rabbit anti kchip1  (Alomone Labs)


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    Structured Review

    Alomone Labs rabbit anti kchip1
    Intrathecal injection of <t>Kv4.3/KChIP1/DPP10</t> cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p
    Rabbit Anti Kchip1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control"

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p
    Figure Legend Snippet: Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p

    Techniques Used: Injection, Western Blot, Isolation

    KChIP1 or KChIP2 ASO reduces all Kv4 complex components in the DRGs and induces mechanical hypersensitivity. Rats were intrathecally injected with vehicle, LacZ ASO, KChIP1 ASO, or KChIP2 ASO during D1–D3. A , B , KChIP1 ASO induces bilateral mechanical hypersensitivity during D1–D5. Thermal hypersensitivity was not detected. L, Left side; R, right side. Data are mean ± SEM ( n = 6). * p
    Figure Legend Snippet: KChIP1 or KChIP2 ASO reduces all Kv4 complex components in the DRGs and induces mechanical hypersensitivity. Rats were intrathecally injected with vehicle, LacZ ASO, KChIP1 ASO, or KChIP2 ASO during D1–D3. A , B , KChIP1 ASO induces bilateral mechanical hypersensitivity during D1–D5. Thermal hypersensitivity was not detected. L, Left side; R, right side. Data are mean ± SEM ( n = 6). * p

    Techniques Used: Allele-specific Oligonucleotide, Injection

    Intrathecal injection of Kv4.3 ASO reduces all Kv4 complex components in the L4–L6 DRGs. Rats were intrathecally injected with Kv4.3 ASO twice daily for 3 consecutive days (D1–D3) and killed on day 4 (D4) or D7. Rats injected with vehicle (V) or LacZ ASO (Z) were used as controls. A , In the L5 DRG of rats treated with Kv4.3 ASO, Kv4.3-, KChIP1-, KChIP2-, and DPP10-IR were greatly reduced on D4 but returned to the normal levels on D7. Scale bar, 40 μm. B–E , Quantitative data of A . C , C7 DRG. L , L5 DRG. F–I , Western blotting was performed using total proteins ( F , G ) or plasma membrane proteins ( H , I ) isolated from the bilateral L4–L6 DRGs on D4. Kv4.3 ASO treatment reduces Kv4.3, KChIP1, and DPP10 in both protein preparations. Bands of GAPDH and cadherin were loading controls for total proteins and plasma membrane proteins, respectively. Data are mean ± SD ( n = 3). ** p
    Figure Legend Snippet: Intrathecal injection of Kv4.3 ASO reduces all Kv4 complex components in the L4–L6 DRGs. Rats were intrathecally injected with Kv4.3 ASO twice daily for 3 consecutive days (D1–D3) and killed on day 4 (D4) or D7. Rats injected with vehicle (V) or LacZ ASO (Z) were used as controls. A , In the L5 DRG of rats treated with Kv4.3 ASO, Kv4.3-, KChIP1-, KChIP2-, and DPP10-IR were greatly reduced on D4 but returned to the normal levels on D7. Scale bar, 40 μm. B–E , Quantitative data of A . C , C7 DRG. L , L5 DRG. F–I , Western blotting was performed using total proteins ( F , G ) or plasma membrane proteins ( H , I ) isolated from the bilateral L4–L6 DRGs on D4. Kv4.3 ASO treatment reduces Kv4.3, KChIP1, and DPP10 in both protein preparations. Bands of GAPDH and cadherin were loading controls for total proteins and plasma membrane proteins, respectively. Data are mean ± SD ( n = 3). ** p

    Techniques Used: Injection, Allele-specific Oligonucleotide, Western Blot, Isolation

    Detection of a Kv4.3/KChIP1/KChIP2/DPP10 complex in the DRG. Total proteins (Total), plasma membrane proteins (PM), and rough ER proteins (rER) were isolated from rat lumbar DRGs, respectively. A , Representative Western blot data show Kv4.3, KChIP1, KChIP2, and DPP10 in each protein preparation. Cadherin and calnexin are markers for the PM and rER, respectively. The purity of PM proteins was confirmed by the presence of cadherin and the absence of calnexin, whereas the purity of rER proteins was confirmed by the presence of calnexin and the absence of cadherin. B , C , In addition to immunoprecipitation of Kv4.3, rabbit anti-Kv4.3 antibody (α-Kv4.3) coimmunoprecipitates KChIP1, KChIP2, and DPP10 from the PM proteins ( B ) and rER proteins ( C ), respectively. Nonspecific rabbit IgG was used as a control of immunoprecipitation, and “extract” indicates a bead-only loading control.
    Figure Legend Snippet: Detection of a Kv4.3/KChIP1/KChIP2/DPP10 complex in the DRG. Total proteins (Total), plasma membrane proteins (PM), and rough ER proteins (rER) were isolated from rat lumbar DRGs, respectively. A , Representative Western blot data show Kv4.3, KChIP1, KChIP2, and DPP10 in each protein preparation. Cadherin and calnexin are markers for the PM and rER, respectively. The purity of PM proteins was confirmed by the presence of cadherin and the absence of calnexin, whereas the purity of rER proteins was confirmed by the presence of calnexin and the absence of cadherin. B , C , In addition to immunoprecipitation of Kv4.3, rabbit anti-Kv4.3 antibody (α-Kv4.3) coimmunoprecipitates KChIP1, KChIP2, and DPP10 from the PM proteins ( B ) and rER proteins ( C ), respectively. Nonspecific rabbit IgG was used as a control of immunoprecipitation, and “extract” indicates a bead-only loading control.

    Techniques Used: Isolation, Western Blot, Immunoprecipitation

    The excitability of IB4 + nociceptors is enhanced after knockdown of Kv4.3, KChIP1, or DPP10. FAM-tagged ASO for LacZ, Kv4.3, KChIP1, or DPP10 was intrathecally injected into the rat by lumbar puncture, and the bilateral L4–L6 DRGs were isolated 5 h later. DRG neurons were dissociated and cultured for 20–24 h before whole-cell patch-clamp recording. A , Top, Only small DRG neurons (soma diameter ≤ 30 μm; bright-field, BF) with both FAM (green) and Alexa594-conjugated IB4 (red) signals were analyzed. Scale bar, 20 μm. Bottom, Responses to the depolarizing current pulses (100 and 300 pA; 1 s). B , The resting membrane potential (Vrest) in each ASO group. n = 9–12 as indicated in D . * p
    Figure Legend Snippet: The excitability of IB4 + nociceptors is enhanced after knockdown of Kv4.3, KChIP1, or DPP10. FAM-tagged ASO for LacZ, Kv4.3, KChIP1, or DPP10 was intrathecally injected into the rat by lumbar puncture, and the bilateral L4–L6 DRGs were isolated 5 h later. DRG neurons were dissociated and cultured for 20–24 h before whole-cell patch-clamp recording. A , Top, Only small DRG neurons (soma diameter ≤ 30 μm; bright-field, BF) with both FAM (green) and Alexa594-conjugated IB4 (red) signals were analyzed. Scale bar, 20 μm. Bottom, Responses to the depolarizing current pulses (100 and 300 pA; 1 s). B , The resting membrane potential (Vrest) in each ASO group. n = 9–12 as indicated in D . * p

