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  • 88
    NeuroMab kchip2
    <t>KChIP2</t> represses miR-34b/c expression by direct interaction with a putative DRE motif in promoter. ( A ) A region from −500 to −191 of the miR-34b/c promoter was cloned into the promoterless luciferase construct, pGL4.10. This construct was co-transfected into COS-7 cells in the presence of KChIP2.3 (n = 3), KChIP2.6 (n = 8), or KChIP2.3 (n = 3) and compared to GFP alone. Renillin (pGL4.74) was used as a normalization control. Results are depicted as a % change in activity compared to GFP alone. ( B ) IgG and KChIP2 ChIP-PCR conducted on native adult rat cardiomyocytes. The target primer site residing within the cloned promoter was evaluated for enrichment following pull down (n = 3), showing significant enrichment of the target region. ( C ) Luciferase assay conducted in COS-7 cells to evaluate the outcome of deleting the putative DRE site in the miR-34b/c promoter. COS-7 cells were transfected with the same WT reporter construct inserted into the pGL4.10 vector or with the DRE motif deleted, both in the presence of KChIP2.6. Activity was normalized to renillin (pGL4.74). Deletion of a putative KChIP2 interaction site (DRE motif) partially abolished the repressive effect KChIP2.6 had over the miR-34b/c promoter (n = 4) compared to WT (n = 9). ( D ) COS-7 cells transfected with KChIP2.6 and the pGL4.10 containing the WT miR-34b/c promoter were treated with or without 10 mM caffeine for 6 hr, leading to promoter activation (n = 4). Results were normalized to renillin activity. Data presented as mean ± SEM. *p
    Kchip2, supplied by NeuroMab, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    Santa Cruz Biotechnology kchip2
    Upregulation of K + channel protein by Pyr. A : representative examples of Western blots of Kv4.2, Kv4.3, <t>KChIP2,</t> and Kv1.5 protein in suspensions of isolated myocytes from post-MI and sham-operated hearts. B : mean densitometric measurements of channel subunits are expressed relative to GAPDH. * P
    Kchip2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    85
    Abcam kchip2
    Upregulation of K + channel protein by Pyr. A : representative examples of Western blots of Kv4.2, Kv4.3, <t>KChIP2,</t> and Kv1.5 protein in suspensions of isolated myocytes from post-MI and sham-operated hearts. B : mean densitometric measurements of channel subunits are expressed relative to GAPDH. * P
    Kchip2, supplied by Abcam, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    88
    Boston Therapeutics kchip2
    Effects of NS5806 on cloned <t>Kv4.3/KChIP2/DPP6‐L</t> channels in HEK293 cells. A, Representative current traces elicited by the depolarizing voltage steps from −40 to +40 mV for 2 seconds from a holding potential of −80 mV at different transfection ratios of Kv4.3: KChIP2: DPP6‐L (Left). The superimposed current traces at +40 mV in the absence and presence of NS5806 are shown on the right. B, Effect of 10 μM NS5806 on the peak current of the Kv4.3/KChIP2/DPP6‐L currents produced by different subunit transfection ratios, measured at +40 mV. C, The time constant of inactivation ( τ ) of Kv4.3/KChIP2/DPP6‐L currents produced by different subunit transfection ratios (n = 22). D, I–V relationships of Kv4.3/KChIP2/DPP6‐L peak current density at plasmid ratio 1:1:1 before and after 10 μM NS5806 (n = 18, * P
    Kchip2, supplied by Boston Therapeutics, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    KChIP2 represses miR-34b/c expression by direct interaction with a putative DRE motif in promoter. ( A ) A region from −500 to −191 of the miR-34b/c promoter was cloned into the promoterless luciferase construct, pGL4.10. This construct was co-transfected into COS-7 cells in the presence of KChIP2.3 (n = 3), KChIP2.6 (n = 8), or KChIP2.3 (n = 3) and compared to GFP alone. Renillin (pGL4.74) was used as a normalization control. Results are depicted as a % change in activity compared to GFP alone. ( B ) IgG and KChIP2 ChIP-PCR conducted on native adult rat cardiomyocytes. The target primer site residing within the cloned promoter was evaluated for enrichment following pull down (n = 3), showing significant enrichment of the target region. ( C ) Luciferase assay conducted in COS-7 cells to evaluate the outcome of deleting the putative DRE site in the miR-34b/c promoter. COS-7 cells were transfected with the same WT reporter construct inserted into the pGL4.10 vector or with the DRE motif deleted, both in the presence of KChIP2.6. Activity was normalized to renillin (pGL4.74). Deletion of a putative KChIP2 interaction site (DRE motif) partially abolished the repressive effect KChIP2.6 had over the miR-34b/c promoter (n = 4) compared to WT (n = 9). ( D ) COS-7 cells transfected with KChIP2.6 and the pGL4.10 containing the WT miR-34b/c promoter were treated with or without 10 mM caffeine for 6 hr, leading to promoter activation (n = 4). Results were normalized to renillin activity. Data presented as mean ± SEM. *p

