Structured Review

Millipore nd7 23 cells
( a ) Family of classical currents recorded from <t>ND7/23</t> cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .
Nd7 23 Cells, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels"

Article Title: A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels

Journal: eLife

doi: 10.7554/eLife.77558

( a ) Family of classical currents recorded from ND7/23 cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .
Figure Legend Snippet: ( a ) Family of classical currents recorded from ND7/23 cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .

Techniques Used: Expressing, Recombinant, Activation Assay


Figure Legend Snippet:

Techniques Used: Transfection, Construct, shRNA, Recombinant, Plasmid Preparation, Sequencing, Mutagenesis, Software


Structured Review

Millipore nd7 23 cells
Changes in whole cell Ca2+ currents in differentiated <t>ND7/23</t> cells following HSV-1 infection and treatment with IL-6. A-C) Example of whole cell T-type Ca2+ currents generated in a differentiated ND7/23 cell following HSV-1 infection and treatment with IL-6. Differentiated ND7/23 cells were infected overnight with HSV-1. After a 24 h infection period, cells were treated with IL-6 (20 ng/mL) for another 24 h. Recordings from control (non-treated) and treatment groups were performed at the end of the 48 h period. In this and subsequent figures, the voltage step protocol is shown below the current trace. Note that the transient component (arrow) generated by voltage step to −20 mV from a holding potential of −110 mV was eliminated following HSV-1 infection (A,B). Stimulation with IL-6 reverses the inhibitory effect of HSV-1 infection on T-type Ca2+ currents (B,C). Scale bars in A are the same for B and C. D). Normalized current-voltage (I-V) relationship generated by the activation of T-type Ca2+ channels in differentiated ND7/23 cells (non-infected vs. HSV+IL-6 treated cells). Current amplitudes at different voltages were normalized to that generated by a voltage step to −20 mV from a holding potential of −110 mV (I/I −20). E) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel F. F) Mean T-type Ca2+ current densities generated in ND7/23 cells following HSV-1 infection and treatment with IL-6. T-type Ca2+ current density was calculated from the peak current amplitude generated by a voltage step to –20 mV from a holding potential of −110 mV. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cells.
Nd7 23 Cells, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Regulation of T-type Ca 2+ channel expression by interleukin-6 in sensory-like ND7/23 cells post herpes simplex virus (HSV-1) infection"

Article Title: Regulation of T-type Ca 2+ channel expression by interleukin-6 in sensory-like ND7/23 cells post herpes simplex virus (HSV-1) infection

Journal: Journal of neurochemistry

doi: 10.1111/jnc.14697

Changes in whole cell Ca2+ currents in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A-C) Example of whole cell T-type Ca2+ currents generated in a differentiated ND7/23 cell following HSV-1 infection and treatment with IL-6. Differentiated ND7/23 cells were infected overnight with HSV-1. After a 24 h infection period, cells were treated with IL-6 (20 ng/mL) for another 24 h. Recordings from control (non-treated) and treatment groups were performed at the end of the 48 h period. In this and subsequent figures, the voltage step protocol is shown below the current trace. Note that the transient component (arrow) generated by voltage step to −20 mV from a holding potential of −110 mV was eliminated following HSV-1 infection (A,B). Stimulation with IL-6 reverses the inhibitory effect of HSV-1 infection on T-type Ca2+ currents (B,C). Scale bars in A are the same for B and C. D). Normalized current-voltage (I-V) relationship generated by the activation of T-type Ca2+ channels in differentiated ND7/23 cells (non-infected vs. HSV+IL-6 treated cells). Current amplitudes at different voltages were normalized to that generated by a voltage step to −20 mV from a holding potential of −110 mV (I/I −20). E) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel F. F) Mean T-type Ca2+ current densities generated in ND7/23 cells following HSV-1 infection and treatment with IL-6. T-type Ca2+ current density was calculated from the peak current amplitude generated by a voltage step to –20 mV from a holding potential of −110 mV. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cells.
Figure Legend Snippet: Changes in whole cell Ca2+ currents in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A-C) Example of whole cell T-type Ca2+ currents generated in a differentiated ND7/23 cell following HSV-1 infection and treatment with IL-6. Differentiated ND7/23 cells were infected overnight with HSV-1. After a 24 h infection period, cells were treated with IL-6 (20 ng/mL) for another 24 h. Recordings from control (non-treated) and treatment groups were performed at the end of the 48 h period. In this and subsequent figures, the voltage step protocol is shown below the current trace. Note that the transient component (arrow) generated by voltage step to −20 mV from a holding potential of −110 mV was eliminated following HSV-1 infection (A,B). Stimulation with IL-6 reverses the inhibitory effect of HSV-1 infection on T-type Ca2+ currents (B,C). Scale bars in A are the same for B and C. D). Normalized current-voltage (I-V) relationship generated by the activation of T-type Ca2+ channels in differentiated ND7/23 cells (non-infected vs. HSV+IL-6 treated cells). Current amplitudes at different voltages were normalized to that generated by a voltage step to −20 mV from a holding potential of −110 mV (I/I −20). E) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel F. F) Mean T-type Ca2+ current densities generated in ND7/23 cells following HSV-1 infection and treatment with IL-6. T-type Ca2+ current density was calculated from the peak current amplitude generated by a voltage step to –20 mV from a holding potential of −110 mV. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cells.