    Techniques Used: Allele-specific Oligonucleotide, Injection, Isolation, Cell Culture, Patch Clamp

    Intrathecal cDNA injection does not suppress SNL-evoked glial activation and macrophage proliferation in the injured DRGs. Rats were intrathecally injected with Kv4.3/KChP1/DPP10 cDNAs on D4 and killed on D7 or D14 after SNL. A , Sections of the ipsilateral L5 DRG were immunostained for GFAP and Iba1, respectively. Scale bar, 48 μm. B , C , Quantitative data of A . GFAP + or Iba1 + area shows no significant difference (N.S.) between SNL rats and the SNL rats treated with Kv4.3/KChIP1/DPP10 cDNAs. Data are mean ± SD ( n = 3), compared with SNL on the same day by Student's t test.
    Figure Legend Snippet: Intrathecal cDNA injection does not suppress SNL-evoked glial activation and macrophage proliferation in the injured DRGs. Rats were intrathecally injected with Kv4.3/KChP1/DPP10 cDNAs on D4 and killed on D7 or D14 after SNL. A , Sections of the ipsilateral L5 DRG were immunostained for GFAP and Iba1, respectively. Scale bar, 48 μm. B , C , Quantitative data of A . GFAP + or Iba1 + area shows no significant difference (N.S.) between SNL rats and the SNL rats treated with Kv4.3/KChIP1/DPP10 cDNAs. Data are mean ± SD ( n = 3), compared with SNL on the same day by Student's t test.

    Techniques Used: Injection, Activation Assay

    Intrathecal ASO injections do not affect KChIP1, KChIP2, and DPP10 expression in the spinal cord. Rats were intrathecally injected with ASO for LacZ (Z), Kv4.3, KChIP1, KChIP2, or DPP10 during D1–D3 and killed on D4. Sections of the L5 spinal cord segment were immunostained. A–C , KChIP1-, KChIP2-, or DPP10-IR in the dorsal spinal cord (on either side) is similar between each ASO group and the vehicle (V) group. Scale bar, 210 μm. D–F , Quantitative data of A–C . Data are mean ± SD ( n = 3), compared with vehicle by Student's t test.
    Figure Legend Snippet: Intrathecal ASO injections do not affect KChIP1, KChIP2, and DPP10 expression in the spinal cord. Rats were intrathecally injected with ASO for LacZ (Z), Kv4.3, KChIP1, KChIP2, or DPP10 during D1–D3 and killed on D4. Sections of the L5 spinal cord segment were immunostained. A–C , KChIP1-, KChIP2-, or DPP10-IR in the dorsal spinal cord (on either side) is similar between each ASO group and the vehicle (V) group. Scale bar, 210 μm. D–F , Quantitative data of A–C . Data are mean ± SD ( n = 3), compared with vehicle by Student's t test.

    Techniques Used: Allele-specific Oligonucleotide, Expressing, Injection

    Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs attenuates SNL-evoked pain. Rats received the SNL surgery following the baseline (BL) measurement on D0. Mechanical and thermal hypersensitivity developed in the hindpaw at the ipsilateral (ipsi) but not contralateral (contra) side ( A , B ). After intrathecal injection (inj.) of Kv4.3 cDNA ( A , B ) or Kv4.3/KChIP1/DPP10 cDNAs ( C , D ) at the ipsilateral side on D4, mechanical hypersensitivity was attenuated ( A , C ), but thermal hypersensitivity remained ( B , D ). Data are mean ± SEM ( n = 6). * p
    Figure Legend Snippet: Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs attenuates SNL-evoked pain. Rats received the SNL surgery following the baseline (BL) measurement on D0. Mechanical and thermal hypersensitivity developed in the hindpaw at the ipsilateral (ipsi) but not contralateral (contra) side ( A , B ). After intrathecal injection (inj.) of Kv4.3 cDNA ( A , B ) or Kv4.3/KChIP1/DPP10 cDNAs ( C , D ) at the ipsilateral side on D4, mechanical hypersensitivity was attenuated ( A , C ), but thermal hypersensitivity remained ( B , D ). Data are mean ± SEM ( n = 6). * p

    Techniques Used: Injection

    2) Product Images from "K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control"

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p
    Figure Legend Snippet: Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p

    Techniques Used: Injection, Western Blot, Isolation

    KChIP1 or KChIP2 ASO reduces all Kv4 complex components in the DRGs and induces mechanical hypersensitivity. Rats were intrathecally injected with vehicle, LacZ ASO, KChIP1 ASO, or KChIP2 ASO during D1–D3. A , B , KChIP1 ASO induces bilateral mechanical hypersensitivity during D1–D5. Thermal hypersensitivity was not detected. L, Left side; R, right side. Data are mean ± SEM ( n = 6). * p
    Figure Legend Snippet: KChIP1 or KChIP2 ASO reduces all Kv4 complex components in the DRGs and induces mechanical hypersensitivity. Rats were intrathecally injected with vehicle, LacZ ASO, KChIP1 ASO, or KChIP2 ASO during D1–D3. A , B , KChIP1 ASO induces bilateral mechanical hypersensitivity during D1–D5. Thermal hypersensitivity was not detected. L, Left side; R, right side. Data are mean ± SEM ( n = 6). * p

    Techniques Used: Allele-specific Oligonucleotide, Injection

    Intrathecal injection of Kv4.3 ASO reduces all Kv4 complex components in the L4–L6 DRGs. Rats were intrathecally injected with Kv4.3 ASO twice daily for 3 consecutive days (D1–D3) and killed on day 4 (D4) or D7. Rats injected with vehicle (V) or LacZ ASO (Z) were used as controls. A , In the L5 DRG of rats treated with Kv4.3 ASO, Kv4.3-, KChIP1-, KChIP2-, and DPP10-IR were greatly reduced on D4 but returned to the normal levels on D7. Scale bar, 40 μm. B–E , Quantitative data of A . C , C7 DRG. L , L5 DRG. F–I , Western blotting was performed using total proteins ( F , G ) or plasma membrane proteins ( H , I ) isolated from the bilateral L4–L6 DRGs on D4. Kv4.3 ASO treatment reduces Kv4.3, KChIP1, and DPP10 in both protein preparations. Bands of GAPDH and cadherin were loading controls for total proteins and plasma membrane proteins, respectively. Data are mean ± SD ( n = 3). ** p
    Figure Legend Snippet: Intrathecal injection of Kv4.3 ASO reduces all Kv4 complex components in the L4–L6 DRGs. Rats were intrathecally injected with Kv4.3 ASO twice daily for 3 consecutive days (D1–D3) and killed on day 4 (D4) or D7. Rats injected with vehicle (V) or LacZ ASO (Z) were used as controls. A , In the L5 DRG of rats treated with Kv4.3 ASO, Kv4.3-, KChIP1-, KChIP2-, and DPP10-IR were greatly reduced on D4 but returned to the normal levels on D7. Scale bar, 40 μm. B–E , Quantitative data of A . C , C7 DRG. L , L5 DRG. F–I , Western blotting was performed using total proteins ( F , G ) or plasma membrane proteins ( H , I ) isolated from the bilateral L4–L6 DRGs on D4. Kv4.3 ASO treatment reduces Kv4.3, KChIP1, and DPP10 in both protein preparations. Bands of GAPDH and cadherin were loading controls for total proteins and plasma membrane proteins, respectively. Data are mean ± SD ( n = 3). ** p