    Journal: eLife

    Article Title: KChIP2 is a core transcriptional regulator of cardiac excitability

    doi: 10.7554/eLife.17304

    Figure Lengend Snippet: KChIP2 represses miR-34b/c expression by direct interaction with a putative DRE motif in promoter. ( A ) A region from −500 to −191 of the miR-34b/c promoter was cloned into the promoterless luciferase construct, pGL4.10. This construct was co-transfected into COS-7 cells in the presence of KChIP2.3 (n = 3), KChIP2.6 (n = 8), or KChIP2.3 (n = 3) and compared to GFP alone. Renillin (pGL4.74) was used as a normalization control. Results are depicted as a % change in activity compared to GFP alone. ( B ) IgG and KChIP2 ChIP-PCR conducted on native adult rat cardiomyocytes. The target primer site residing within the cloned promoter was evaluated for enrichment following pull down (n = 3), showing significant enrichment of the target region. ( C ) Luciferase assay conducted in COS-7 cells to evaluate the outcome of deleting the putative DRE site in the miR-34b/c promoter. COS-7 cells were transfected with the same WT reporter construct inserted into the pGL4.10 vector or with the DRE motif deleted, both in the presence of KChIP2.6. Activity was normalized to renillin (pGL4.74). Deletion of a putative KChIP2 interaction site (DRE motif) partially abolished the repressive effect KChIP2.6 had over the miR-34b/c promoter (n = 4) compared to WT (n = 9). ( D ) COS-7 cells transfected with KChIP2.6 and the pGL4.10 containing the WT miR-34b/c promoter were treated with or without 10 mM caffeine for 6 hr, leading to promoter activation (n = 4). Results were normalized to renillin activity. Data presented as mean ± SEM. *p

    Article Snippet: Overexpression of miR34b and c precursors dampens currents (Ito only in human cells as there is compensatory expression of Kv4.2 in mouse CMs), while over expression of KChIP2 restores currents dampened after PE treatment of NRVC.

    Techniques: Expressing, Clone Assay, Luciferase, Construct, Transfection, Activity Assay, Chromatin Immunoprecipitation, Polymerase Chain Reaction, Plasmid Preparation, Activation Assay

    Preservation of the KChIP2/miR-34b/c axis in human heart failure. ( A ) Human tissue taken from the left ventricle of non-failing (NF) (n = 8) and failing patients (n = 20) evaluating KChIP2 and miR-34b/c RNA expression. KChIP2 levels were normalized to GAPDH and miR expression to small nucleolar RNA U6. ( B ) Evaluation of the human miR-34b/c reveals a conserved DRE motif in proximity of the miR-34b stem loop (−242 bp), as predicted by MatInspector, suggesting conservation of KChIP2 activity in the regulation of miR-34b/c expression. ( C ) Human heart failure tissue evaluating RNA levels for SCN5A , SCN1B , and KCND3 . Significant reductions in heart failure samples (n = 20) were observed for SCN5A and KCND3 , but not for SCN1B , compared to non-failing tissue (n = 8). ( D ) Alignment of the 3’-UTR of SCN5A, SCN1B, and KCND3 genes with miRs-34b/c from human. Grayed letters indicate variation in sequence between miR-34b and −34c. A single site of interaction is indicated for SCN5A, matching observations in the rat, while KCND3 has three potential sites, compared to two observed in the rat. Notably, SCN1B miR-34b/c targeting is not conserved in human shown by imperfect hybridization in the seed region. Data presented as mean ± SEM. *p

