anti k v 2 1 rabbit polyclonal antibody  (Alomone Labs)

Journal: Cells

Article Title: Increased K V 2.1 Channel Clustering Underlies the Reduction of Delayed Rectifier K + Currents in Hippocampal Neurons of the Tg2576 Alzheimer’s Disease Mouse

doi: 10.3390/cells11182820

Figure Lengend Snippet: Effect of the intracellular diffusion of the anti-K V 2.1 monoclonal antibody on I DR recorded in the WT and Tg2576 primary hippocampal neurons. ( A ) Time-dependent inhibitory effect of the anti-K V 2.1 monoclonal antibody (10 µg mL − 1 ) on I DR recorded in WT and Tg2576 primary hippocampal pyramidal neurons. ( B ) Quantification of I DR densities, at +40 mV, before (Control) and after 6 min of the anti-K V 2.1 intracellular diffusion (+K V 2.1Ab). Data are expressed as percentage of WT and Tg2576 internal controls. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. internal controls. ( C ) Superimposed representative traces of I DR at +40 mV recorded before and after 6 min of intracellular diffusion of the anti-K V 2.1 antibody ( top ), and representative traces resulting from the subtraction of the currents resistant to the anti-K V 2.1 antibody from the initial currents ( bottom ) in WT ( left ) and Tg2576 ( right ) neurons. ( D ) Representative traces of I DR recorded in control conditions and upon 6 min of intracellular diffusion of the anti-K V 2.1 monoclonal antibody (10 µg mL − 1 ) in WT ( left ) and Tg2576 ( right ) primary hippocampal pyramidal neurons. Protocols are shown in the lower part of the panel. ( E ) I/V relationships for the I DR recorded in control conditions and upon 6 min of intracellular diffusion of the anti-K V 2.1 antibody in the WT ( left ) and Tg2576 primary hippocampal neurons ( right ). ( F ) Steady-state activation curves of I DR recorded in WT and Tg2576 hippocampal neurons in control conditions and in WT neurons upon 6 min of intracellular diffusion of the anti-K V 2.1 antibody. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. WT.

Article Snippet: To this aim, both the Tg2576 and WT hippocampal neurons were fixed and stained with the anti-K V 2.1 rabbit polyclonal antibody (1:1000, Alomone Labs, Jerusalem, Israel) and subjected to imaging on a confocal microscope.

Techniques: Diffusion-based Assay, Activation Assay

Journal: Cells

Article Title: Increased K V 2.1 Channel Clustering Underlies the Reduction of Delayed Rectifier K + Currents in Hippocampal Neurons of the Tg2576 Alzheimer’s Disease Mouse

doi: 10.3390/cells11182820

Figure Lengend Snippet: K V 2.1 clustering and effect of glutamate on I DR in WT and Tg2576 primary hippocampal pyramidal neurons. ( A ) Representative confocal images of pyramidal neurons from Tg2576 ( c , d ) and WT ( a , b ) primary hippocampal cultures stained with anti-K V 2.1 antibody (green). On the right, a magnification of neuronal somata from the confocal images shown on the left. ( B ) Time-dependent stimulatory effect of glutamate (10 µM) on I DR recorded in WT and Tg2576 primary hippocampal pyramidal neurons. ( C ) Quantification of I DR densities, at +40 mV, before (Control) and after 11 min of 10 µM glutamate exposure (Glu). Data are represented as percentage of WT and Tg2576 internal controls. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. internal controls. ( D ) Representative traces of I DR recorded in control conditions and upon 11 min of 10 µM glutamate exposure in WT ( left ) and Tg2576 ( right ) primary hippocampal pyramidal neurons. Protocols are shown in the lower part of the panel. ( E ) I/V relationships for the I DR recorded in control conditions and upon 11 min of 10 µM glutamate exposure in the WT ( left ) and Tg2576 primary hippocampal neurons ( right ). ( F ) Steady-state activation curves of I DR recorded in WT and Tg2576 hippocampal neurons in control conditions and in Tg2576 neurons upon 11 min of 10 µM glutamate exposure. Values are expressed as mean ± SEM of 3 independent experimental sessions.