    Techniques Used: Injection, Allele-specific Oligonucleotide, Western Blot, Isolation

    Detection of a Kv4.3/KChIP1/KChIP2/DPP10 complex in the DRG. Total proteins (Total), plasma membrane proteins (PM), and rough ER proteins (rER) were isolated from rat lumbar DRGs, respectively. A , Representative Western blot data show Kv4.3, KChIP1, KChIP2, and DPP10 in each protein preparation. Cadherin and calnexin are markers for the PM and rER, respectively. The purity of PM proteins was confirmed by the presence of cadherin and the absence of calnexin, whereas the purity of rER proteins was confirmed by the presence of calnexin and the absence of cadherin. B , C , In addition to immunoprecipitation of Kv4.3, rabbit anti-Kv4.3 antibody (α-Kv4.3) coimmunoprecipitates KChIP1, KChIP2, and DPP10 from the PM proteins ( B ) and rER proteins ( C ), respectively. Nonspecific rabbit IgG was used as a control of immunoprecipitation, and “extract” indicates a bead-only loading control.
    Figure Legend Snippet: Detection of a Kv4.3/KChIP1/KChIP2/DPP10 complex in the DRG. Total proteins (Total), plasma membrane proteins (PM), and rough ER proteins (rER) were isolated from rat lumbar DRGs, respectively. A , Representative Western blot data show Kv4.3, KChIP1, KChIP2, and DPP10 in each protein preparation. Cadherin and calnexin are markers for the PM and rER, respectively. The purity of PM proteins was confirmed by the presence of cadherin and the absence of calnexin, whereas the purity of rER proteins was confirmed by the presence of calnexin and the absence of cadherin. B , C , In addition to immunoprecipitation of Kv4.3, rabbit anti-Kv4.3 antibody (α-Kv4.3) coimmunoprecipitates KChIP1, KChIP2, and DPP10 from the PM proteins ( B ) and rER proteins ( C ), respectively. Nonspecific rabbit IgG was used as a control of immunoprecipitation, and “extract” indicates a bead-only loading control.

    Techniques Used: Isolation, Western Blot, Immunoprecipitation

    The excitability of IB4 + nociceptors is enhanced after knockdown of Kv4.3, KChIP1, or DPP10. FAM-tagged ASO for LacZ, Kv4.3, KChIP1, or DPP10 was intrathecally injected into the rat by lumbar puncture, and the bilateral L4–L6 DRGs were isolated 5 h later. DRG neurons were dissociated and cultured for 20–24 h before whole-cell patch-clamp recording. A , Top, Only small DRG neurons (soma diameter ≤ 30 μm; bright-field, BF) with both FAM (green) and Alexa594-conjugated IB4 (red) signals were analyzed. Scale bar, 20 μm. Bottom, Responses to the depolarizing current pulses (100 and 300 pA; 1 s). B , The resting membrane potential (Vrest) in each ASO group. n = 9–12 as indicated in D . * p
    Figure Legend Snippet: The excitability of IB4 + nociceptors is enhanced after knockdown of Kv4.3, KChIP1, or DPP10. FAM-tagged ASO for LacZ, Kv4.3, KChIP1, or DPP10 was intrathecally injected into the rat by lumbar puncture, and the bilateral L4–L6 DRGs were isolated 5 h later. DRG neurons were dissociated and cultured for 20–24 h before whole-cell patch-clamp recording. A , Top, Only small DRG neurons (soma diameter ≤ 30 μm; bright-field, BF) with both FAM (green) and Alexa594-conjugated IB4 (red) signals were analyzed. Scale bar, 20 μm. Bottom, Responses to the depolarizing current pulses (100 and 300 pA; 1 s). B , The resting membrane potential (Vrest) in each ASO group. n = 9–12 as indicated in D . * p

    Techniques Used: Allele-specific Oligonucleotide, Injection, Isolation, Cell Culture, Patch Clamp

    Intrathecal cDNA injection does not suppress SNL-evoked glial activation and macrophage proliferation in the injured DRGs. Rats were intrathecally injected with Kv4.3/KChP1/DPP10 cDNAs on D4 and killed on D7 or D14 after SNL. A , Sections of the ipsilateral L5 DRG were immunostained for GFAP and Iba1, respectively. Scale bar, 48 μm. B , C , Quantitative data of A . GFAP + or Iba1 + area shows no significant difference (N.S.) between SNL rats and the SNL rats treated with Kv4.3/KChIP1/DPP10 cDNAs. Data are mean ± SD ( n = 3), compared with SNL on the same day by Student's t test.
    Figure Legend Snippet: Intrathecal cDNA injection does not suppress SNL-evoked glial activation and macrophage proliferation in the injured DRGs. Rats were intrathecally injected with Kv4.3/KChP1/DPP10 cDNAs on D4 and killed on D7 or D14 after SNL. A , Sections of the ipsilateral L5 DRG were immunostained for GFAP and Iba1, respectively. Scale bar, 48 μm. B , C , Quantitative data of A . GFAP + or Iba1 + area shows no significant difference (N.S.) between SNL rats and the SNL rats treated with Kv4.3/KChIP1/DPP10 cDNAs. Data are mean ± SD ( n = 3), compared with SNL on the same day by Student's t test.

    Techniques Used: Injection, Activation Assay

    Intrathecal ASO injections do not affect KChIP1, KChIP2, and DPP10 expression in the spinal cord. Rats were intrathecally injected with ASO for LacZ (Z), Kv4.3, KChIP1, KChIP2, or DPP10 during D1–D3 and killed on D4. Sections of the L5 spinal cord segment were immunostained. A–C , KChIP1-, KChIP2-, or DPP10-IR in the dorsal spinal cord (on either side) is similar between each ASO group and the vehicle (V) group. Scale bar, 210 μm. D–F , Quantitative data of A–C . Data are mean ± SD ( n = 3), compared with vehicle by Student's t test.
    Figure Legend Snippet: Intrathecal ASO injections do not affect KChIP1, KChIP2, and DPP10 expression in the spinal cord. Rats were intrathecally injected with ASO for LacZ (Z), Kv4.3, KChIP1, KChIP2, or DPP10 during D1–D3 and killed on D4. Sections of the L5 spinal cord segment were immunostained. A–C , KChIP1-, KChIP2-, or DPP10-IR in the dorsal spinal cord (on either side) is similar between each ASO group and the vehicle (V) group. Scale bar, 210 μm. D–F , Quantitative data of A–C . Data are mean ± SD ( n = 3), compared with vehicle by Student's t test.

