rabbit anti kv1 1  (Alomone Labs)


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    Name:
    Anti Kv1 1 KCNA1 extracellular Antibody
    Description:
    Anti KV1 1 KCNA1 extracellular Antibody APC 161 is a highly specific antibody directed against an epitope of the rat protein The antibody can be used in western blot immunohistochemistry indirect flow cytometry and live cell imaging applications It has been designed to recognize KV1 1 from human rat and mouse samples
    Catalog Number:
    APC-161
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunocytochemistry, Immunofluorescence, Indirect Flow Cytometry, Live Cell Imaging, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Rabbit
    Isotype:
    Rabbit IgG
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    Structured Review

    Alomone Labs rabbit anti kv1 1
    Anti Kv1 1 KCNA1 extracellular Antibody
    Anti KV1 1 KCNA1 extracellular Antibody APC 161 is a highly specific antibody directed against an epitope of the rat protein The antibody can be used in western blot immunohistochemistry indirect flow cytometry and live cell imaging applications It has been designed to recognize KV1 1 from human rat and mouse samples
    https://www.bioz.com/result/rabbit anti kv1 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti kv1 1 - by Bioz Stars, 2021-09
    93/100 stars

    Images

    1) Product Images from "Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization"

    Article Title: Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    doi: 10.1073/pnas.1608763114

    Kv1.1 channels determine spike width. ( A ) Example recordings from one neuron before and after 20 nM DTx-K application. This neurotoxin had no effect on somatic spikes but led to broadening of presynaptic action potentials. ( B ) Presynaptic spike widths
    Figure Legend Snippet: Kv1.1 channels determine spike width. ( A ) Example recordings from one neuron before and after 20 nM DTx-K application. This neurotoxin had no effect on somatic spikes but led to broadening of presynaptic action potentials. ( B ) Presynaptic spike widths

    Techniques Used:

    Blockade or deletion of Kv1.1 does not prevent analog modulation of presynaptic spike width. ( A ) Trace analysis from one wild-type cell showing bidirectional changes in presynaptic spike width by subthreshold somatic current injections before evoking
    Figure Legend Snippet: Blockade or deletion of Kv1.1 does not prevent analog modulation of presynaptic spike width. ( A ) Trace analysis from one wild-type cell showing bidirectional changes in presynaptic spike width by subthreshold somatic current injections before evoking

    Techniques Used:

    2) Product Images from "The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta"

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    Journal: BMC Biology

    doi: 10.1186/s12915-020-00878-1

    ARTD10 inhibition reduces the proportion of the inactivating Kv1.1 current and enhances spontaneous excitation in hippocampal neurons. a Left, whole cell currents of mouse hippocampal neurons in the presence of tetrodotoxin with and without an inhibitor of ARTD10 (OUL35). Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. b Resting membrane potential (RMP) and spontaneous spikes/s from control and OUL35 treated hippocampal neurons. * p
    Figure Legend Snippet: ARTD10 inhibition reduces the proportion of the inactivating Kv1.1 current and enhances spontaneous excitation in hippocampal neurons. a Left, whole cell currents of mouse hippocampal neurons in the presence of tetrodotoxin with and without an inhibitor of ARTD10 (OUL35). Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. b Resting membrane potential (RMP) and spontaneous spikes/s from control and OUL35 treated hippocampal neurons. * p

    Techniques Used: Inhibition

    Scheme illustrating the interplay of PKA, PKCδ, and ARTD10 in the regulation of Kv1.1. The regulation of a phosphatase by PKCδ is hypothetical. Current traces above the schemes of the Kv1.1 channels illustrate the typical inactivation pattern of phosphorylated vs. un-phosphorylated Kv1.1α. I/F, IBMX/forskolin; PMA, phorbol-myristate-acetate
    Figure Legend Snippet: Scheme illustrating the interplay of PKA, PKCδ, and ARTD10 in the regulation of Kv1.1. The regulation of a phosphatase by PKCδ is hypothetical. Current traces above the schemes of the Kv1.1 channels illustrate the typical inactivation pattern of phosphorylated vs. un-phosphorylated Kv1.1α. I/F, IBMX/forskolin; PMA, phorbol-myristate-acetate

