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pkcε translocation inhibitor ii  (Millipore)

 
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    Structured Review

    Millipore pkcε translocation inhibitor ii
    <t>PKC</t> mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε <t>translocation</t> inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.
    Pkcε Translocation Inhibitor Ii, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pkcε translocation inhibitor ii/product/Millipore
    Average 90 stars, based on 1 article reviews
    pkcε translocation inhibitor ii - by Bioz Stars, 2026-03
    90/100 stars

    Images

    1) Product Images from "Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus"

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    Journal: Alcohol, clinical & experimental research

    doi: 10.1111/acer.15342

    PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.
    Figure Legend Snippet: PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Techniques Used: Produced, Derivative Assay, Inhibition, Translocation Assay, Transferring

    Summary of inhibitors and results ( n = cell numbers).
    Figure Legend Snippet: Summary of inhibitors and results ( n = cell numbers).

    Techniques Used: Translocation Assay, Negative Control

    Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).
    Figure Legend Snippet: Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Techniques Used: Transferring

    Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.
    Figure Legend Snippet: Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Techniques Used: Translocation Assay, Membrane, Injection, Control

    T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).
    Figure Legend Snippet: T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Techniques Used: Membrane, Control



    Similar Products

    pkcε translocation inhibitor ii  (Millipore)
    90
    Millipore pkcε translocation inhibitor ii
    <t>PKC</t> mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε <t>translocation</t> inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.
    Pkcε Translocation Inhibitor Ii, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pkcε translocation inhibitor ii/product/Millipore
    Average 90 stars, based on 1 article reviews
    pkcε translocation inhibitor ii - by Bioz Stars, 2026-03
    90/100 stars
    		  Buy from Supplier
    pkcε translocation inhibitor ii, #530993, (calbiochem)  (Millipore)
    90
    Millipore pkcε translocation inhibitor ii, #530993, (calbiochem)
    <t>PKC</t> mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε <t>translocation</t> inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.
    Pkcε Translocation Inhibitor Ii, #530993, (Calbiochem), supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pkcε translocation inhibitor ii, #530993, (calbiochem)/product/Millipore
    Average 90 stars, based on 1 article reviews
    pkcε translocation inhibitor ii, #530993, (calbiochem) - by Bioz Stars, 2026-03
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: PKC mediates a T channel gain of function during alcohol withdrawal. (A–C) Representative traces of T-type current inactivation curves for (A) Air, (B) WD, and (C) WD + PKC (−) groups, respectively, elicited at −50 mV from holding potentials ranging from −135 to −60 mV for 1 s (inset). (D, E) Alcohol WD produced a significant depolarizing shift in the inactivation curve of native T-type calcium current. The depolarizing shift was blocked by PKC peptide inhibitors, including PKC epsilon-specific inhibitors. (F) V 50 derived from the inactivation curve ~5 h. into the 4th alcohol WD in C57BL/6 mice was analyzed. The significant depolarizing shift for V 50 was blocked by the PKC peptide inhibitor (PKC (−), 10 μM). This inhibition was mimicked by specific PKCε isoform inhibitors (#530993, 539522; 5 μM) but not a PKCε translocation inhibitor inactive peptide (#539542; 5 μM). All drugs were delivered through the internal pipette solution. Statistics for V 50 showed F (6, 73) = 3.87, p = 0.0021 (One-Way ANOVA). In the plot * indicates p <0.05 and ** indicates p <0.01.

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Produced, Derivative Assay, Inhibition, Translocation Assay, Transferring

    Summary of inhibitors and results ( n = cell numbers).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Summary of inhibitors and results ( n = cell numbers).

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Translocation Assay, Negative Control

    Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Kinetic changes of T-channel during the application of PKC inhibitors recorded from the reuniens after 5 h into 4th alcohol withdrawal. (A, B) PKCε inhibitor (#530993, 5 μM) was applied through the bath solution, it significantly reduced rise time (A. paired t test, p = 0.0311, n = 6); increased rise slope (B. paired t test, p = 0.0266, n = 6); (C) Rise time did not show a significant main effect [ F (4, 53) = 2.205, p = 0.0809], although Dunnett’s post hoc test showed a significant difference between WD and WD plus PKCε (−), (#529522, p = 0.0223.* p <0.05). All drugs were delivered through the patch pipette internal solution, including the PKC peptide inhibitor (10 μM), and PKCε inhibitors (#530993, 5 μM; #539522, 5 μM).

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Transferring

    Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: Midline thalamic neurons exhibit more spikes per low-threshold Ca 2+ burst during alcohol withdrawal. PKCε translocation inhibitor peptide (#539522) reduced the number of spikes/burst after 4th WD. (A–E) representative traces for the bursts elicited near resting membrane potential by prepulse negative current injection of −200 pA, 800 ms. (F) Statistics for the bursts induced by prepulse negative current injection of −200 pA. One-way ANOVA: F (4, 56) = 6.321, p = 0.0003, Dunnett’s multiple comparisons test, WD and Control, p = 0.0013; WD and Air exposed, p = 0.0461; WD and WD + PKCε (−), p = 0.0469; WD and WD + PKCε inactive peptide, p = 0.9990. In the plots * indicates p <0.05, and ** indicates p <0.01.

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Translocation Assay, Membrane, Injection, Control

    T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Journal: Alcohol, clinical & experimental research

    Article Title: Protein kinase C epsilon-mediated modulation of T-type calcium channels underlies alcohol withdrawal hyperexcitability in the midline thalamus

    doi: 10.1111/acer.15342

    Figure Lengend Snippet: T-current-mediated bursting was elicited near resting membrane potential from a series of hyperpolarizing prepulse current injections. Using a procedure analogous to the voltage clamp inactivation protocol (current injections started from 0 to −400 pA, −50 pA step, 500 ms of duration), we measured T-current-mediated bursting. Control (A) and air-exposed (B) conditions elicit 1–3 action potentials/burst. After the 4th WD (C), the cells responded with increased numbers of spikes/burst, which were reduced by the PKC ε inhibitor (D) but not the PKC ε inhibitor inactive peptide (E).

    Article Snippet: #530993 (Calbiochem) , PKCε translocation inhibitor II , WD vs WD + PKCε (−) , Reduction (p = 0.013), n = 23 , 9.579 ± 8.048.

    Techniques: Membrane, Control