    Techniques Used: Allele-specific Oligonucleotide, Expressing, Injection

    Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs attenuates SNL-evoked pain. Rats received the SNL surgery following the baseline (BL) measurement on D0. Mechanical and thermal hypersensitivity developed in the hindpaw at the ipsilateral (ipsi) but not contralateral (contra) side ( A , B ). After intrathecal injection (inj.) of Kv4.3 cDNA ( A , B ) or Kv4.3/KChIP1/DPP10 cDNAs ( C , D ) at the ipsilateral side on D4, mechanical hypersensitivity was attenuated ( A , C ), but thermal hypersensitivity remained ( B , D ). Data are mean ± SEM ( n = 6). * p
    Figure Legend Snippet: Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs attenuates SNL-evoked pain. Rats received the SNL surgery following the baseline (BL) measurement on D0. Mechanical and thermal hypersensitivity developed in the hindpaw at the ipsilateral (ipsi) but not contralateral (contra) side ( A , B ). After intrathecal injection (inj.) of Kv4.3 cDNA ( A , B ) or Kv4.3/KChIP1/DPP10 cDNAs ( C , D ) at the ipsilateral side on D4, mechanical hypersensitivity was attenuated ( A , C ), but thermal hypersensitivity remained ( B , D ). Data are mean ± SEM ( n = 6). * p

    Techniques Used: Injection

    3) Product Images from "Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation"

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    Journal: Nature Communications

    doi: 10.1038/ncomms10190

    Atrial APDs of KCNIP1-knockdown or overexpression hearts are comparable to control hearts. ( a ) Representative atrial action potentials of KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts at a baseline pacing rate of 188 beats per min. Action potentials were recorded by using the microelectrode and disrupted patch method. ( b ) Quantification of atrial APD at 90% repolarization. The mean APD was comparable between KCNIP1 MO, KCNIP1 OE and the CTL hearts. N =3 experiments for each group. Error bars, s.d. Mann–Whitney U -test.
    Figure Legend Snippet: Atrial APDs of KCNIP1-knockdown or overexpression hearts are comparable to control hearts. ( a ) Representative atrial action potentials of KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts at a baseline pacing rate of 188 beats per min. Action potentials were recorded by using the microelectrode and disrupted patch method. ( b ) Quantification of atrial APD at 90% repolarization. The mean APD was comparable between KCNIP1 MO, KCNIP1 OE and the CTL hearts. N =3 experiments for each group. Error bars, s.d. Mann–Whitney U -test.

    Techniques Used: Over Expression, CTL Assay, MANN-WHITNEY

    Individuals with insertion in intron 1 of KCNIP1 have a higher KCNIP1 mRNA expression. ( a ) Top panel: The detection of insertion/deletion in intron 1 of human KCNIP1 was performed by PCR amplification of genomic DNA with primers targeting the sequences within the CNV segment in intron 1 of human KCNIP1 . No PCR band indicates homozygous deletion (copy number (CN)=0) (patients 1–4, 9 and 10); the presence of one PCR band (479 bp) indicates homozygous insertion (CN=2)(patients 5–8). Middle and lower panels: KCNIP1 and GAPDH mRNA expressions were semiquantified by PCR with reverse transcription and visualized by electrophoresis. White blood cell mRNA samples from those with KCNIP1 intron homozygous insertion (patients 5–8) show higher PCR band density, indicating a higher KCNIP1 mRNA level. Arrows indicate the locations of PCR bands. ( b ) Quantification of KCNIP1 expression (normalized to GAPDH) in patients with CN=0 and those with CN=2. Data are representative of three independent experiments. Error bars, s.d. Mann–Whitney U -test; * P
    Figure Legend Snippet: Individuals with insertion in intron 1 of KCNIP1 have a higher KCNIP1 mRNA expression. ( a ) Top panel: The detection of insertion/deletion in intron 1 of human KCNIP1 was performed by PCR amplification of genomic DNA with primers targeting the sequences within the CNV segment in intron 1 of human KCNIP1 . No PCR band indicates homozygous deletion (copy number (CN)=0) (patients 1–4, 9 and 10); the presence of one PCR band (479 bp) indicates homozygous insertion (CN=2)(patients 5–8). Middle and lower panels: KCNIP1 and GAPDH mRNA expressions were semiquantified by PCR with reverse transcription and visualized by electrophoresis. White blood cell mRNA samples from those with KCNIP1 intron homozygous insertion (patients 5–8) show higher PCR band density, indicating a higher KCNIP1 mRNA level. Arrows indicate the locations of PCR bands. ( b ) Quantification of KCNIP1 expression (normalized to GAPDH) in patients with CN=0 and those with CN=2. Data are representative of three independent experiments. Error bars, s.d. Mann–Whitney U -test; * P

    Techniques Used: Expressing, Polymerase Chain Reaction, Amplification, Electrophoresis, MANN-WHITNEY

    Co-immunoprecipitation shows a biochemical association between KCHIP1 and KV4.2/4.3. ( a , b ) Tissue samples from adult rat heart were lysed and immunoprecipitated (IP) with anti-KCHIP1. The membranes were then immunoblotted (IB) using anti-KV4.2/4.3 ( a ) and anti-Cav1.2 ( b ). Beads conjugated with IgG isotype were used as negative control (NC). There is a biochemical association between KCHIP1 and KV4.2/4.3 ( a ), but no association between KCHIP1 and Cav1.2 ( b ). Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 6 .
    Figure Legend Snippet: Co-immunoprecipitation shows a biochemical association between KCHIP1 and KV4.2/4.3. ( a , b ) Tissue samples from adult rat heart were lysed and immunoprecipitated (IP) with anti-KCHIP1. The membranes were then immunoblotted (IB) using anti-KV4.2/4.3 ( a ) and anti-Cav1.2 ( b ). Beads conjugated with IgG isotype were used as negative control (NC). There is a biochemical association between KCHIP1 and KV4.2/4.3 ( a ), but no association between KCHIP1 and Cav1.2 ( b ). Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 6 .

    Techniques Used: Immunoprecipitation, Negative Control

    KCNIP1 -knockdown and overexpression modulates APD shortening at high atrial rates. ( a ) Representative atrial action potential tracings at increasing pacing rates for KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts are shown. At pacing cycle length (PCL) 200 ms, the CTL and KCNIP1 -overexpression hearts could sustain 1 to 1 pacing rate, but the KCNIP1 -knockdown heart could not, and 2 to 1 capture is noted, indicating that the KCNIP1 -knockdown heart could not maintain as higher rates as the CTL heart. At even shorter PCL (170 ms), only the KCNIP1 -overexpression heart could sustain 1 to 1 high pacing rate, but the KCNIP1 -knockdown and CTL hearts could not (2 to 1 capture), indicating that the KCNIP1 -overexpression heart could maintain higher rates than the CTL heart. Interestingly, at this high-rate pacing, atrial tachyarrhythmia or AF could be induced in the KCNIP1 -overexpression heart. ( b ) Summary data for three independent experiments demonstrating the relationship of PCL and APD from CTL, KCNIP1 -knockdown and overexpression hearts are shown. With increasing rate (decreased PCL), APD shortens accordingly to facilitate maintenance of high rate in all the three groups. However, less APD shortening is observed in the KCNIP1 -knockdown hearts. The maximal pacing rate is lower in the KCNIP1 -knockdown hearts and higher in the KCNIP1 -overexpression hearts, compared to that of the CTL hearts. N =3 experiments for each group. Error bars, s.d.
    Figure Legend Snippet: KCNIP1 -knockdown and overexpression modulates APD shortening at high atrial rates. ( a ) Representative atrial action potential tracings at increasing pacing rates for KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts are shown. At pacing cycle length (PCL) 200 ms, the CTL and KCNIP1 -overexpression hearts could sustain 1 to 1 pacing rate, but the KCNIP1 -knockdown heart could not, and 2 to 1 capture is noted, indicating that the KCNIP1 -knockdown heart could not maintain as higher rates as the CTL heart. At even shorter PCL (170 ms), only the KCNIP1 -overexpression heart could sustain 1 to 1 high pacing rate, but the KCNIP1 -knockdown and CTL hearts could not (2 to 1 capture), indicating that the KCNIP1 -overexpression heart could maintain higher rates than the CTL heart. Interestingly, at this high-rate pacing, atrial tachyarrhythmia or AF could be induced in the KCNIP1 -overexpression heart. ( b ) Summary data for three independent experiments demonstrating the relationship of PCL and APD from CTL, KCNIP1 -knockdown and overexpression hearts are shown. With increasing rate (decreased PCL), APD shortens accordingly to facilitate maintenance of high rate in all the three groups. However, less APD shortening is observed in the KCNIP1 -knockdown hearts. The maximal pacing rate is lower in the KCNIP1 -knockdown hearts and higher in the KCNIP1 -overexpression hearts, compared to that of the CTL hearts. N =3 experiments for each group. Error bars, s.d.