    Techniques Used:

    ARTD10 inhibition enhances excitability of hippocampal neurons via Kv1.1. a Left, representative current clamp recordings of APs elicited by step current pulses in control neurons and neurons treated with OUL35. Right, bar graphs represent the rheobase and the latency to the first spike. For cells with a RMP more positive than − 60 mV, the membrane potential was adjusted to ~ − 60 mV. b The number of spikes elicited by step current pulses were counted and for stimuli from 10 to 30 pA they were fitted with a linear function. Right, bar graphs summarize the AP amplitude from neurons with and without OUL35 treatment. c Left, bar graphs representing the rheobase. Right, summary of spikes/s with and without the Kv1 inhibitor α-dendrotoxin (DTX) and from neurons with and without OUL35 treatment. * p
    Figure Legend Snippet: ARTD10 inhibition enhances excitability of hippocampal neurons via Kv1.1. a Left, representative current clamp recordings of APs elicited by step current pulses in control neurons and neurons treated with OUL35. Right, bar graphs represent the rheobase and the latency to the first spike. For cells with a RMP more positive than − 60 mV, the membrane potential was adjusted to ~ − 60 mV. b The number of spikes elicited by step current pulses were counted and for stimuli from 10 to 30 pA they were fitted with a linear function. Right, bar graphs summarize the AP amplitude from neurons with and without OUL35 treatment. c Left, bar graphs representing the rheobase. Right, summary of spikes/s with and without the Kv1 inhibitor α-dendrotoxin (DTX) and from neurons with and without OUL35 treatment. * p

    Techniques Used: Inhibition

    Inactivation of Kv1.1 is regulated by Kvβ and phosphorylation at S446. a Representative recordings, I steady-state / I peak ( I s / I p ), and peak current amplitudes of Kv1.1 with or without co-expression of Kvβ1.1 in HeLa cells. b Representative recordings and I s / I p before and after the application of either IBMX/forskolin (I/F) or of the phorbol ester PMA. c Representative recordings, I s / I p , and peak current amplitudes of the phosphorylation-deficient mutant Kv1.1 S446A co-expressed with Kvβ1.1. d Representative recordings, I s / I p , and peak current amplitudes of Kv1.1 after 1.5 h pre-incubation with a phosphatase inhibitor cocktail. * p
    Figure Legend Snippet: Inactivation of Kv1.1 is regulated by Kvβ and phosphorylation at S446. a Representative recordings, I steady-state / I peak ( I s / I p ), and peak current amplitudes of Kv1.1 with or without co-expression of Kvβ1.1 in HeLa cells. b Representative recordings and I s / I p before and after the application of either IBMX/forskolin (I/F) or of the phorbol ester PMA. c Representative recordings, I s / I p , and peak current amplitudes of the phosphorylation-deficient mutant Kv1.1 S446A co-expressed with Kvβ1.1. d Representative recordings, I s / I p , and peak current amplitudes of Kv1.1 after 1.5 h pre-incubation with a phosphatase inhibitor cocktail. * p

    Techniques Used: Expressing, Mutagenesis, Incubation

    ARTD10 leads to phosphorylation of Kv1.1 at S446. a , b Left, Representative current traces of wild type ( a ) or the phosphorylation-deficient mutant ( b ) of Kv1.1 overexpressed in three different HeLa cell lines. Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. * p
    Figure Legend Snippet: ARTD10 leads to phosphorylation of Kv1.1 at S446. a , b Left, Representative current traces of wild type ( a ) or the phosphorylation-deficient mutant ( b ) of Kv1.1 overexpressed in three different HeLa cell lines. Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. * p