    Journal: eLife

    Article Title: KChIP2 is a core transcriptional regulator of cardiac excitability

    doi: 10.7554/eLife.17304

    Figure Lengend Snippet: Preservation of the KChIP2/miR-34b/c axis in human heart failure. ( A ) Human tissue taken from the left ventricle of non-failing (NF) (n = 8) and failing patients (n = 20) evaluating KChIP2 and miR-34b/c RNA expression. KChIP2 levels were normalized to GAPDH and miR expression to small nucleolar RNA U6. ( B ) Evaluation of the human miR-34b/c reveals a conserved DRE motif in proximity of the miR-34b stem loop (−242 bp), as predicted by MatInspector, suggesting conservation of KChIP2 activity in the regulation of miR-34b/c expression. ( C ) Human heart failure tissue evaluating RNA levels for SCN5A , SCN1B , and KCND3 . Significant reductions in heart failure samples (n = 20) were observed for SCN5A and KCND3 , but not for SCN1B , compared to non-failing tissue (n = 8). ( D ) Alignment of the 3’-UTR of SCN5A, SCN1B, and KCND3 genes with miRs-34b/c from human. Grayed letters indicate variation in sequence between miR-34b and −34c. A single site of interaction is indicated for SCN5A, matching observations in the rat, while KCND3 has three potential sites, compared to two observed in the rat. Notably, SCN1B miR-34b/c targeting is not conserved in human shown by imperfect hybridization in the seed region. Data presented as mean ± SEM. *p

    Article Snippet: Overexpression of miR34b and c precursors dampens currents (Ito only in human cells as there is compensatory expression of Kv4.2 in mouse CMs), while over expression of KChIP2 restores currents dampened after PE treatment of NRVC.

    Techniques: Preserving, RNA Expression, Expressing, Activity Assay, Sequencing, Hybridization

    In vitro cardiac disease signaling links KChIP2 loss with miR-34 elevation. ( A ) Real-time qPCR evaluation of relative kcnip2 following treatment with 100 μM PE for 48 hr in NRVM (n = 6). Results normalized to ribosomal protein RPL27. ( B ) Evaluation of miR-34b (n = 8) and miR-34c (n = 7) relative expression in NRVM under control (no PE with Ad.GFP), 100 μM PE with Ad.GFP, or 100 μM PE with Ad.KChIP2 to maintain KChIP2 expression during the 48 hr treatment. Expression levels were normalized to small nucleolar RNA, U87. ( C ) The same treatment conditions in ( B ), evaluating relative mRNA expression for SCN5A (n = 10), SCN1B (n = 10), and KCND3 (n = 7). ( D ) Functional current-voltage measurements of I Na from NRVM under control (n = 29), PE+Ad.GFP (n = 27), and PE+Ad.KChIP2 (n = 30). ( E ) I/V curve for I to,f recordings in control (n = 7), PE+Ad.GFP (n = 9) and PE+Ad.KChIP2 (n = 9). Data presented as mean ± SEM. *p

    Journal: eLife

    Article Title: KChIP2 is a core transcriptional regulator of cardiac excitability