    Techniques Used: Over Expression, CTL Assay, Mass Spectrometry

    Knockdown of KCNIP1 downregulates transient outward currents in atrial myocytes. ( a ) Transient outward current (Ito) was obtained by a family of depolarization steps from −80 mV, and was measured as the 4-aminopyridine (4-AP)-sensitive peak current (10 mM). (left upper) Voltage protocol. Right panel shows the representative recordings of 4-AP sensitive currents of the control (CTL) and KCNIP1 knockdown (KCNIP1 KD) atrial myocytes, respectively. (left lower) Efficiency of knockdown represented by decreased KCHIP1 protein level. ( b ) Representative current density–voltage relationships of 4-AP sensitive currents in CTL and KCNIP1 KD atrial myocytes. N =3 experiments for each group. Error bars, s.d. Full-length blots are presented in Supplementary Fig. 7 .
    Figure Legend Snippet: Knockdown of KCNIP1 downregulates transient outward currents in atrial myocytes. ( a ) Transient outward current (Ito) was obtained by a family of depolarization steps from −80 mV, and was measured as the 4-aminopyridine (4-AP)-sensitive peak current (10 mM). (left upper) Voltage protocol. Right panel shows the representative recordings of 4-AP sensitive currents of the control (CTL) and KCNIP1 knockdown (KCNIP1 KD) atrial myocytes, respectively. (left lower) Efficiency of knockdown represented by decreased KCHIP1 protein level. ( b ) Representative current density–voltage relationships of 4-AP sensitive currents in CTL and KCNIP1 KD atrial myocytes. N =3 experiments for each group. Error bars, s.d. Full-length blots are presented in Supplementary Fig. 7 .

    Techniques Used: CTL Assay

    Basal expressions of KCNIP s in the mammalian heart. Total RNA was isolated and PCR with reverse transcription (RT-PCR) products with primer pairs specific to rat KCNIP s were visualized by electrophoresis. ( a ) The RT-PCR results of a positive control for KCNIP1-4 (K1-4) from a representative sample of rat brain. ( b ) The RT-PCR results of representative left atrium (LA), right atrium (RA), left ventricle (LV) and right ventricle (RV). KCNIP1-3 mRNAs could be detected in the mammalian LA, RA, LV and RV. GP, glyceraldehyde 3-phosphate dehydrogenase; M, molecular weight maker. Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 4 .
    Figure Legend Snippet: Basal expressions of KCNIP s in the mammalian heart. Total RNA was isolated and PCR with reverse transcription (RT-PCR) products with primer pairs specific to rat KCNIP s were visualized by electrophoresis. ( a ) The RT-PCR results of a positive control for KCNIP1-4 (K1-4) from a representative sample of rat brain. ( b ) The RT-PCR results of representative left atrium (LA), right atrium (RA), left ventricle (LV) and right ventricle (RV). KCNIP1-3 mRNAs could be detected in the mammalian LA, RA, LV and RV. GP, glyceraldehyde 3-phosphate dehydrogenase; M, molecular weight maker. Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 4 .

    Techniques Used: Isolation, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Electrophoresis, Positive Control, Molecular Weight

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    Alomone Labs rabbit anti kchip1
    Intrathecal injection of <t>Kv4.3/KChIP1/DPP10</t> cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p
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    Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs rescues SNL-evoked Kv4 complex downregulation in the injured DRGs. Rats were killed on D7 after sham operation, SNL, SNL with Kv4.3 cDNA injection (SNL + Kv4.3) on D4, or SNL with coinjection of Kv4.3/KChIP1/DPP10 cDNAs (SNL + Kv4.3/KChIP1/DPP10) on D4. A , The ipsilateral L5 DRG was immunostained for Kv4.3, KChIP1, or DPP10. Scale bar, 40 μm. B , Quantification of IR in A . C–F , Western blotting was performed using total proteins ( C , D ) or plasma membrane proteins ( E , F ) isolated from the ipsilateral L5/L6 DRGs, respectively. Data are mean ± SD ( n = 3). * p

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Injection, Western Blot, Isolation

    KChIP1 or KChIP2 ASO reduces all Kv4 complex components in the DRGs and induces mechanical hypersensitivity. Rats were intrathecally injected with vehicle, LacZ ASO, KChIP1 ASO, or KChIP2 ASO during D1–D3. A , B , KChIP1 ASO induces bilateral mechanical hypersensitivity during D1–D5. Thermal hypersensitivity was not detected. L, Left side; R, right side. Data are mean ± SEM ( n = 6). * p

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: KChIP1 or KChIP2 ASO reduces all Kv4 complex components in the DRGs and induces mechanical hypersensitivity. Rats were intrathecally injected with vehicle, LacZ ASO, KChIP1 ASO, or KChIP2 ASO during D1–D3. A , B , KChIP1 ASO induces bilateral mechanical hypersensitivity during D1–D5. Thermal hypersensitivity was not detected. L, Left side; R, right side. Data are mean ± SEM ( n = 6). * p

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Allele-specific Oligonucleotide, Injection

    Intrathecal injection of Kv4.3 ASO reduces all Kv4 complex components in the L4–L6 DRGs. Rats were intrathecally injected with Kv4.3 ASO twice daily for 3 consecutive days (D1–D3) and killed on day 4 (D4) or D7. Rats injected with vehicle (V) or LacZ ASO (Z) were used as controls. A , In the L5 DRG of rats treated with Kv4.3 ASO, Kv4.3-, KChIP1-, KChIP2-, and DPP10-IR were greatly reduced on D4 but returned to the normal levels on D7. Scale bar, 40 μm. B–E , Quantitative data of A . C , C7 DRG. L , L5 DRG. F–I , Western blotting was performed using total proteins ( F , G ) or plasma membrane proteins ( H , I ) isolated from the bilateral L4–L6 DRGs on D4. Kv4.3 ASO treatment reduces Kv4.3, KChIP1, and DPP10 in both protein preparations. Bands of GAPDH and cadherin were loading controls for total proteins and plasma membrane proteins, respectively. Data are mean ± SD ( n = 3). ** p