    Techniques Used: Mutagenesis

    Kv1.1 is regulated by PKCδ in HeLa cells. a , b Wild type Kv1.1 or mutant Kv1.1-S446A were co-expressed with Kvβ1 and either the catalytic domain (CAT) or a dominant negative mutant (DN) of PKCδ. Bar graphs represent I steady-state / I peak ( I s / I p ) and peak current amplitudes
    Figure Legend Snippet: Kv1.1 is regulated by PKCδ in HeLa cells. a , b Wild type Kv1.1 or mutant Kv1.1-S446A were co-expressed with Kvβ1 and either the catalytic domain (CAT) or a dominant negative mutant (DN) of PKCδ. Bar graphs represent I steady-state / I peak ( I s / I p ) and peak current amplitudes

    Techniques Used: Mutagenesis, Dominant Negative Mutation

    Related Articles

    Western Blot:

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta
    Article Snippet: .. For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451). ..

    Sequencing:

    Article Title: Potassium channels Kv1.1, Kv1.2 and Kv1.6 influence excitability of rat visceral sensory neurons
    Article Snippet: .. Two Kv1.1 antibodies were used: a mouse monoclonal antibody (Upstate Biotechnology) raised against a C-terminal peptide (residues 458-476) of rat Kv1.1 and a rabbit polyclonal Kv1.1 (Alomone Labs) raised against a fusion protein with sequence corresponding to residues 416-495. ..

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  • 93
    Alomone Labs rabbit anti kv1 1
    <t>Kv1.1</t> channels determine spike width. ( A ) Example recordings from one neuron before and after 20 nM DTx-K application. This neurotoxin had no effect on somatic spikes but led to broadening of presynaptic action potentials. ( B ) Presynaptic spike widths
    Rabbit Anti Kv1 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti kv1 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti kv1 1 - by Bioz Stars, 2021-09
    93/100 stars
      Buy from Supplier

    Image Search Results


    Kv1.1 channels determine spike width. ( A ) Example recordings from one neuron before and after 20 nM DTx-K application. This neurotoxin had no effect on somatic spikes but led to broadening of presynaptic action potentials. ( B ) Presynaptic spike widths

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization

    doi: 10.1073/pnas.1608763114

    Figure Lengend Snippet: Kv1.1 channels determine spike width. ( A ) Example recordings from one neuron before and after 20 nM DTx-K application. This neurotoxin had no effect on somatic spikes but led to broadening of presynaptic action potentials. ( B ) Presynaptic spike widths

    Article Snippet: Membranes were immunoblotted with the respective antibodies: rabbit anti-Kv1.1 (APC-161, Alomone Labs; 1:800), anti-Kv1.2 (APC-010, 1:1,500), anti-Kv1.3 (APC-101, 1:1,000), anti-Kv1.4 (APC-167, 1:500), anti-Kv1.6 (APC-003, 1:2,000), and anti-SNAP25 (Abcam ab5666; 1:2,000) at 4 °C overnight.

    Techniques:

    Blockade or deletion of Kv1.1 does not prevent analog modulation of presynaptic spike width. ( A ) Trace analysis from one wild-type cell showing bidirectional changes in presynaptic spike width by subthreshold somatic current injections before evoking

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization

    doi: 10.1073/pnas.1608763114

    Figure Lengend Snippet: Blockade or deletion of Kv1.1 does not prevent analog modulation of presynaptic spike width. ( A ) Trace analysis from one wild-type cell showing bidirectional changes in presynaptic spike width by subthreshold somatic current injections before evoking

    Article Snippet: Membranes were immunoblotted with the respective antibodies: rabbit anti-Kv1.1 (APC-161, Alomone Labs; 1:800), anti-Kv1.2 (APC-010, 1:1,500), anti-Kv1.3 (APC-101, 1:1,000), anti-Kv1.4 (APC-167, 1:500), anti-Kv1.6 (APC-003, 1:2,000), and anti-SNAP25 (Abcam ab5666; 1:2,000) at 4 °C overnight.