Article Snippet: To this aim, both the Tg2576 and WT hippocampal neurons were fixed and stained with the anti-K V 2.1 rabbit polyclonal antibody (1:1000, Alomone Labs, Jerusalem, Israel) and subjected to imaging on a confocal microscope.

Techniques: Staining, Activation Assay

Journal: Cells

Article Title: Increased K V 2.1 Channel Clustering Underlies the Reduction of Delayed Rectifier K + Currents in Hippocampal Neurons of the Tg2576 Alzheimer’s Disease Mouse

doi: 10.3390/cells11182820

Figure Lengend Snippet: Effect of the anti-K V 2.1 monoclonal antibody on the positive modulation of I DR by glutamate in WT and Tg2576 primary hippocampal neurons. ( A ) Superimposed representative traces of I DR at +40 mV recorded before (Control) and after 11 min of 10 µM glutamate (Glu), and representative traces recorded before and after the intracellular diffusion of the anti-K V 2.1 antibody and after 11 min of 10 µM glutamate exposure in the presence of the anti-K V 2.1 antibody. ( B ) Quantification of I DR densities, at +40 mV, in control conditions and upon 11 min of 10 µM glutamate exposure with (+K V 2.1Ab) and without the anti-K V 2.1 antibody (−K V 2.1Ab) in the recording pipette. Data are expressed as percentage of WT and Tg2576 internal controls. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. control; ** p < 0.001 vs. GLU + K V 2.1Ab.

Article Snippet: To this aim, both the Tg2576 and WT hippocampal neurons were fixed and stained with the anti-K V 2.1 rabbit polyclonal antibody (1:1000, Alomone Labs, Jerusalem, Israel) and subjected to imaging on a confocal microscope.

Techniques: Diffusion-based Assay, Transferring

Journal: Cells

Article Title: Increased K V 2.1 Channel Clustering Underlies the Reduction of Delayed Rectifier K + Currents in Hippocampal Neurons of the Tg2576 Alzheimer’s Disease Mouse

doi: 10.3390/cells11182820

Figure Lengend Snippet: Effect of the intracellular diffusion of the anti-K V 2.1 monoclonal antibody on I DR recorded in the WT and Tg2576 primary hippocampal neurons. ( A ) Time-dependent inhibitory effect of the anti-K V 2.1 monoclonal antibody (10 µg mL − 1 ) on I DR recorded in WT and Tg2576 primary hippocampal pyramidal neurons. ( B ) Quantification of I DR densities, at +40 mV, before (Control) and after 6 min of the anti-K V 2.1 intracellular diffusion (+K V 2.1Ab). Data are expressed as percentage of WT and Tg2576 internal controls. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. internal controls. ( C ) Superimposed representative traces of I DR at +40 mV recorded before and after 6 min of intracellular diffusion of the anti-K V 2.1 antibody ( top ), and representative traces resulting from the subtraction of the currents resistant to the anti-K V 2.1 antibody from the initial currents ( bottom ) in WT ( left ) and Tg2576 ( right ) neurons. ( D ) Representative traces of I DR recorded in control conditions and upon 6 min of intracellular diffusion of the anti-K V 2.1 monoclonal antibody (10 µg mL − 1 ) in WT ( left ) and Tg2576 ( right ) primary hippocampal pyramidal neurons. Protocols are shown in the lower part of the panel. ( E ) I/V relationships for the I DR recorded in control conditions and upon 6 min of intracellular diffusion of the anti-K V 2.1 antibody in the WT ( left ) and Tg2576 primary hippocampal neurons ( right ). ( F ) Steady-state activation curves of I DR recorded in WT and Tg2576 hippocampal neurons in control conditions and in WT neurons upon 6 min of intracellular diffusion of the anti-K V 2.1 antibody. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. WT.