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: Intrathecal injection of Kv4.3 ASO reduces all Kv4 complex components in the L4–L6 DRGs. Rats were intrathecally injected with Kv4.3 ASO twice daily for 3 consecutive days (D1–D3) and killed on day 4 (D4) or D7. Rats injected with vehicle (V) or LacZ ASO (Z) were used as controls. A , In the L5 DRG of rats treated with Kv4.3 ASO, Kv4.3-, KChIP1-, KChIP2-, and DPP10-IR were greatly reduced on D4 but returned to the normal levels on D7. Scale bar, 40 μm. B–E , Quantitative data of A . C , C7 DRG. L , L5 DRG. F–I , Western blotting was performed using total proteins ( F , G ) or plasma membrane proteins ( H , I ) isolated from the bilateral L4–L6 DRGs on D4. Kv4.3 ASO treatment reduces Kv4.3, KChIP1, and DPP10 in both protein preparations. Bands of GAPDH and cadherin were loading controls for total proteins and plasma membrane proteins, respectively. Data are mean ± SD ( n = 3). ** p

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Injection, Allele-specific Oligonucleotide, Western Blot, Isolation

    Detection of a Kv4.3/KChIP1/KChIP2/DPP10 complex in the DRG. Total proteins (Total), plasma membrane proteins (PM), and rough ER proteins (rER) were isolated from rat lumbar DRGs, respectively. A , Representative Western blot data show Kv4.3, KChIP1, KChIP2, and DPP10 in each protein preparation. Cadherin and calnexin are markers for the PM and rER, respectively. The purity of PM proteins was confirmed by the presence of cadherin and the absence of calnexin, whereas the purity of rER proteins was confirmed by the presence of calnexin and the absence of cadherin. B , C , In addition to immunoprecipitation of Kv4.3, rabbit anti-Kv4.3 antibody (α-Kv4.3) coimmunoprecipitates KChIP1, KChIP2, and DPP10 from the PM proteins ( B ) and rER proteins ( C ), respectively. Nonspecific rabbit IgG was used as a control of immunoprecipitation, and “extract” indicates a bead-only loading control.

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: Detection of a Kv4.3/KChIP1/KChIP2/DPP10 complex in the DRG. Total proteins (Total), plasma membrane proteins (PM), and rough ER proteins (rER) were isolated from rat lumbar DRGs, respectively. A , Representative Western blot data show Kv4.3, KChIP1, KChIP2, and DPP10 in each protein preparation. Cadherin and calnexin are markers for the PM and rER, respectively. The purity of PM proteins was confirmed by the presence of cadherin and the absence of calnexin, whereas the purity of rER proteins was confirmed by the presence of calnexin and the absence of cadherin. B , C , In addition to immunoprecipitation of Kv4.3, rabbit anti-Kv4.3 antibody (α-Kv4.3) coimmunoprecipitates KChIP1, KChIP2, and DPP10 from the PM proteins ( B ) and rER proteins ( C ), respectively. Nonspecific rabbit IgG was used as a control of immunoprecipitation, and “extract” indicates a bead-only loading control.

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Isolation, Western Blot, Immunoprecipitation

    The excitability of IB4 + nociceptors is enhanced after knockdown of Kv4.3, KChIP1, or DPP10. FAM-tagged ASO for LacZ, Kv4.3, KChIP1, or DPP10 was intrathecally injected into the rat by lumbar puncture, and the bilateral L4–L6 DRGs were isolated 5 h later. DRG neurons were dissociated and cultured for 20–24 h before whole-cell patch-clamp recording. A , Top, Only small DRG neurons (soma diameter ≤ 30 μm; bright-field, BF) with both FAM (green) and Alexa594-conjugated IB4 (red) signals were analyzed. Scale bar, 20 μm. Bottom, Responses to the depolarizing current pulses (100 and 300 pA; 1 s). B , The resting membrane potential (Vrest) in each ASO group. n = 9–12 as indicated in D . * p

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: The excitability of IB4 + nociceptors is enhanced after knockdown of Kv4.3, KChIP1, or DPP10. FAM-tagged ASO for LacZ, Kv4.3, KChIP1, or DPP10 was intrathecally injected into the rat by lumbar puncture, and the bilateral L4–L6 DRGs were isolated 5 h later. DRG neurons were dissociated and cultured for 20–24 h before whole-cell patch-clamp recording. A , Top, Only small DRG neurons (soma diameter ≤ 30 μm; bright-field, BF) with both FAM (green) and Alexa594-conjugated IB4 (red) signals were analyzed. Scale bar, 20 μm. Bottom, Responses to the depolarizing current pulses (100 and 300 pA; 1 s). B , The resting membrane potential (Vrest) in each ASO group. n = 9–12 as indicated in D . * p

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Allele-specific Oligonucleotide, Injection, Isolation, Cell Culture, Patch Clamp

    Intrathecal cDNA injection does not suppress SNL-evoked glial activation and macrophage proliferation in the injured DRGs. Rats were intrathecally injected with Kv4.3/KChP1/DPP10 cDNAs on D4 and killed on D7 or D14 after SNL. A , Sections of the ipsilateral L5 DRG were immunostained for GFAP and Iba1, respectively. Scale bar, 48 μm. B , C , Quantitative data of A . GFAP + or Iba1 + area shows no significant difference (N.S.) between SNL rats and the SNL rats treated with Kv4.3/KChIP1/DPP10 cDNAs. Data are mean ± SD ( n = 3), compared with SNL on the same day by Student's t test.

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: Intrathecal cDNA injection does not suppress SNL-evoked glial activation and macrophage proliferation in the injured DRGs. Rats were intrathecally injected with Kv4.3/KChP1/DPP10 cDNAs on D4 and killed on D7 or D14 after SNL. A , Sections of the ipsilateral L5 DRG were immunostained for GFAP and Iba1, respectively. Scale bar, 48 μm. B , C , Quantitative data of A . GFAP + or Iba1 + area shows no significant difference (N.S.) between SNL rats and the SNL rats treated with Kv4.3/KChIP1/DPP10 cDNAs. Data are mean ± SD ( n = 3), compared with SNL on the same day by Student's t test.

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Injection, Activation Assay

    Intrathecal ASO injections do not affect KChIP1, KChIP2, and DPP10 expression in the spinal cord. Rats were intrathecally injected with ASO for LacZ (Z), Kv4.3, KChIP1, KChIP2, or DPP10 during D1–D3 and killed on D4. Sections of the L5 spinal cord segment were immunostained. A–C , KChIP1-, KChIP2-, or DPP10-IR in the dorsal spinal cord (on either side) is similar between each ASO group and the vehicle (V) group. Scale bar, 210 μm. D–F , Quantitative data of A–C . Data are mean ± SD ( n = 3), compared with vehicle by Student's t test.

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: Intrathecal ASO injections do not affect KChIP1, KChIP2, and DPP10 expression in the spinal cord. Rats were intrathecally injected with ASO for LacZ (Z), Kv4.3, KChIP1, KChIP2, or DPP10 during D1–D3 and killed on D4. Sections of the L5 spinal cord segment were immunostained. A–C , KChIP1-, KChIP2-, or DPP10-IR in the dorsal spinal cord (on either side) is similar between each ASO group and the vehicle (V) group. Scale bar, 210 μm. D–F , Quantitative data of A–C . Data are mean ± SD ( n = 3), compared with vehicle by Student's t test.

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Allele-specific Oligonucleotide, Expressing, Injection

    Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs attenuates SNL-evoked pain. Rats received the SNL surgery following the baseline (BL) measurement on D0. Mechanical and thermal hypersensitivity developed in the hindpaw at the ipsilateral (ipsi) but not contralateral (contra) side ( A , B ). After intrathecal injection (inj.) of Kv4.3 cDNA ( A , B ) or Kv4.3/KChIP1/DPP10 cDNAs ( C , D ) at the ipsilateral side on D4, mechanical hypersensitivity was attenuated ( A , C ), but thermal hypersensitivity remained ( B , D ). Data are mean ± SEM ( n = 6). * p

    Journal: The Journal of Neuroscience

    Article Title: K+ Channel Modulatory Subunits KChIP and DPP Participate in Kv4-Mediated Mechanical Pain Control

    doi: 10.1523/JNEUROSCI.1619-16.2017

    Figure Lengend Snippet: Intrathecal injection of Kv4.3/KChIP1/DPP10 cDNAs attenuates SNL-evoked pain. Rats received the SNL surgery following the baseline (BL) measurement on D0. Mechanical and thermal hypersensitivity developed in the hindpaw at the ipsilateral (ipsi) but not contralateral (contra) side ( A , B ). After intrathecal injection (inj.) of Kv4.3 cDNA ( A , B ) or Kv4.3/KChIP1/DPP10 cDNAs ( C , D ) at the ipsilateral side on D4, mechanical hypersensitivity was attenuated ( A , C ), but thermal hypersensitivity remained ( B , D ). Data are mean ± SEM ( n = 6). * p

    Article Snippet: Primary antibodies and their dilution factors were mouse anti-cadherin (1:500; Sigma catalog #C1821, RRID:AB_476826), goat anti-calnexin (1:500; Santa Cruz Biotechnology catalog #sc6465, RRID:AB_2069146), rabbit anti-DPP10 (1:500; customer made by GeneTex, RRID:AB_236936), rabbit anti-GAPDH (1:5000; GeneTex catalog #GTX100118, RRID:AB_1080976), rabbit anti-KChIP1 (1:500; Alomone Labs catalog #APC-141, RRID:AB_10917754), mouse anti-KChIP2 (1:400; NeuroMab catalog #75-004, RRID:AB_2280942), and rabbit anti-Kv4.3 (1:500; customer made by GeneTex, RRID:AB_845371).

    Techniques: Injection

    Atrial APDs of KCNIP1-knockdown or overexpression hearts are comparable to control hearts. ( a ) Representative atrial action potentials of KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts at a baseline pacing rate of 188 beats per min. Action potentials were recorded by using the microelectrode and disrupted patch method. ( b ) Quantification of atrial APD at 90% repolarization. The mean APD was comparable between KCNIP1 MO, KCNIP1 OE and the CTL hearts. N =3 experiments for each group. Error bars, s.d. Mann–Whitney U -test.

    Journal: Nature Communications

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    doi: 10.1038/ncomms10190

    Figure Lengend Snippet: Atrial APDs of KCNIP1-knockdown or overexpression hearts are comparable to control hearts. ( a ) Representative atrial action potentials of KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts at a baseline pacing rate of 188 beats per min. Action potentials were recorded by using the microelectrode and disrupted patch method. ( b ) Quantification of atrial APD at 90% repolarization. The mean APD was comparable between KCNIP1 MO, KCNIP1 OE and the CTL hearts. N =3 experiments for each group. Error bars, s.d. Mann–Whitney U -test.

    Article Snippet: For immunoprecipitation , protein lysates were incubated with 1 μg ml−1 of the anti-KCHIP1 antibody (Alomone Labs) overnight at 4 °C.

    Techniques: Over Expression, CTL Assay, MANN-WHITNEY

    Individuals with insertion in intron 1 of KCNIP1 have a higher KCNIP1 mRNA expression. ( a ) Top panel: The detection of insertion/deletion in intron 1 of human KCNIP1 was performed by PCR amplification of genomic DNA with primers targeting the sequences within the CNV segment in intron 1 of human KCNIP1 . No PCR band indicates homozygous deletion (copy number (CN)=0) (patients 1–4, 9 and 10); the presence of one PCR band (479 bp) indicates homozygous insertion (CN=2)(patients 5–8). Middle and lower panels: KCNIP1 and GAPDH mRNA expressions were semiquantified by PCR with reverse transcription and visualized by electrophoresis. White blood cell mRNA samples from those with KCNIP1 intron homozygous insertion (patients 5–8) show higher PCR band density, indicating a higher KCNIP1 mRNA level. Arrows indicate the locations of PCR bands. ( b ) Quantification of KCNIP1 expression (normalized to GAPDH) in patients with CN=0 and those with CN=2. Data are representative of three independent experiments. Error bars, s.d. Mann–Whitney U -test; * P

    Journal: Nature Communications

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    doi: 10.1038/ncomms10190

    Figure Lengend Snippet: Individuals with insertion in intron 1 of KCNIP1 have a higher KCNIP1 mRNA expression. ( a ) Top panel: The detection of insertion/deletion in intron 1 of human KCNIP1 was performed by PCR amplification of genomic DNA with primers targeting the sequences within the CNV segment in intron 1 of human KCNIP1 . No PCR band indicates homozygous deletion (copy number (CN)=0) (patients 1–4, 9 and 10); the presence of one PCR band (479 bp) indicates homozygous insertion (CN=2)(patients 5–8). Middle and lower panels: KCNIP1 and GAPDH mRNA expressions were semiquantified by PCR with reverse transcription and visualized by electrophoresis. White blood cell mRNA samples from those with KCNIP1 intron homozygous insertion (patients 5–8) show higher PCR band density, indicating a higher KCNIP1 mRNA level. Arrows indicate the locations of PCR bands. ( b ) Quantification of KCNIP1 expression (normalized to GAPDH) in patients with CN=0 and those with CN=2. Data are representative of three independent experiments. Error bars, s.d. Mann–Whitney U -test; * P

    Article Snippet: For immunoprecipitation , protein lysates were incubated with 1 μg ml−1 of the anti-KCHIP1 antibody (Alomone Labs) overnight at 4 °C.

    Techniques: Expressing, Polymerase Chain Reaction, Amplification, Electrophoresis, MANN-WHITNEY

    Co-immunoprecipitation shows a biochemical association between KCHIP1 and KV4.2/4.3. ( a , b ) Tissue samples from adult rat heart were lysed and immunoprecipitated (IP) with anti-KCHIP1. The membranes were then immunoblotted (IB) using anti-KV4.2/4.3 ( a ) and anti-Cav1.2 ( b ). Beads conjugated with IgG isotype were used as negative control (NC). There is a biochemical association between KCHIP1 and KV4.2/4.3 ( a ), but no association between KCHIP1 and Cav1.2 ( b ). Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 6 .

    Journal: Nature Communications

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    doi: 10.1038/ncomms10190

    Figure Lengend Snippet: Co-immunoprecipitation shows a biochemical association between KCHIP1 and KV4.2/4.3. ( a , b ) Tissue samples from adult rat heart were lysed and immunoprecipitated (IP) with anti-KCHIP1. The membranes were then immunoblotted (IB) using anti-KV4.2/4.3 ( a ) and anti-Cav1.2 ( b ). Beads conjugated with IgG isotype were used as negative control (NC). There is a biochemical association between KCHIP1 and KV4.2/4.3 ( a ), but no association between KCHIP1 and Cav1.2 ( b ). Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 6 .

    Article Snippet: For immunoprecipitation , protein lysates were incubated with 1 μg ml−1 of the anti-KCHIP1 antibody (Alomone Labs) overnight at 4 °C.

    Techniques: Immunoprecipitation, Negative Control

    KCNIP1 -knockdown and overexpression modulates APD shortening at high atrial rates. ( a ) Representative atrial action potential tracings at increasing pacing rates for KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts are shown. At pacing cycle length (PCL) 200 ms, the CTL and KCNIP1 -overexpression hearts could sustain 1 to 1 pacing rate, but the KCNIP1 -knockdown heart could not, and 2 to 1 capture is noted, indicating that the KCNIP1 -knockdown heart could not maintain as higher rates as the CTL heart. At even shorter PCL (170 ms), only the KCNIP1 -overexpression heart could sustain 1 to 1 high pacing rate, but the KCNIP1 -knockdown and CTL hearts could not (2 to 1 capture), indicating that the KCNIP1 -overexpression heart could maintain higher rates than the CTL heart. Interestingly, at this high-rate pacing, atrial tachyarrhythmia or AF could be induced in the KCNIP1 -overexpression heart. ( b ) Summary data for three independent experiments demonstrating the relationship of PCL and APD from CTL, KCNIP1 -knockdown and overexpression hearts are shown. With increasing rate (decreased PCL), APD shortens accordingly to facilitate maintenance of high rate in all the three groups. However, less APD shortening is observed in the KCNIP1 -knockdown hearts. The maximal pacing rate is lower in the KCNIP1 -knockdown hearts and higher in the KCNIP1 -overexpression hearts, compared to that of the CTL hearts. N =3 experiments for each group. Error bars, s.d.

    Journal: Nature Communications

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    doi: 10.1038/ncomms10190

    Figure Lengend Snippet: KCNIP1 -knockdown and overexpression modulates APD shortening at high atrial rates. ( a ) Representative atrial action potential tracings at increasing pacing rates for KCNIP1 -knockdown (KCNIP1 MO), overexpression (KCNIP1 OE) and control (CTL) hearts are shown. At pacing cycle length (PCL) 200 ms, the CTL and KCNIP1 -overexpression hearts could sustain 1 to 1 pacing rate, but the KCNIP1 -knockdown heart could not, and 2 to 1 capture is noted, indicating that the KCNIP1 -knockdown heart could not maintain as higher rates as the CTL heart. At even shorter PCL (170 ms), only the KCNIP1 -overexpression heart could sustain 1 to 1 high pacing rate, but the KCNIP1 -knockdown and CTL hearts could not (2 to 1 capture), indicating that the KCNIP1 -overexpression heart could maintain higher rates than the CTL heart. Interestingly, at this high-rate pacing, atrial tachyarrhythmia or AF could be induced in the KCNIP1 -overexpression heart. ( b ) Summary data for three independent experiments demonstrating the relationship of PCL and APD from CTL, KCNIP1 -knockdown and overexpression hearts are shown. With increasing rate (decreased PCL), APD shortens accordingly to facilitate maintenance of high rate in all the three groups. However, less APD shortening is observed in the KCNIP1 -knockdown hearts. The maximal pacing rate is lower in the KCNIP1 -knockdown hearts and higher in the KCNIP1 -overexpression hearts, compared to that of the CTL hearts. N =3 experiments for each group. Error bars, s.d.

    Article Snippet: For immunoprecipitation , protein lysates were incubated with 1 μg ml−1 of the anti-KCHIP1 antibody (Alomone Labs) overnight at 4 °C.

    Techniques: Over Expression, CTL Assay, Mass Spectrometry

    Knockdown of KCNIP1 downregulates transient outward currents in atrial myocytes. ( a ) Transient outward current (Ito) was obtained by a family of depolarization steps from −80 mV, and was measured as the 4-aminopyridine (4-AP)-sensitive peak current (10 mM). (left upper) Voltage protocol. Right panel shows the representative recordings of 4-AP sensitive currents of the control (CTL) and KCNIP1 knockdown (KCNIP1 KD) atrial myocytes, respectively. (left lower) Efficiency of knockdown represented by decreased KCHIP1 protein level. ( b ) Representative current density–voltage relationships of 4-AP sensitive currents in CTL and KCNIP1 KD atrial myocytes. N =3 experiments for each group. Error bars, s.d. Full-length blots are presented in Supplementary Fig. 7 .

    Journal: Nature Communications

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    doi: 10.1038/ncomms10190

    Figure Lengend Snippet: Knockdown of KCNIP1 downregulates transient outward currents in atrial myocytes. ( a ) Transient outward current (Ito) was obtained by a family of depolarization steps from −80 mV, and was measured as the 4-aminopyridine (4-AP)-sensitive peak current (10 mM). (left upper) Voltage protocol. Right panel shows the representative recordings of 4-AP sensitive currents of the control (CTL) and KCNIP1 knockdown (KCNIP1 KD) atrial myocytes, respectively. (left lower) Efficiency of knockdown represented by decreased KCHIP1 protein level. ( b ) Representative current density–voltage relationships of 4-AP sensitive currents in CTL and KCNIP1 KD atrial myocytes. N =3 experiments for each group. Error bars, s.d. Full-length blots are presented in Supplementary Fig. 7 .

    Article Snippet: For immunoprecipitation , protein lysates were incubated with 1 μg ml−1 of the anti-KCHIP1 antibody (Alomone Labs) overnight at 4 °C.

    Techniques: CTL Assay

    Basal expressions of KCNIP s in the mammalian heart. Total RNA was isolated and PCR with reverse transcription (RT-PCR) products with primer pairs specific to rat KCNIP s were visualized by electrophoresis. ( a ) The RT-PCR results of a positive control for KCNIP1-4 (K1-4) from a representative sample of rat brain. ( b ) The RT-PCR results of representative left atrium (LA), right atrium (RA), left ventricle (LV) and right ventricle (RV). KCNIP1-3 mRNAs could be detected in the mammalian LA, RA, LV and RV. GP, glyceraldehyde 3-phosphate dehydrogenase; M, molecular weight maker. Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 4 .

    Journal: Nature Communications

    Article Title: Genome-wide screening identifies a KCNIP1 copy number variant as a genetic predictor for atrial fibrillation

    doi: 10.1038/ncomms10190

    Figure Lengend Snippet: Basal expressions of KCNIP s in the mammalian heart. Total RNA was isolated and PCR with reverse transcription (RT-PCR) products with primer pairs specific to rat KCNIP s were visualized by electrophoresis. ( a ) The RT-PCR results of a positive control for KCNIP1-4 (K1-4) from a representative sample of rat brain. ( b ) The RT-PCR results of representative left atrium (LA), right atrium (RA), left ventricle (LV) and right ventricle (RV). KCNIP1-3 mRNAs could be detected in the mammalian LA, RA, LV and RV. GP, glyceraldehyde 3-phosphate dehydrogenase; M, molecular weight maker. Data are representative of three independent experiments. Full-length blots are presented in Supplementary Fig. 4 .

    Article Snippet: For immunoprecipitation , protein lysates were incubated with 1 μg ml−1 of the anti-KCHIP1 antibody (Alomone Labs) overnight at 4 °C.

    Techniques: Isolation, Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction, Electrophoresis, Positive Control, Molecular Weight