machine learning and molecular docking techniques. DCM transcriptome datasets (GSE120895, GSE9800, GSE29819) are integrated. Disease-related genes are screened through differential expression analysis and weighted gene co-expression network analysis (WGCNA). Potential targets of DEHP are predicted using CHEMBL, SwissTargetPrediction, and PharmMapper databases. The associated targets of DEHP and DCM are identified via intersection analysis, and a multi-algorithm machine learning framework is used to further screen core genes. Finally, molecular docking is performed to verify the binding affinity between DEHP and core targets. A total of 1364 potential targets of DEHP are identified. Intersection with 61 DCM-related genes yields 11 key targets. Functional enrichment analysis shows that these genes are involved in ion homeostasis, metabolic reprogramming, and regulation of inflammatory pathways. Machine learning further screens eight core genes: ABAT, ACE2, BLM, C3, IGFBP2, KCNIP2, NPPA, and TYMS. Molecular docking confirms that DEHP has strong binding specificity with all eight core proteins. - Source: PubMed
Publication date: 2026/01/22
Xia XiaoHu LanshuoTao ShiyiLi JunHuang Xuanchun - Histone deacetylase (HDAC) inhibitors are approved for cancer treatment and are being investigated for a wide range of other diseases. Despite their therapeutic promise, clinical studies have reported cardiac side effects, particularly electrocardiogram (EKG) abnormalities, with QT interval prolongation being one of the most consistently reported findings. The mechanisms underlying these cardiac effects remain unclear. In this study, we investigated the role of HDAC3 in cardiac electrophysiology. We found that postnatal depletion of cardiac HDAC3 in mice caused QT interval prolongation, recapitulating the EKG abnormalities reported with HDAC inhibitor use. Adult-onset inducible depletion of cardiac HDAC3 induced additional EKG abnormalities, including T-wave flattening, inversion, and biphasic T waves, which are also observed clinically. Loss of HDAC3 deacetylase activity, without affecting HDAC3 protein levels, was sufficient to induce QT prolongation. Disruption of HDAC3 function altered the expression of ion channel genes, including the downregulation of potassium channel genes such as , , and . Moreover, a single dose of HDAC inhibitors, romidepsin or mocetinostat, caused reversible QT prolongation in mice. Consistent with these findings, HDAC inhibitor treatment altered the expression of potassium channel genes, with a predominant downregulation of multiple Kcn family members, including , , and . These findings establish HDAC3 enzymatic activity as a key regulator of cardiac repolarization and provide mechanistic insight into HDAC inhibitor-associated cardiotoxicity. - Source: PubMed
Publication date: 2026/05/14
Lu JiaoWard ChristopherQian SichongZhang LileiChang JiangSun Zheng - The present study aimed to discover novel KChIP ligands as pharmacological tools for modulating the K4.3/KChIP channels. A multidisciplinary approach, combining medicinal chemistry and electrophysiology studies, led to the successfully identification of a novel K4.3/KChIP modulator (IQM-22110). Its design was guided by the previous knowledge of the (phenylacetamido)benzoic acid moiety as suitable scaffold, along with virtual screening of a focused chemical library that suggested improved KChIP3 binding upon incorporation of an additional aromatic ring. IQM-22110 was selected for synthesis and identified as a potent KChIP3 ligand. Its electrophysiological effects on K4.3/KChIP3 currents indicate that IQM-22110 binds to a high affinity site in K4.3/KChIP3 channels that it is not present in K4.3/KChIP2 or K4.3. To the best of our knowledge, here we describe the first KChIP3 ligand that selectively modulates K4.3/KChIP3 versus K4.3/KChIP2 and K4.3 channels at nanomolar concentration. Since KChIP2 is predominantly expressed in cardiac tissue, this selectivity may enable the development of K4.3/KChIP3-targeted therapeutics with reduced risk of cardiac side effects. Computational and site-directed mutagenesis studies allowed the identification of IQM-22110's binding site on KChIP3. Knowledge gained from structural and functional studies with this novel KChIP3 ligand could establish the basis for drug discovery programs fostering treatments for diseases in which K4.3/KChIPs channels are involved. - Source: PubMed
Publication date: 2026/03/21
Socuellamos Paula GViedma-Barba Carmende Benito-Bueno AngelaBonache Maria AngelesRopero MariaDiez SaraElizalde PabloMarín-Olivero IreneRedondo-Moya MariaNaranjo Jose RamonGonzalez-Vera Juan AOrte AngelPerez-Lara AngelMartin-Martinez MercedesValenzuela CarmenGutierrez-Rodriguez Marta - Sudden unexpected death in epilepsy (SUDEP) is one of the most frequent causes of death in patients with epilepsy, though the pathogenesis of SUDEP has not been well elucidated. Here, we report novel heterozygous KCND3 variants, p.V401L and p.V401M, identified in young patients with refractory epilepsy (RE) and neurodevelopmental disorders, and the functional properties of these variants. We aimed to investigate the electrophysiological changes in de novo KCND3 variants and analyse the pharmacological effects of quinidine on these variants. Chinese hamster ovary (CHO) cells were transiently co-transfected with wild-type (WT) and/or variant KCND3 and Kcnip2. Transient outward potassium currents (I) were recorded using the whole-cell patch-clamp method. The inhibitory effect of quinidine on I was evaluated. In electrophysiological analysis, CHO cells expressing the variant channels showed a significant increase in current density compared with those expressing WT channels. The I activation curves were shifted significantly to the left, and significantly slower inactivation time constants were observed in both variant channels. Recovery from inactivation of the variant channels was significantly slower than that of WT. Quinidine suppressed I in a concentration-dependent manner and accelerated the slow inactivation of variant channels. In conclusion, de novo KCND3 variants identified in patients with RE and neurodevelopmental disorders showed gain and loss of function effects on I. These patients may be at risk of developing early repolarization syndrome, leading to SUDEP. Increased I was suppressed by quinidine, suggesting that it may be an effective therapy for RE and possibly for preventing SUDEP. - Source: PubMed
Publication date: 2025/11/05
Tserenlkham ByambajavTakayama KoichiroZankov Dimitar PGallentine William BCuddapah Vishnu AnandCohen StaceySonoda KeikoHorie MinoruOhno Seiko