    Techniques:

    ARTD10 inhibition reduces the proportion of the inactivating Kv1.1 current and enhances spontaneous excitation in hippocampal neurons. a Left, whole cell currents of mouse hippocampal neurons in the presence of tetrodotoxin with and without an inhibitor of ARTD10 (OUL35). Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. b Resting membrane potential (RMP) and spontaneous spikes/s from control and OUL35 treated hippocampal neurons. * p

    Journal: BMC Biology

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    doi: 10.1186/s12915-020-00878-1

    Figure Lengend Snippet: ARTD10 inhibition reduces the proportion of the inactivating Kv1.1 current and enhances spontaneous excitation in hippocampal neurons. a Left, whole cell currents of mouse hippocampal neurons in the presence of tetrodotoxin with and without an inhibitor of ARTD10 (OUL35). Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. b Resting membrane potential (RMP) and spontaneous spikes/s from control and OUL35 treated hippocampal neurons. * p

    Article Snippet: For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451).

    Techniques: Inhibition

    Scheme illustrating the interplay of PKA, PKCδ, and ARTD10 in the regulation of Kv1.1. The regulation of a phosphatase by PKCδ is hypothetical. Current traces above the schemes of the Kv1.1 channels illustrate the typical inactivation pattern of phosphorylated vs. un-phosphorylated Kv1.1α. I/F, IBMX/forskolin; PMA, phorbol-myristate-acetate

    Journal: BMC Biology

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    doi: 10.1186/s12915-020-00878-1

    Figure Lengend Snippet: Scheme illustrating the interplay of PKA, PKCδ, and ARTD10 in the regulation of Kv1.1. The regulation of a phosphatase by PKCδ is hypothetical. Current traces above the schemes of the Kv1.1 channels illustrate the typical inactivation pattern of phosphorylated vs. un-phosphorylated Kv1.1α. I/F, IBMX/forskolin; PMA, phorbol-myristate-acetate

    Article Snippet: For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451).

    Techniques:

    ARTD10 inhibition enhances excitability of hippocampal neurons via Kv1.1. a Left, representative current clamp recordings of APs elicited by step current pulses in control neurons and neurons treated with OUL35. Right, bar graphs represent the rheobase and the latency to the first spike. For cells with a RMP more positive than − 60 mV, the membrane potential was adjusted to ~ − 60 mV. b The number of spikes elicited by step current pulses were counted and for stimuli from 10 to 30 pA they were fitted with a linear function. Right, bar graphs summarize the AP amplitude from neurons with and without OUL35 treatment. c Left, bar graphs representing the rheobase. Right, summary of spikes/s with and without the Kv1 inhibitor α-dendrotoxin (DTX) and from neurons with and without OUL35 treatment. * p

    Journal: BMC Biology

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    doi: 10.1186/s12915-020-00878-1

    Figure Lengend Snippet: ARTD10 inhibition enhances excitability of hippocampal neurons via Kv1.1. a Left, representative current clamp recordings of APs elicited by step current pulses in control neurons and neurons treated with OUL35. Right, bar graphs represent the rheobase and the latency to the first spike. For cells with a RMP more positive than − 60 mV, the membrane potential was adjusted to ~ − 60 mV. b The number of spikes elicited by step current pulses were counted and for stimuli from 10 to 30 pA they were fitted with a linear function. Right, bar graphs summarize the AP amplitude from neurons with and without OUL35 treatment. c Left, bar graphs representing the rheobase. Right, summary of spikes/s with and without the Kv1 inhibitor α-dendrotoxin (DTX) and from neurons with and without OUL35 treatment. * p

    Article Snippet: For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451).

    Techniques: Inhibition

    Inactivation of Kv1.1 is regulated by Kvβ and phosphorylation at S446. a Representative recordings, I steady-state / I peak ( I s / I p ), and peak current amplitudes of Kv1.1 with or without co-expression of Kvβ1.1 in HeLa cells. b Representative recordings and I s / I p before and after the application of either IBMX/forskolin (I/F) or of the phorbol ester PMA. c Representative recordings, I s / I p , and peak current amplitudes of the phosphorylation-deficient mutant Kv1.1 S446A co-expressed with Kvβ1.1. d Representative recordings, I s / I p , and peak current amplitudes of Kv1.1 after 1.5 h pre-incubation with a phosphatase inhibitor cocktail. * p

    Journal: BMC Biology

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    doi: 10.1186/s12915-020-00878-1

    Figure Lengend Snippet: Inactivation of Kv1.1 is regulated by Kvβ and phosphorylation at S446. a Representative recordings, I steady-state / I peak ( I s / I p ), and peak current amplitudes of Kv1.1 with or without co-expression of Kvβ1.1 in HeLa cells. b Representative recordings and I s / I p before and after the application of either IBMX/forskolin (I/F) or of the phorbol ester PMA. c Representative recordings, I s / I p , and peak current amplitudes of the phosphorylation-deficient mutant Kv1.1 S446A co-expressed with Kvβ1.1. d Representative recordings, I s / I p , and peak current amplitudes of Kv1.1 after 1.5 h pre-incubation with a phosphatase inhibitor cocktail. * p

    Article Snippet: For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451).

    Techniques: Expressing, Mutagenesis, Incubation

    ARTD10 leads to phosphorylation of Kv1.1 at S446. a , b Left, Representative current traces of wild type ( a ) or the phosphorylation-deficient mutant ( b ) of Kv1.1 overexpressed in three different HeLa cell lines. Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. * p

    Journal: BMC Biology

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    doi: 10.1186/s12915-020-00878-1

    Figure Lengend Snippet: ARTD10 leads to phosphorylation of Kv1.1 at S446. a , b Left, Representative current traces of wild type ( a ) or the phosphorylation-deficient mutant ( b ) of Kv1.1 overexpressed in three different HeLa cell lines. Right, bar graphs representing I steady-state / I peak ( I s / I p ) and peak current amplitudes. * p

    Article Snippet: For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451).

    Techniques: Mutagenesis

    Kv1.1 is regulated by PKCδ in HeLa cells. a , b Wild type Kv1.1 or mutant Kv1.1-S446A were co-expressed with Kvβ1 and either the catalytic domain (CAT) or a dominant negative mutant (DN) of PKCδ. Bar graphs represent I steady-state / I peak ( I s / I p ) and peak current amplitudes

    Journal: BMC Biology

    Article Title: The mono-ADP-ribosyltransferase ARTD10 regulates the voltage-gated K+ channel Kv1.1 through protein kinase C delta

    doi: 10.1186/s12915-020-00878-1

    Figure Lengend Snippet: Kv1.1 is regulated by PKCδ in HeLa cells. a , b Wild type Kv1.1 or mutant Kv1.1-S446A were co-expressed with Kvβ1 and either the catalytic domain (CAT) or a dominant negative mutant (DN) of PKCδ. Bar graphs represent I steady-state / I peak ( I s / I p ) and peak current amplitudes

    Article Snippet: For immunoblots, proteins were transferred to PVDF membranes (Roche, Mannheim, Germany), and the membrane was blocked for 1 h at RT in 5% non-fat milk in TBS-T (137 mM NaCl, 2.7 mM KCl, 25 mM Tris, 0.1% Tween-20), and probed overnight at 4 °C with the following primary antibodies: rabbit polyclonal anti-Kv1.1 (Alomone Labs, # APC-161 and APC-009), rabbit polyclonal anti-PKCδ (Santa Cruz, # sc-937), rabbit polyclonal anti-phospho-PKCδ (Tyr311) (Cell Signaling, # 2055), rat monoclonal anti-ARTD10 (Merck, #5H11), or mouse monoclonal anti-acetylated tubulin (Sigma-Aldrich, # T7451).

    Techniques: Mutagenesis, Dominant Negative Mutation