    doi: 10.7554/eLife.17304

    Figure Lengend Snippet: In vitro cardiac disease signaling links KChIP2 loss with miR-34 elevation. ( A ) Real-time qPCR evaluation of relative kcnip2 following treatment with 100 μM PE for 48 hr in NRVM (n = 6). Results normalized to ribosomal protein RPL27. ( B ) Evaluation of miR-34b (n = 8) and miR-34c (n = 7) relative expression in NRVM under control (no PE with Ad.GFP), 100 μM PE with Ad.GFP, or 100 μM PE with Ad.KChIP2 to maintain KChIP2 expression during the 48 hr treatment. Expression levels were normalized to small nucleolar RNA, U87. ( C ) The same treatment conditions in ( B ), evaluating relative mRNA expression for SCN5A (n = 10), SCN1B (n = 10), and KCND3 (n = 7). ( D ) Functional current-voltage measurements of I Na from NRVM under control (n = 29), PE+Ad.GFP (n = 27), and PE+Ad.KChIP2 (n = 30). ( E ) I/V curve for I to,f recordings in control (n = 7), PE+Ad.GFP (n = 9) and PE+Ad.KChIP2 (n = 9). Data presented as mean ± SEM. *p

    Article Snippet: Overexpression of miR34b and c precursors dampens currents (Ito only in human cells as there is compensatory expression of Kv4.2 in mouse CMs), while over expression of KChIP2 restores currents dampened after PE treatment of NRVC.

    Techniques: In Vitro, Real-time Polymerase Chain Reaction, Expressing, Functional Assay

    miR-34 regulation linked to changes in KChIP2 expression. ( A ) Results of miRNA microarray showing the log 2 of the fold changes in miR expression following 72 hr of KChIP2 siRNA treatment. Arrow identifies miR-34b and −34c amongst the panel of altered miRNAs. Analysis of miRNAs for mRNA targets using TargetScan 7.1 was restricted to those above two fold induction (dashed line) ( B ) Tables showing the list of those miRNAs showing at least a two fold increase or decrease following KChIP2 silencing. ( C ) Alignment of the 3’-UTR of SCN5A, SCN1B, and KCND3 genes with miRs-34b/c from rat, showing hybridization of the seed region. Grayed letters indicate variation in sequence between miR-34b and −34c. A single site of interaction is indicated for SCN5A and SCN1B while two sites exist for KCND3. ( D ) Real-time qPCR analysis showing percent change of miR-34b/c expression from control cells in NRVM transfected with KChIP2.3 (n = 5), KChIP2.6 (n = 6), KChIP2.4 (n = 4), or KChIP2 siRNA (n = 4–5). ( E ) Cytosolic, membrane, and nuclear fractions of native adult rat heart tissue. KChIP2 nuclear localization was assessed by using lactate dehydrogenase (LDH), Serca2a, and Lamin-B as cytoplasmic, membrane, and nuclear markers respectively. ( F ) Representative z-stack images of adult rat ventricular myocyte. Nuclear stained regions (DAPI, blue) show the absence of cytosolic protein LDH (green), while KChIP2 (red) staining reveals significant colocalization. Data presented as mean ± SEM. *p

    Journal: eLife

    Article Title: KChIP2 is a core transcriptional regulator of cardiac excitability

    doi: 10.7554/eLife.17304

    Figure Lengend Snippet: miR-34 regulation linked to changes in KChIP2 expression. ( A ) Results of miRNA microarray showing the log 2 of the fold changes in miR expression following 72 hr of KChIP2 siRNA treatment. Arrow identifies miR-34b and −34c amongst the panel of altered miRNAs. Analysis of miRNAs for mRNA targets using TargetScan 7.1 was restricted to those above two fold induction (dashed line) ( B ) Tables showing the list of those miRNAs showing at least a two fold increase or decrease following KChIP2 silencing. ( C ) Alignment of the 3’-UTR of SCN5A, SCN1B, and KCND3 genes with miRs-34b/c from rat, showing hybridization of the seed region. Grayed letters indicate variation in sequence between miR-34b and −34c. A single site of interaction is indicated for SCN5A and SCN1B while two sites exist for KCND3. ( D ) Real-time qPCR analysis showing percent change of miR-34b/c expression from control cells in NRVM transfected with KChIP2.3 (n = 5), KChIP2.6 (n = 6), KChIP2.4 (n = 4), or KChIP2 siRNA (n = 4–5). ( E ) Cytosolic, membrane, and nuclear fractions of native adult rat heart tissue. KChIP2 nuclear localization was assessed by using lactate dehydrogenase (LDH), Serca2a, and Lamin-B as cytoplasmic, membrane, and nuclear markers respectively. ( F ) Representative z-stack images of adult rat ventricular myocyte. Nuclear stained regions (DAPI, blue) show the absence of cytosolic protein LDH (green), while KChIP2 (red) staining reveals significant colocalization. Data presented as mean ± SEM. *p