Techniques Used: Infection, Generated, Activation Assay

Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A, B, C) HSV-1 infection causes a leftward shift in current densities. D) IL-6 treatment for 24 h reverses the HSV-1 evoked shift in current densities. The number of cells analyzed under each condition was: control (n=22), +IL-6 (n=15), +HSV (n=22), and HSV+Il-6 (n=25) from at least 3 different cell cultures.
Figure Legend Snippet: Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A, B, C) HSV-1 infection causes a leftward shift in current densities. D) IL-6 treatment for 24 h reverses the HSV-1 evoked shift in current densities. The number of cells analyzed under each condition was: control (n=22), +IL-6 (n=15), +HSV (n=22), and HSV+Il-6 (n=25) from at least 3 different cell cultures.

Techniques Used: Generated, Infection

Effect of HSV-1 infection on Na+ currents generated in differentiated ND7/23 cells following treatment with IL-6. A-B) Examples of whole cell Na+ currents generated in a differentiated ND7/23 cell following HSV-1 infection. Note that the inward Na+ current generated by voltage step to +20 mV from a holding potential of −100 mV was eliminated following HSV-1 infection. C) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel D. D) Infection of differentiated ND7/23 cells with HSV-1 causes a significant reduction in the density of Na+ currents under all conditions tested (* denotes p < 0.05 vs. HSV-1 infected cells). IL-6 treatment does not reverse the inhibitory effect of HSV-1 infection on Na+ current densities. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures.
Figure Legend Snippet: Effect of HSV-1 infection on Na+ currents generated in differentiated ND7/23 cells following treatment with IL-6. A-B) Examples of whole cell Na+ currents generated in a differentiated ND7/23 cell following HSV-1 infection. Note that the inward Na+ current generated by voltage step to +20 mV from a holding potential of −100 mV was eliminated following HSV-1 infection. C) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel D. D) Infection of differentiated ND7/23 cells with HSV-1 causes a significant reduction in the density of Na+ currents under all conditions tested (* denotes p < 0.05 vs. HSV-1 infected cells). IL-6 treatment does not reverse the inhibitory effect of HSV-1 infection on Na+ current densities. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures.

Techniques Used: Infection, Generated

Effect of HSV-1 infection and treatment with IL-6 on the expression of the Cav3.2 transcripts and channel proteins. A) HSV-1 infection of differentiated ND7/23 cells evokes a considerable increase in the expression of Cav3.2 mRNA as assessed by real time PCR analysis. IL-6 does not alter the expression of Cav3.2 mRNA in control or HSV-1 infected cells. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures). B) Western blot analysis showing changers in the expression of Cav3.2 channel protein following HSV-1 infection and treatment with IL-6. Note that HSV-1 infection caused a significant reduction in Cav3.2 protein expression. IL-6 did not reverse the reduction in Cav3.2 protein expression. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures).
Figure Legend Snippet: Effect of HSV-1 infection and treatment with IL-6 on the expression of the Cav3.2 transcripts and channel proteins. A) HSV-1 infection of differentiated ND7/23 cells evokes a considerable increase in the expression of Cav3.2 mRNA as assessed by real time PCR analysis. IL-6 does not alter the expression of Cav3.2 mRNA in control or HSV-1 infected cells. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures). B) Western blot analysis showing changers in the expression of Cav3.2 channel protein following HSV-1 infection and treatment with IL-6. Note that HSV-1 infection caused a significant reduction in Cav3.2 protein expression. IL-6 did not reverse the reduction in Cav3.2 protein expression. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures).