Article Snippet: Following three washes in PBS, cells were blocked in PBS containing 3% of BSA for 30 min, and then incubated overnight at 4 °C with the rabbit anti-K V 2.1 antibody (1:1000, Alomone Labs, Jerusalem, Israel).

Techniques: Diffusion-based Assay, Activation Assay

Journal: Cells

Article Title: Increased K V 2.1 Channel Clustering Underlies the Reduction of Delayed Rectifier K + Currents in Hippocampal Neurons of the Tg2576 Alzheimer’s Disease Mouse

doi: 10.3390/cells11182820

Figure Lengend Snippet: K V 2.1 clustering and effect of glutamate on I DR in WT and Tg2576 primary hippocampal pyramidal neurons. ( A ) Representative confocal images of pyramidal neurons from Tg2576 ( c , d ) and WT ( a , b ) primary hippocampal cultures stained with anti-K V 2.1 antibody (green). On the right, a magnification of neuronal somata from the confocal images shown on the left. ( B ) Time-dependent stimulatory effect of glutamate (10 µM) on I DR recorded in WT and Tg2576 primary hippocampal pyramidal neurons. ( C ) Quantification of I DR densities, at +40 mV, before (Control) and after 11 min of 10 µM glutamate exposure (Glu). Data are represented as percentage of WT and Tg2576 internal controls. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. internal controls. ( D ) Representative traces of I DR recorded in control conditions and upon 11 min of 10 µM glutamate exposure in WT ( left ) and Tg2576 ( right ) primary hippocampal pyramidal neurons. Protocols are shown in the lower part of the panel. ( E ) I/V relationships for the I DR recorded in control conditions and upon 11 min of 10 µM glutamate exposure in the WT ( left ) and Tg2576 primary hippocampal neurons ( right ). ( F ) Steady-state activation curves of I DR recorded in WT and Tg2576 hippocampal neurons in control conditions and in Tg2576 neurons upon 11 min of 10 µM glutamate exposure. Values are expressed as mean ± SEM of 3 independent experimental sessions.

Article Snippet: Following three washes in PBS, cells were blocked in PBS containing 3% of BSA for 30 min, and then incubated overnight at 4 °C with the rabbit anti-K V 2.1 antibody (1:1000, Alomone Labs, Jerusalem, Israel).

Techniques: Staining, Activation Assay

Journal: Cells

Article Title: Increased K V 2.1 Channel Clustering Underlies the Reduction of Delayed Rectifier K + Currents in Hippocampal Neurons of the Tg2576 Alzheimer’s Disease Mouse

doi: 10.3390/cells11182820

Figure Lengend Snippet: Effect of the anti-K V 2.1 monoclonal antibody on the positive modulation of I DR by glutamate in WT and Tg2576 primary hippocampal neurons. ( A ) Superimposed representative traces of I DR at +40 mV recorded before (Control) and after 11 min of 10 µM glutamate (Glu), and representative traces recorded before and after the intracellular diffusion of the anti-K V 2.1 antibody and after 11 min of 10 µM glutamate exposure in the presence of the anti-K V 2.1 antibody. ( B ) Quantification of I DR densities, at +40 mV, in control conditions and upon 11 min of 10 µM glutamate exposure with (+K V 2.1Ab) and without the anti-K V 2.1 antibody (−K V 2.1Ab) in the recording pipette. Data are expressed as percentage of WT and Tg2576 internal controls. Values are expressed as mean ± SEM of 3 independent experimental sessions. * p < 0.001 vs. control; ** p < 0.001 vs. GLU + K V 2.1Ab.

Article Snippet: Following three washes in PBS, cells were blocked in PBS containing 3% of BSA for 30 min, and then incubated overnight at 4 °C with the rabbit anti-K V 2.1 antibody (1:1000, Alomone Labs, Jerusalem, Israel).

Techniques: Diffusion-based Assay, Transferring