    Article Snippet: Overexpression of miR34b and c precursors dampens currents (Ito only in human cells as there is compensatory expression of Kv4.2 in mouse CMs), while over expression of KChIP2 restores currents dampened after PE treatment of NRVC.

    Techniques: Expressing, Microarray, Hybridization, Sequencing, Real-time Polymerase Chain Reaction, Transfection, Staining

    Upregulation of K + channel protein by Pyr. A : representative examples of Western blots of Kv4.2, Kv4.3, KChIP2, and Kv1.5 protein in suspensions of isolated myocytes from post-MI and sham-operated hearts. B : mean densitometric measurements of channel subunits are expressed relative to GAPDH. * P

    Journal: American Journal of Physiology. Heart and Circulatory Physiology

    Article Title: Regulation of Kv4 channel expression in failing rat heart by the thioredoxin system

    doi: 10.1152/ajpheart.91446.2007

    Figure Lengend Snippet: Upregulation of K + channel protein by Pyr. A : representative examples of Western blots of Kv4.2, Kv4.3, KChIP2, and Kv1.5 protein in suspensions of isolated myocytes from post-MI and sham-operated hearts. B : mean densitometric measurements of channel subunits are expressed relative to GAPDH. * P

    Article Snippet: The pyruvate-stimulated upregulation of Kv4.2 and Kv4.3 mRNA was blocked when myocytes were pretreated for 30 min with 10 nmol/l AF, whereas this inhibitor did not change the pyruvate response of KChIP2.

    Techniques: Western Blot, Isolation

    Upregulation of K + channel expression by Pyr. A : mRNA levels of Kv4.2, Kv4.3, and KChIP2 in isolated myocytes from post-MI (black bars) and sham-operated hearts were measured by real-time PCR. Mean data for the post-MI group are expressed relative to sham. * P

    Journal: American Journal of Physiology. Heart and Circulatory Physiology

    Article Title: Regulation of Kv4 channel expression in failing rat heart by the thioredoxin system

    doi: 10.1152/ajpheart.91446.2007

    Figure Lengend Snippet: Upregulation of K + channel expression by Pyr. A : mRNA levels of Kv4.2, Kv4.3, and KChIP2 in isolated myocytes from post-MI (black bars) and sham-operated hearts were measured by real-time PCR. Mean data for the post-MI group are expressed relative to sham. * P

    Article Snippet: The pyruvate-stimulated upregulation of Kv4.2 and Kv4.3 mRNA was blocked when myocytes were pretreated for 30 min with 10 nmol/l AF, whereas this inhibitor did not change the pyruvate response of KChIP2.

    Techniques: Expressing, Isolation, Real-time Polymerase Chain Reaction

    Effects of NS5806 on cloned Kv4.3/KChIP2/DPP6‐L channels in HEK293 cells. A, Representative current traces elicited by the depolarizing voltage steps from −40 to +40 mV for 2 seconds from a holding potential of −80 mV at different transfection ratios of Kv4.3: KChIP2: DPP6‐L (Left). The superimposed current traces at +40 mV in the absence and presence of NS5806 are shown on the right. B, Effect of 10 μM NS5806 on the peak current of the Kv4.3/KChIP2/DPP6‐L currents produced by different subunit transfection ratios, measured at +40 mV. C, The time constant of inactivation ( τ ) of Kv4.3/KChIP2/DPP6‐L currents produced by different subunit transfection ratios (n = 22). D, I–V relationships of Kv4.3/KChIP2/DPP6‐L peak current density at plasmid ratio 1:1:1 before and after 10 μM NS5806 (n = 18, * P