Techniques Used: Infection, Expressing, Real-time Polymerase Chain Reaction, Western Blot

IL-6 increases the expression of Cav3.2 channel proteins on the membrane following HSV-1 infection of differentiated ND7/23 cells (A). The effect of IL-6 post HSV-1 infection was quantified on biotinylated proteins to assess changes in Cav3.2 channel proteins on the membrane. * denotes p ≤ 0.05 vs. control (non-treated) cells; n=4 (number of independent cell cultures). B-C) Inhibition of protein trafficking with brefeldin-A (BFA, 1 μg/mL) reduces T-type Ca2+ channel functional expression as assessed by whole cell recordings. Effect of brefeldin-A on cell capacitance (B) and T-type Ca2+ current density (C) on differentiated ND7/23 cells. Note that brefeldin-A evoked a significant reduction in the cell capacitance of IL-6 or HSV-1/IL-6 treated cells. T-type Ca2+ current density was significantly reduced following HSV-1/IL-6 treatment of ND7/23 cells. The number of cells recorded under each condition is presented in parenthesis in panel C from 2 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6. D-G) Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following treatment with brefeldin-A. Treatment of ND7/23 cells with brefeldin-A caused a leftward shift in current densities.
Figure Legend Snippet: IL-6 increases the expression of Cav3.2 channel proteins on the membrane following HSV-1 infection of differentiated ND7/23 cells (A). The effect of IL-6 post HSV-1 infection was quantified on biotinylated proteins to assess changes in Cav3.2 channel proteins on the membrane. * denotes p ≤ 0.05 vs. control (non-treated) cells; n=4 (number of independent cell cultures). B-C) Inhibition of protein trafficking with brefeldin-A (BFA, 1 μg/mL) reduces T-type Ca2+ channel functional expression as assessed by whole cell recordings. Effect of brefeldin-A on cell capacitance (B) and T-type Ca2+ current density (C) on differentiated ND7/23 cells. Note that brefeldin-A evoked a significant reduction in the cell capacitance of IL-6 or HSV-1/IL-6 treated cells. T-type Ca2+ current density was significantly reduced following HSV-1/IL-6 treatment of ND7/23 cells. The number of cells recorded under each condition is presented in parenthesis in panel C from 2 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6. D-G) Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following treatment with brefeldin-A. Treatment of ND7/23 cells with brefeldin-A caused a leftward shift in current densities.

Techniques Used: Expressing, Infection, Inhibition, Functional Assay, Generated

Effect of ERK1/2 activation on the functional expression of T-type Ca2+ channels in differentiated ND7/23 cells. A) Effect of cell differentiation and HSV-1 infection on ERK activation as assessed by changes in phosphorylated ERK (p-ERK). Note that differentiated cells (following 4 d culture in differentiation media-DM) expressed higher levels of p-ERK compared with ND7/23 cells cultured in growth media (GM). Infection of differentiated ND7/23 cells with HSV-1 evoked a significant reduction in p-ERK. Overall changes in p-ERK was normalized to total ERK (t-ERK) expression under each culture condition (number of independent cell cultures n=3). B) Time course of ERK activation following stimulation of differentiated ND7/23 cells with IL-6 (20 ng/mL). Immunoblot analysis was used to determine changes in ERK activation by assessing the levels of phosphorylated and total ERK. ERK activation in differentiated ND7/23 cells can be inhibited by pre-treatment with the ERK blocker U0126 (10 μM). In these experiments, cultures were pre-treated with U0126 for 1 h prior to stimulation with IL-6 (number of independent cell cultures n=4). C) In HSV-1 infected cells, IL-6 evokes an increased in ERK activation (number of independent cell cultures n=4). D) The ERK inhibitor U0126 blocked the stimulatory effect of IL-6 on T-type Ca2+ channel expression. Note that 1 h treatment with U0126 did not alter the functional expression of T-type Ca2+ channels, suggesting a lack of an allosteric effect on channels already present in the membrane. Overnight incubation with U0126 prevents the normal expression of T-type Ca2+ channels on the membrane. In HSV-1 infected cells treated with IL-6, inhibition of ERK activity with U0126 caused a completed disruption of channel expression. The number of cells recorded under each condition is presented in parenthesis from 2 independent cell cultures. * denotes p ≤ 0.05 vs. control (non-infected cultures); ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6.
Figure Legend Snippet: Effect of ERK1/2 activation on the functional expression of T-type Ca2+ channels in differentiated ND7/23 cells. A) Effect of cell differentiation and HSV-1 infection on ERK activation as assessed by changes in phosphorylated ERK (p-ERK). Note that differentiated cells (following 4 d culture in differentiation media-DM) expressed higher levels of p-ERK compared with ND7/23 cells cultured in growth media (GM). Infection of differentiated ND7/23 cells with HSV-1 evoked a significant reduction in p-ERK. Overall changes in p-ERK was normalized to total ERK (t-ERK) expression under each culture condition (number of independent cell cultures n=3). B) Time course of ERK activation following stimulation of differentiated ND7/23 cells with IL-6 (20 ng/mL). Immunoblot analysis was used to determine changes in ERK activation by assessing the levels of phosphorylated and total ERK. ERK activation in differentiated ND7/23 cells can be inhibited by pre-treatment with the ERK blocker U0126 (10 μM). In these experiments, cultures were pre-treated with U0126 for 1 h prior to stimulation with IL-6 (number of independent cell cultures n=4). C) In HSV-1 infected cells, IL-6 evokes an increased in ERK activation (number of independent cell cultures n=4). D) The ERK inhibitor U0126 blocked the stimulatory effect of IL-6 on T-type Ca2+ channel expression. Note that 1 h treatment with U0126 did not alter the functional expression of T-type Ca2+ channels, suggesting a lack of an allosteric effect on channels already present in the membrane. Overnight incubation with U0126 prevents the normal expression of T-type Ca2+ channels on the membrane. In HSV-1 infected cells treated with IL-6, inhibition of ERK activity with U0126 caused a completed disruption of channel expression. The number of cells recorded under each condition is presented in parenthesis from 2 independent cell cultures. * denotes p ≤ 0.05 vs. control (non-infected cultures); ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6.

Techniques Used: Activation Assay, Functional Assay, Expressing, Cell Differentiation, Infection, Cell Culture, Western Blot, Incubation, Inhibition, Activity Assay

Effect of HSV-1 infection on IL-6 secretion, and its contribution to viral replication and release. A) IL-6 release was assessed from the supernatant of HSV-1 infected HCEC as assessed by ELISA (* denotes p < 0.05 vs. HSV-1 infected cells for 6 h; number of independent cell cultures n=3). B) IL-6 evokes a considerable increase in the expression of the HSV-1 TK following infection of differentiated ND7/23 cells (* denotes p < 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4). C) IL-6 had no effect on plaque formation following HSV-1 infection of differentiated ND7/23 cells (p > 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4).
Figure Legend Snippet: Effect of HSV-1 infection on IL-6 secretion, and its contribution to viral replication and release. A) IL-6 release was assessed from the supernatant of HSV-1 infected HCEC as assessed by ELISA (* denotes p < 0.05 vs. HSV-1 infected cells for 6 h; number of independent cell cultures n=3). B) IL-6 evokes a considerable increase in the expression of the HSV-1 TK following infection of differentiated ND7/23 cells (* denotes p < 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4). C) IL-6 had no effect on plaque formation following HSV-1 infection of differentiated ND7/23 cells (p > 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4).

Techniques Used: Infection, Enzyme-linked Immunosorbent Assay, Expressing


Structured Review

Millipore nd7 23 cells
Changes in whole cell Ca2+ currents in differentiated <t>ND7/23</t> cells following HSV-1 infection and treatment with IL-6. A-C) Example of whole cell T-type Ca2+ currents generated in a differentiated ND7/23 cell following HSV-1 infection and treatment with IL-6. Differentiated ND7/23 cells were infected overnight with HSV-1. After a 24 h infection period, cells were treated with IL-6 (20 ng/mL) for another 24 h. Recordings from control (non-treated) and treatment groups were performed at the end of the 48 h period. In this and subsequent figures, the voltage step protocol is shown below the current trace. Note that the transient component (arrow) generated by voltage step to −20 mV from a holding potential of −110 mV was eliminated following HSV-1 infection (A,B). Stimulation with IL-6 reverses the inhibitory effect of HSV-1 infection on T-type Ca2+ currents (B,C). Scale bars in A are the same for B and C. D). Normalized current-voltage (I-V) relationship generated by the activation of T-type Ca2+ channels in differentiated ND7/23 cells (non-infected vs. HSV+IL-6 treated cells). Current amplitudes at different voltages were normalized to that generated by a voltage step to −20 mV from a holding potential of −110 mV (I/I −20). E) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel F. F) Mean T-type Ca2+ current densities generated in ND7/23 cells following HSV-1 infection and treatment with IL-6. T-type Ca2+ current density was calculated from the peak current amplitude generated by a voltage step to –20 mV from a holding potential of −110 mV. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cells.
Nd7 23 Cells, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/nd7 23 cells/product/Millipore
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
nd7 23 cells - by Bioz Stars, 2023-02
86/100 stars

Images

1) Product Images from "Regulation of T-type Ca 2+ channel expression by interleukin-6 in sensory-like ND7/23 cells post herpes simplex virus (HSV-1) infection"

Article Title: Regulation of T-type Ca 2+ channel expression by interleukin-6 in sensory-like ND7/23 cells post herpes simplex virus (HSV-1) infection

Journal: Journal of neurochemistry

doi: 10.1111/jnc.14697

Changes in whole cell Ca2+ currents in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A-C) Example of whole cell T-type Ca2+ currents generated in a differentiated ND7/23 cell following HSV-1 infection and treatment with IL-6. Differentiated ND7/23 cells were infected overnight with HSV-1. After a 24 h infection period, cells were treated with IL-6 (20 ng/mL) for another 24 h. Recordings from control (non-treated) and treatment groups were performed at the end of the 48 h period. In this and subsequent figures, the voltage step protocol is shown below the current trace. Note that the transient component (arrow) generated by voltage step to −20 mV from a holding potential of −110 mV was eliminated following HSV-1 infection (A,B). Stimulation with IL-6 reverses the inhibitory effect of HSV-1 infection on T-type Ca2+ currents (B,C). Scale bars in A are the same for B and C. D). Normalized current-voltage (I-V) relationship generated by the activation of T-type Ca2+ channels in differentiated ND7/23 cells (non-infected vs. HSV+IL-6 treated cells). Current amplitudes at different voltages were normalized to that generated by a voltage step to −20 mV from a holding potential of −110 mV (I/I −20). E) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel F. F) Mean T-type Ca2+ current densities generated in ND7/23 cells following HSV-1 infection and treatment with IL-6. T-type Ca2+ current density was calculated from the peak current amplitude generated by a voltage step to –20 mV from a holding potential of −110 mV. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cells.
Figure Legend Snippet: Changes in whole cell Ca2+ currents in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A-C) Example of whole cell T-type Ca2+ currents generated in a differentiated ND7/23 cell following HSV-1 infection and treatment with IL-6. Differentiated ND7/23 cells were infected overnight with HSV-1. After a 24 h infection period, cells were treated with IL-6 (20 ng/mL) for another 24 h. Recordings from control (non-treated) and treatment groups were performed at the end of the 48 h period. In this and subsequent figures, the voltage step protocol is shown below the current trace. Note that the transient component (arrow) generated by voltage step to −20 mV from a holding potential of −110 mV was eliminated following HSV-1 infection (A,B). Stimulation with IL-6 reverses the inhibitory effect of HSV-1 infection on T-type Ca2+ currents (B,C). Scale bars in A are the same for B and C. D). Normalized current-voltage (I-V) relationship generated by the activation of T-type Ca2+ channels in differentiated ND7/23 cells (non-infected vs. HSV+IL-6 treated cells). Current amplitudes at different voltages were normalized to that generated by a voltage step to −20 mV from a holding potential of −110 mV (I/I −20). E) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel F. F) Mean T-type Ca2+ current densities generated in ND7/23 cells following HSV-1 infection and treatment with IL-6. T-type Ca2+ current density was calculated from the peak current amplitude generated by a voltage step to –20 mV from a holding potential of −110 mV. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cells.

Techniques Used: Infection, Generated, Activation Assay

Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A, B, C) HSV-1 infection causes a leftward shift in current densities. D) IL-6 treatment for 24 h reverses the HSV-1 evoked shift in current densities. The number of cells analyzed under each condition was: control (n=22), +IL-6 (n=15), +HSV (n=22), and HSV+Il-6 (n=25) from at least 3 different cell cultures.
Figure Legend Snippet: Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following HSV-1 infection and treatment with IL-6. A, B, C) HSV-1 infection causes a leftward shift in current densities. D) IL-6 treatment for 24 h reverses the HSV-1 evoked shift in current densities. The number of cells analyzed under each condition was: control (n=22), +IL-6 (n=15), +HSV (n=22), and HSV+Il-6 (n=25) from at least 3 different cell cultures.

Techniques Used: Generated, Infection

Effect of HSV-1 infection on Na+ currents generated in differentiated ND7/23 cells following treatment with IL-6. A-B) Examples of whole cell Na+ currents generated in a differentiated ND7/23 cell following HSV-1 infection. Note that the inward Na+ current generated by voltage step to +20 mV from a holding potential of −100 mV was eliminated following HSV-1 infection. C) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel D. D) Infection of differentiated ND7/23 cells with HSV-1 causes a significant reduction in the density of Na+ currents under all conditions tested (* denotes p < 0.05 vs. HSV-1 infected cells). IL-6 treatment does not reverse the inhibitory effect of HSV-1 infection on Na+ current densities. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures.
Figure Legend Snippet: Effect of HSV-1 infection on Na+ currents generated in differentiated ND7/23 cells following treatment with IL-6. A-B) Examples of whole cell Na+ currents generated in a differentiated ND7/23 cell following HSV-1 infection. Note that the inward Na+ current generated by voltage step to +20 mV from a holding potential of −100 mV was eliminated following HSV-1 infection. C) Comparison of cell capacitance in ND7/23 cells following HSV-1 infection and treatment with IL-6. The number of cells recorded under each condition is presented in parenthesis in panel D. D) Infection of differentiated ND7/23 cells with HSV-1 causes a significant reduction in the density of Na+ currents under all conditions tested (* denotes p < 0.05 vs. HSV-1 infected cells). IL-6 treatment does not reverse the inhibitory effect of HSV-1 infection on Na+ current densities. The number of cells recorded under each condition is presented in parenthesis from at least 3 different cell cultures.

Techniques Used: Infection, Generated

Effect of HSV-1 infection and treatment with IL-6 on the expression of the Cav3.2 transcripts and channel proteins. A) HSV-1 infection of differentiated ND7/23 cells evokes a considerable increase in the expression of Cav3.2 mRNA as assessed by real time PCR analysis. IL-6 does not alter the expression of Cav3.2 mRNA in control or HSV-1 infected cells. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures). B) Western blot analysis showing changers in the expression of Cav3.2 channel protein following HSV-1 infection and treatment with IL-6. Note that HSV-1 infection caused a significant reduction in Cav3.2 protein expression. IL-6 did not reverse the reduction in Cav3.2 protein expression. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures).
Figure Legend Snippet: Effect of HSV-1 infection and treatment with IL-6 on the expression of the Cav3.2 transcripts and channel proteins. A) HSV-1 infection of differentiated ND7/23 cells evokes a considerable increase in the expression of Cav3.2 mRNA as assessed by real time PCR analysis. IL-6 does not alter the expression of Cav3.2 mRNA in control or HSV-1 infected cells. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures). B) Western blot analysis showing changers in the expression of Cav3.2 channel protein following HSV-1 infection and treatment with IL-6. Note that HSV-1 infection caused a significant reduction in Cav3.2 protein expression. IL-6 did not reverse the reduction in Cav3.2 protein expression. * denotes p ≤ 0.05 vs. control (non-treated) cells; ns denotes no significant difference (p > 0.05); n=4 (number of independent cell cultures).

Techniques Used: Infection, Expressing, Real-time Polymerase Chain Reaction, Western Blot

IL-6 increases the expression of Cav3.2 channel proteins on the membrane following HSV-1 infection of differentiated ND7/23 cells (A). The effect of IL-6 post HSV-1 infection was quantified on biotinylated proteins to assess changes in Cav3.2 channel proteins on the membrane. * denotes p ≤ 0.05 vs. control (non-treated) cells; n=4 (number of independent cell cultures). B-C) Inhibition of protein trafficking with brefeldin-A (BFA, 1 μg/mL) reduces T-type Ca2+ channel functional expression as assessed by whole cell recordings. Effect of brefeldin-A on cell capacitance (B) and T-type Ca2+ current density (C) on differentiated ND7/23 cells. Note that brefeldin-A evoked a significant reduction in the cell capacitance of IL-6 or HSV-1/IL-6 treated cells. T-type Ca2+ current density was significantly reduced following HSV-1/IL-6 treatment of ND7/23 cells. The number of cells recorded under each condition is presented in parenthesis in panel C from 2 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6. D-G) Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following treatment with brefeldin-A. Treatment of ND7/23 cells with brefeldin-A caused a leftward shift in current densities.
Figure Legend Snippet: IL-6 increases the expression of Cav3.2 channel proteins on the membrane following HSV-1 infection of differentiated ND7/23 cells (A). The effect of IL-6 post HSV-1 infection was quantified on biotinylated proteins to assess changes in Cav3.2 channel proteins on the membrane. * denotes p ≤ 0.05 vs. control (non-treated) cells; n=4 (number of independent cell cultures). B-C) Inhibition of protein trafficking with brefeldin-A (BFA, 1 μg/mL) reduces T-type Ca2+ channel functional expression as assessed by whole cell recordings. Effect of brefeldin-A on cell capacitance (B) and T-type Ca2+ current density (C) on differentiated ND7/23 cells. Note that brefeldin-A evoked a significant reduction in the cell capacitance of IL-6 or HSV-1/IL-6 treated cells. T-type Ca2+ current density was significantly reduced following HSV-1/IL-6 treatment of ND7/23 cells. The number of cells recorded under each condition is presented in parenthesis in panel C from 2 different cell cultures. * denotes p ≤ 0.05 vs. control (non-treated) cells; ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6. D-G) Density plot of T-type Ca2+ currents generated in differentiated ND7/23 cells following treatment with brefeldin-A. Treatment of ND7/23 cells with brefeldin-A caused a leftward shift in current densities.

Techniques Used: Expressing, Infection, Inhibition, Functional Assay, Generated

Effect of ERK1/2 activation on the functional expression of T-type Ca2+ channels in differentiated ND7/23 cells. A) Effect of cell differentiation and HSV-1 infection on ERK activation as assessed by changes in phosphorylated ERK (p-ERK). Note that differentiated cells (following 4 d culture in differentiation media-DM) expressed higher levels of p-ERK compared with ND7/23 cells cultured in growth media (GM). Infection of differentiated ND7/23 cells with HSV-1 evoked a significant reduction in p-ERK. Overall changes in p-ERK was normalized to total ERK (t-ERK) expression under each culture condition (number of independent cell cultures n=3). B) Time course of ERK activation following stimulation of differentiated ND7/23 cells with IL-6 (20 ng/mL). Immunoblot analysis was used to determine changes in ERK activation by assessing the levels of phosphorylated and total ERK. ERK activation in differentiated ND7/23 cells can be inhibited by pre-treatment with the ERK blocker U0126 (10 μM). In these experiments, cultures were pre-treated with U0126 for 1 h prior to stimulation with IL-6 (number of independent cell cultures n=4). C) In HSV-1 infected cells, IL-6 evokes an increased in ERK activation (number of independent cell cultures n=4). D) The ERK inhibitor U0126 blocked the stimulatory effect of IL-6 on T-type Ca2+ channel expression. Note that 1 h treatment with U0126 did not alter the functional expression of T-type Ca2+ channels, suggesting a lack of an allosteric effect on channels already present in the membrane. Overnight incubation with U0126 prevents the normal expression of T-type Ca2+ channels on the membrane. In HSV-1 infected cells treated with IL-6, inhibition of ERK activity with U0126 caused a completed disruption of channel expression. The number of cells recorded under each condition is presented in parenthesis from 2 independent cell cultures. * denotes p ≤ 0.05 vs. control (non-infected cultures); ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6.
Figure Legend Snippet: Effect of ERK1/2 activation on the functional expression of T-type Ca2+ channels in differentiated ND7/23 cells. A) Effect of cell differentiation and HSV-1 infection on ERK activation as assessed by changes in phosphorylated ERK (p-ERK). Note that differentiated cells (following 4 d culture in differentiation media-DM) expressed higher levels of p-ERK compared with ND7/23 cells cultured in growth media (GM). Infection of differentiated ND7/23 cells with HSV-1 evoked a significant reduction in p-ERK. Overall changes in p-ERK was normalized to total ERK (t-ERK) expression under each culture condition (number of independent cell cultures n=3). B) Time course of ERK activation following stimulation of differentiated ND7/23 cells with IL-6 (20 ng/mL). Immunoblot analysis was used to determine changes in ERK activation by assessing the levels of phosphorylated and total ERK. ERK activation in differentiated ND7/23 cells can be inhibited by pre-treatment with the ERK blocker U0126 (10 μM). In these experiments, cultures were pre-treated with U0126 for 1 h prior to stimulation with IL-6 (number of independent cell cultures n=4). C) In HSV-1 infected cells, IL-6 evokes an increased in ERK activation (number of independent cell cultures n=4). D) The ERK inhibitor U0126 blocked the stimulatory effect of IL-6 on T-type Ca2+ channel expression. Note that 1 h treatment with U0126 did not alter the functional expression of T-type Ca2+ channels, suggesting a lack of an allosteric effect on channels already present in the membrane. Overnight incubation with U0126 prevents the normal expression of T-type Ca2+ channels on the membrane. In HSV-1 infected cells treated with IL-6, inhibition of ERK activity with U0126 caused a completed disruption of channel expression. The number of cells recorded under each condition is presented in parenthesis from 2 independent cell cultures. * denotes p ≤ 0.05 vs. control (non-infected cultures); ** denotes p ≤ 0.05 vs. HSV-1 infected cell cultures treated with IL-6.

Techniques Used: Activation Assay, Functional Assay, Expressing, Cell Differentiation, Infection, Cell Culture, Western Blot, Incubation, Inhibition, Activity Assay

Effect of HSV-1 infection on IL-6 secretion, and its contribution to viral replication and release. A) IL-6 release was assessed from the supernatant of HSV-1 infected HCEC as assessed by ELISA (* denotes p < 0.05 vs. HSV-1 infected cells for 6 h; number of independent cell cultures n=3). B) IL-6 evokes a considerable increase in the expression of the HSV-1 TK following infection of differentiated ND7/23 cells (* denotes p < 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4). C) IL-6 had no effect on plaque formation following HSV-1 infection of differentiated ND7/23 cells (p > 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4).
Figure Legend Snippet: Effect of HSV-1 infection on IL-6 secretion, and its contribution to viral replication and release. A) IL-6 release was assessed from the supernatant of HSV-1 infected HCEC as assessed by ELISA (* denotes p < 0.05 vs. HSV-1 infected cells for 6 h; number of independent cell cultures n=3). B) IL-6 evokes a considerable increase in the expression of the HSV-1 TK following infection of differentiated ND7/23 cells (* denotes p < 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4). C) IL-6 had no effect on plaque formation following HSV-1 infection of differentiated ND7/23 cells (p > 0.05 vs. HSV-1 infected cells; number of independent cell cultures n=4).

Techniques Used: Infection, Enzyme-linked Immunosorbent Assay, Expressing


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    Millipore nd7 23 cells
    ( a ) Family of classical currents recorded from <t>ND7/23</t> cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .
    Nd7 23 Cells, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore autonomous camkii activity assays nd7 23
    ( a ) Family of classical currents recorded from <t>ND7/23</t> cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .
    Autonomous Camkii Activity Assays Nd7 23, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore hc qds nd7 23
    ( a ) Family of classical currents recorded from <t>ND7/23</t> cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .
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    ( a ) Family of classical currents recorded from ND7/23 cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .

    Journal: eLife

    Article Title: A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels

    doi: 10.7554/eLife.77558

    Figure Lengend Snippet: ( a ) Family of classical currents recorded from ND7/23 cells expressing recombinant Nav1.8. Currents were elicited by 50 ms depolarizing voltage steps from +25 mV to −55 mV in –10 mV increments from a holding potential of –100 mV (inset). ( b ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p<0.0001, 0.0035, 0.0077 vs. control, respectively) and inactivation (p=0.0002, <0.0001, <0.0001 vs. control, respectively) of Nav1.8. ( c ) FHF2B, FHF2A, and FHF4A accelerated the recovery rate from Nav1.8 inactivation. The time constants estimated from single-exponential fits were 29.71 ± 2.54 ms (control), 5.81 ± 1.03 ms (FHF2B, p<0.0001 vs. control), 4.45 ± 0.43 ms (FHF2A, p<0.0001 vs. control), and 5.46 ± 0.40 ms (FHF4A, p<0.0001 vs. control). ( d ) Family of classical currents recorded from HEK293 cells expressing recombinant Nav1.9. Currents were elicited by 50 ms depolarizing voltage steps from +20 mV to −100 mV in –20 mV increments from a holding potential of –120 mV (inset). ( e ) Effects of FHF2B, FHF2A, and FHF4A on steady-state activation (p=0.1832, 0.0171, 0.3215 vs. control, respectively) and inactivation (p=0.175, 0.5978, 0.636 vs. control, respectively) of Nav1.9. ( f ), FHF2B, FHF2A, and FHF4A did not affect the recovery rate from Nav1.9 inactivation. The time constants estimated from single-exponential fits were 38.46 ± 4.64 ms (control), 48.99 ± 6.93 ms (FHF2B, p=0.2041 vs. control), 49.72 ± 6.81 ms (FHF2A, p=0.1745 vs. control), and 31.95 ± 2.84 ms (FHF4A, p=0.4786 vs. control). In ( a–c ), cells were pretreated with 500 nM TTX. In ( c, f ), recovery from inactivation was assayed by the protocol that the cells were prepulsed to 0 mV for 50 ms to inactivate sodium channels and then brought back to –100 mV for increasing recovery durations before the test pulse to 0 mV. Filled circles, open circles, open diamond, and open squares represent control, FHF2B, FHF2A, and FHF4A, respectively. The number of separate cells tested is indicated in parentheses. Data points are shown as mean ± SE. The V 1/2 values for activation and inactivation are summarized in .

    Article Snippet: Cell line (mouse × rat hybridoma nerve) , ND7/23 cells , MilliporeSigma , CAT# 92090903 , .

    Techniques: Expressing, Recombinant, Activation Assay

    Journal: eLife

    Article Title: A-type FHFs mediate resurgent currents through TTX-resistant voltage-gated sodium channels

    doi: 10.7554/eLife.77558

    Figure Lengend Snippet:

    Article Snippet: Cell line (mouse × rat hybridoma nerve) , ND7/23 cells , MilliporeSigma , CAT# 92090903 , .

    Techniques: Transfection, Construct, shRNA, Recombinant, Plasmid Preparation, Sequencing, Mutagenesis, Software