    Journal: The FASEB Journal

    Article Title: Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex, et al. Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex

    doi: 10.1096/fj.201902010RR

    Figure Lengend Snippet: Effects of NS5806 on cloned Kv4.3/KChIP2/DPP6‐L channels in HEK293 cells. A, Representative current traces elicited by the depolarizing voltage steps from −40 to +40 mV for 2 seconds from a holding potential of −80 mV at different transfection ratios of Kv4.3: KChIP2: DPP6‐L (Left). The superimposed current traces at +40 mV in the absence and presence of NS5806 are shown on the right. B, Effect of 10 μM NS5806 on the peak current of the Kv4.3/KChIP2/DPP6‐L currents produced by different subunit transfection ratios, measured at +40 mV. C, The time constant of inactivation ( τ ) of Kv4.3/KChIP2/DPP6‐L currents produced by different subunit transfection ratios (n = 22). D, I–V relationships of Kv4.3/KChIP2/DPP6‐L peak current density at plasmid ratio 1:1:1 before and after 10 μM NS5806 (n = 18, * P

    Article Snippet: However, further structural insights are needed to confirm the direct interaction between KChIP2 and DPP6‐L.

    Techniques: Clone Assay, Transfection, Produced, Plasmid Preparation

    DPP6 and KChIP2 subunits confer the modality of I to channel response to NS5806

    Journal: The FASEB Journal

    Article Title: Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex, et al. Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex

    doi: 10.1096/fj.201902010RR

    Figure Lengend Snippet: DPP6 and KChIP2 subunits confer the modality of I to channel response to NS5806

    Article Snippet: However, further structural insights are needed to confirm the direct interaction between KChIP2 and DPP6‐L.

    Techniques:

    Analysis on the putative interactions between KChIP2 and DPP6‐L. A 1 , Modeling and docking simulation of putative interactions between DPP6‐Lin and KChIP2 . Homology model of KChIP2. A 2 , The top‐ranked model of the intracellular domain of DPP6‐L (DPP6‐Lin). A 3 , Top‐ranked models of both proteins. A 4 , Best scored model of docking KChIP2 with DPP6‐Lin; putative‐interacting residues are indicated. B 1 , Schematic depiction of DPP6‐L and the location of mutated residues within the putative KChIP2 interaction site. B 2 , Representative recordings of Kv4.3/KChIP2/DPP6‐L‐WT and Kv4.3/KChIP2/DPP6‐L‐Mut currents from HEK293 cells using 500 ms square voltage pulses (from −40 to +40 mV; holding potential is −80 mV). B 3 , The time constants of inactivation ( τ ) of Kv4.3/KChIP2/DPP6‐L‐WT and Kv4.3/KChIP2/DPP6‐L‐Mut current traces plotted against voltage (** P

    Journal: The FASEB Journal

    Article Title: Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex, et al. Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex

    doi: 10.1096/fj.201902010RR

    Figure Lengend Snippet: Analysis on the putative interactions between KChIP2 and DPP6‐L. A 1 , Modeling and docking simulation of putative interactions between DPP6‐Lin and KChIP2 . Homology model of KChIP2. A 2 , The top‐ranked model of the intracellular domain of DPP6‐L (DPP6‐Lin). A 3 , Top‐ranked models of both proteins. A 4 , Best scored model of docking KChIP2 with DPP6‐Lin; putative‐interacting residues are indicated. B 1 , Schematic depiction of DPP6‐L and the location of mutated residues within the putative KChIP2 interaction site. B 2 , Representative recordings of Kv4.3/KChIP2/DPP6‐L‐WT and Kv4.3/KChIP2/DPP6‐L‐Mut currents from HEK293 cells using 500 ms square voltage pulses (from −40 to +40 mV; holding potential is −80 mV). B 3 , The time constants of inactivation ( τ ) of Kv4.3/KChIP2/DPP6‐L‐WT and Kv4.3/KChIP2/DPP6‐L‐Mut current traces plotted against voltage (** P

    Article Snippet: However, further structural insights are needed to confirm the direct interaction between KChIP2 and DPP6‐L.

    Techniques: