rabbit anti hcn3  (Alomone Labs)


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    Name:
    Anti HCN3 Antibody
    Description:
    Anti HCN3 Antibody APC 057 is a highly specific antibody directed against an epitope of the rat protein The antibody can be used in western blot and immunohistochemistry applications It has been designed to recognize HCN3 from human rat and mouse samples
    Catalog Number:
    APC-057
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunofluorescence, Immunohistochemistry, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Rabbit
    Isotype:
    Rabbit IgG
    Buy from Supplier


    Structured Review

    Alomone Labs rabbit anti hcn3
    Anti HCN3 Antibody
    Anti HCN3 Antibody APC 057 is a highly specific antibody directed against an epitope of the rat protein The antibody can be used in western blot and immunohistochemistry applications It has been designed to recognize HCN3 from human rat and mouse samples
    https://www.bioz.com/result/rabbit anti hcn3/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti hcn3 - by Bioz Stars, 2021-10
    92/100 stars

    Images

    1) Product Images from "Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits"

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI99986

    The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P
    Figure Legend Snippet: The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P

    Techniques Used: shRNA, Expressing, Over Expression, Injection

    2) Product Images from "Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits"

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI99986

    The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P
    Figure Legend Snippet: The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P

    Techniques Used: shRNA, Expressing, Over Expression, Injection

    3) Product Images from "Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels"

    Article Title: Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms20204995

    HCN3 channel expression in mitochondria isolated from renal cortex and HEK293 cells. ( a ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 with polyclonal antibodies detected only HCN2 (~94 kDa) and HCN3 (~86 kDa) in renal mitochondria. α-tubulin (~50 kDa) and voltage dependent anion channel (VDAC, ~31 kDa) were used as negative and positive controls of mitochondria abundance, respectively. ( b ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M) of control HEK293 cells. ( c ) Immunoblotting of HEK293 cells transfected with HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M). Only HCN3 (86 kDa) and HCN4 (160 kDa) were observed in HEK293 mitochondria. Immunogold electron microscopy localization of HCN3 (arrows) in the inner mitochondrial membrane of mitochondria from ( d ) rat (renal cortex) and ( e ) human kidney. ( f ) Negative control was performed in the absence of the primary antibody.
    Figure Legend Snippet: HCN3 channel expression in mitochondria isolated from renal cortex and HEK293 cells. ( a ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 with polyclonal antibodies detected only HCN2 (~94 kDa) and HCN3 (~86 kDa) in renal mitochondria. α-tubulin (~50 kDa) and voltage dependent anion channel (VDAC, ~31 kDa) were used as negative and positive controls of mitochondria abundance, respectively. ( b ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M) of control HEK293 cells. ( c ) Immunoblotting of HEK293 cells transfected with HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M). Only HCN3 (86 kDa) and HCN4 (160 kDa) were observed in HEK293 mitochondria. Immunogold electron microscopy localization of HCN3 (arrows) in the inner mitochondrial membrane of mitochondria from ( d ) rat (renal cortex) and ( e ) human kidney. ( f ) Negative control was performed in the absence of the primary antibody.

    Techniques Used: Expressing, Isolation, Transfection, Electron Microscopy, Negative Control

    Respiratory parameters for control and HCN3 overexpressed in HEK293 cells. ( a ) Cellular routine respiration; ( b ) leak of respiration; ( c ) respiration associated to oxidative phosphorylation (P); ( d ) respiratory control index (RCI). Data is presented as mean ± SEM, n = 4–5. Unpaired t -test. *** p
    Figure Legend Snippet: Respiratory parameters for control and HCN3 overexpressed in HEK293 cells. ( a ) Cellular routine respiration; ( b ) leak of respiration; ( c ) respiration associated to oxidative phosphorylation (P); ( d ) respiratory control index (RCI). Data is presented as mean ± SEM, n = 4–5. Unpaired t -test. *** p

    Techniques Used:

    Effect of ZD7288 and carbonyl cyanide m-chlorophenylhydrazone (CCCP) on mitochondrial membrane potential (ΔΨm) in HEK293 cells (control) and HEK293 cells transfected with HCN3. ( a ) Visualization by Cytation 5 showing JC-1 red, JC-1 green and merge images of HEK293 cells. ( b ) The JC-1 fluorescence was quantified as the ratio of the red fluorescence (590 nm) to green fluorescence (525 nm) using Cytation 5 and the fluorescence was normalized with HEK293 cells (control) without inhibitor. ZD7288 (50 μM), CCCP (50 μM). Data are mean ± SEM, n = 4–8. *** p
    Figure Legend Snippet: Effect of ZD7288 and carbonyl cyanide m-chlorophenylhydrazone (CCCP) on mitochondrial membrane potential (ΔΨm) in HEK293 cells (control) and HEK293 cells transfected with HCN3. ( a ) Visualization by Cytation 5 showing JC-1 red, JC-1 green and merge images of HEK293 cells. ( b ) The JC-1 fluorescence was quantified as the ratio of the red fluorescence (590 nm) to green fluorescence (525 nm) using Cytation 5 and the fluorescence was normalized with HEK293 cells (control) without inhibitor. ZD7288 (50 μM), CCCP (50 μM). Data are mean ± SEM, n = 4–8. *** p

    Techniques Used: Transfection, Fluorescence

    Inwardly potassium (K + ) currents recorded in isolated mitochondria from the renal cortex and HEK293 cells correspond to HCN3. ( a ) Fluorescence microscopy imaging from isolated mitochondria obtained from the renal cortex. Mitochondria were incubated for 10 min with 5 µM of the fluorescent indicator MitoTracker Green FM. Excitation was 490 nm and emission collected at 525 nm. By fluorescence microscopy it was possible to separate mitochondria from debris during patch clamp experiments. ( b ) Whole-mitochondria voltage clamp currents were recorded with 20 mV steps from −120 mV to +60 mV and a holding potential of 0 mV. Basal shows a representative family of HCN currents obtained from a single mitochondrion and the same family of currents after 2 min of incubation with 50 µM of the inhibitor ZD7288. ( c ) Currents obtained at −120 mV from different independent mitochondria under basal conditions and after addition of ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value. ( d ) HEK293T cells labeled with the fluorescent indicator MitoTracker Green FM. ( e ) Isolated mitochondria from HEK293 cells labeled with MitoTracker Green FM. ( f ) Family of currents obtained in whole-cell configuration and ( g ) in whole-mitochondria, under basal conditions and from cells overexpressing HCN1, HCN2 and HCN3. ( h ) Currents recorded at −120 mV from mitochondria isolated from HEK293 control cells (Basal) and cells overexpressing HCN1, HCN2, HCN3 and HCN3 + ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value.
    Figure Legend Snippet: Inwardly potassium (K + ) currents recorded in isolated mitochondria from the renal cortex and HEK293 cells correspond to HCN3. ( a ) Fluorescence microscopy imaging from isolated mitochondria obtained from the renal cortex. Mitochondria were incubated for 10 min with 5 µM of the fluorescent indicator MitoTracker Green FM. Excitation was 490 nm and emission collected at 525 nm. By fluorescence microscopy it was possible to separate mitochondria from debris during patch clamp experiments. ( b ) Whole-mitochondria voltage clamp currents were recorded with 20 mV steps from −120 mV to +60 mV and a holding potential of 0 mV. Basal shows a representative family of HCN currents obtained from a single mitochondrion and the same family of currents after 2 min of incubation with 50 µM of the inhibitor ZD7288. ( c ) Currents obtained at −120 mV from different independent mitochondria under basal conditions and after addition of ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value. ( d ) HEK293T cells labeled with the fluorescent indicator MitoTracker Green FM. ( e ) Isolated mitochondria from HEK293 cells labeled with MitoTracker Green FM. ( f ) Family of currents obtained in whole-cell configuration and ( g ) in whole-mitochondria, under basal conditions and from cells overexpressing HCN1, HCN2 and HCN3. ( h ) Currents recorded at −120 mV from mitochondria isolated from HEK293 control cells (Basal) and cells overexpressing HCN1, HCN2, HCN3 and HCN3 + ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value.

    Techniques Used: Isolation, Fluorescence, Microscopy, Imaging, Incubation, Patch Clamp, Labeling

    4) Product Images from "Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits"

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI99986

    The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P
    Figure Legend Snippet: The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P

    Techniques Used: shRNA, Expressing, Over Expression, Injection

    5) Product Images from "Age-Dependent Up-Regulation of HCN Channels in Spiral Ganglion Neurons Coincide With Hearing Loss in Mice"

    Article Title: Age-Dependent Up-Regulation of HCN Channels in Spiral Ganglion Neurons Coincide With Hearing Loss in Mice

    Journal: Frontiers in Aging Neuroscience

    doi: 10.3389/fnagi.2018.00353

    Increased expression of hyperpolarization-activated cyclic nucleotide-gated 1 (HCN1) and HCN2 in spiral ganglion neurons (SGNs) of old mice. (A) Auditory brainstem response (ABR) hearing thresholds were measured from young and old mice ( n = 8). Arrows indicate that thresholds exceeded the upper limits of the tucker davis technologies (TDT) ABR system. (B) Real-time PCR of HCN subunits in SGNs from young and old mice, showed a significant increase of HCN1 and HCN2 at the mRNA level in old mice ( n = 6). (C) Western blotting showed HCN1 and HCN2 expression level was significantly increased in the SGNs of old mice, but HCN3 and HCN4 were unchanged ( n = 4). Data are means ± SEM, * p
    Figure Legend Snippet: Increased expression of hyperpolarization-activated cyclic nucleotide-gated 1 (HCN1) and HCN2 in spiral ganglion neurons (SGNs) of old mice. (A) Auditory brainstem response (ABR) hearing thresholds were measured from young and old mice ( n = 8). Arrows indicate that thresholds exceeded the upper limits of the tucker davis technologies (TDT) ABR system. (B) Real-time PCR of HCN subunits in SGNs from young and old mice, showed a significant increase of HCN1 and HCN2 at the mRNA level in old mice ( n = 6). (C) Western blotting showed HCN1 and HCN2 expression level was significantly increased in the SGNs of old mice, but HCN3 and HCN4 were unchanged ( n = 4). Data are means ± SEM, * p

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

    6) Product Images from "Differential regulation of HCN channel isoform expression in thalamic neurons of epileptic and non-epileptic rat strains"

    Article Title: Differential regulation of HCN channel isoform expression in thalamic neurons of epileptic and non-epileptic rat strains

    Journal: Neurobiology of disease

    doi: 10.1016/j.nbd.2011.08.032

    Immunohistochemical characterization of HCN channel localization in dLGN. ( A ) Specific antibodies directed against HCN1 (1 st column), HCN2 (2 nd column), HCN3 (3 rd column), and HCN4 (4 th column) were applied in WAG/Rij (upper row) and ACI (lower row) rats.
    Figure Legend Snippet: Immunohistochemical characterization of HCN channel localization in dLGN. ( A ) Specific antibodies directed against HCN1 (1 st column), HCN2 (2 nd column), HCN3 (3 rd column), and HCN4 (4 th column) were applied in WAG/Rij (upper row) and ACI (lower row) rats.

    Techniques Used: Immunohistochemistry

    Quantitative analyses of postnatal protein expression of HCN channels in dLGN tissue. HCN1 ( A ), HCN3 ( B ), HCN2 ( C ), and HCN4 ( D ) were detected by means of Western blotting (A = ACI, gray bars; W = WAG/Rij, black bars). Data from 4 independent protein
    Figure Legend Snippet: Quantitative analyses of postnatal protein expression of HCN channels in dLGN tissue. HCN1 ( A ), HCN3 ( B ), HCN2 ( C ), and HCN4 ( D ) were detected by means of Western blotting (A = ACI, gray bars; W = WAG/Rij, black bars). Data from 4 independent protein

    Techniques Used: Expressing, Western Blot

    7) Product Images from "Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits"

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI99986

    The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P
    Figure Legend Snippet: The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P

    Techniques Used: shRNA, Expressing, Over Expression, Injection

    Related Articles

    Incubation:

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits
    Article Snippet: .. The membranes were then incubated overnight at 4°C with primary antibodies as follows: rabbit anti-HCN1 (1:500, Alomone Labs), rabbit anti-HCN2 (1:200, Alomone Labs), rabbit anti-HCN3 (1:200, Alomone Labs), or rabbit anti-HCN4 (1:300, Alomone Labs) (clone number provided earlier). ..

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits
    Article Snippet: .. Sections were incubated overnight at 4°C with primary antibody/antibodies, as follows: mouse anti-glutamate (1:1000, MilliporeSigma; catalog MAB5304, RRID:AB_94698), goat anti-GAD67 (1:1000, Abcam; catalog ab80589, RRID:AB_1640532), rabbit anti-histamine (1:1000, MilliporeSigma; catalog AB5885, RRID:AB_177540) and rabbit anti-histamine (1:500, Acris; catalog 22939, RRID:AB_572245), mouse anti-TH (1:2000, MilliporeSigma; catalog T2928, RRID:AB_477569), goat anti-H1 receptor (1:500, Everest Biotech; catalog EB06904, RRID:AB_2230568) and rabbit anti-H1 receptor (1:50, Santa Cruz Biotechnology Inc.; catalog SC20633, RRID:AB_2277328), goat anti-H2 receptor (1:500, Everest Biotech; catalog EB06905, RRID:AB_2121375), rabbit anti-H4 receptor (1:200, Santa Cruz Biotechnology Inc.; catalog SC50313, RRID:AB_2119026), rabbit anti-HCN1 (1:300, Alomone Labs; catalog APC-056, RRID:AB_2039900), rabbit anti-HCN2 (1:100, Alomone Labs; catalog APC-030, RRID:AB_2313726), rabbit anti-HCN3 (1:100, Alomone Labs; catalog APC-057, RRID:AB_2039904), and rabbit anti-HCN4 (1:200, Alomone Labs; catalog APC-052, RRID:AB_2039906). ..

    Article Title: Selective Blockade of HCN1/HCN2 Channels as a Potential Pharmacological Strategy Against Pain
    Article Snippet: .. Cells were then blocked in 1% BSA for 10 min and incubated with rabbit anti-HCN1 [1:300], rabbit anti-HCN2 [1:100], rabbit anti-HCN3 [1:25], rabbit anti-HCN4 [1:200] (Alomone Labs, Israel) antibodies overnight at 4°C and Alexa Fluor 546 anti-rabbit (Invitrogen) secondary antibodies for 2 h. To spot nuclei, the sample was incubated with, 4′, 6-diamidino-2-phenylindole [1:1000] (DAPI, Vectashield Labs, UK) in 0.1% Tween 20 in PBS for 10 min. ..

    Article Title: Hyperpolarization-Activated Cyclic Nucleotide-Gated Ion (HCN) Channels Regulate PC12 Cell Differentiation Toward Sympathetic Neuron
    Article Snippet: .. After washing six times with PBS (5 min for each wash), cells were permeated by incubation in 0.5% Triton X-100 in PBS for 5 min, rinsed six times with PBS, blocked with 10% sheep serum in PBS for 45 min, washed once with 1% sheep serum in PBS, and incubated in a refrigerator (4°C) overnight in the presence or absence of the primary antibodies diluted with 1% sheep serum in PBS: 1:50 dilution for rabbit anti-HCN1 (APC-056), anti-HCN2 (APC-030), anti-HCN3 (APC-057), anti-HCN4 (AGP-004) (Alomone Labs, Jerusalem, Israel), anti-GAP43 (sc-135915) and anti-TH (sc-136100) (Santa Cruz Biotechnology, Inc., United States). ..

    Protease Inhibitor:

    Article Title: Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels
    Article Snippet: .. Anti-HCN1, anti-HCN2, anti-HCN3 and anti-HCN4 were purchased from Alomone (Jerusalem, Israel). cOmplete™ Protease Inhibitor Cocktail Roche, Mexico. ..

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  • 92
    Alomone Labs rabbit anti hcn3
    The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- <t>Hcn3</t> -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P
    Rabbit Anti Hcn3, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P

    Journal: The Journal of Clinical Investigation

    Article Title: Regularizing firing patterns of rat subthalamic neurons ameliorates parkinsonian motor deficits

    doi: 10.1172/JCI99986

    Figure Lengend Snippet: The HCN2 channel is responsible for the histamine-induced amelioration of motor deficits in PD rats. ( A – D ) LV- Hcn1 -shRNA, LV- Hcn2 -shRNA, LV- Hcn3 -shRNA, and LV- Hcn4 -shRNA effectively downregulated the expression of Hcn1 , Hcn2 , Hcn3 , and Hcn4 mRNAs and proteins ( n = 6 from 6 independent experiments) in the STN. ( E ) LV- Hcn2 -oe upregulated the expression of Hcn2 mRNAs and proteins ( n = 6 from 6 independent experiments). ( F – H ) Effects of downregulation and overexpression of the HCN2 channel in the STN on motor deficits of turning behavior ( F , n = 12), adhesive-removal test ( G , n = 10), and locomotor footprints ( H , n = 10) in PD rats with sham operation, saline injection, and histamine injection. Downregulation of the HCN2 channel significantly increased the apomorphine-induced turnings, prolonged contralesional adhesive-removal time, and shortened bilateral stride length, whereas downregulation of the HCN1, HCN3, or HCN4 channel had no effect on these motor deficits. Only the downregulation of HCN2 rather than the HCN1, HCN3, or HCN4 channel blocked the amelioration of turnings, removal time, and stride length of PD rats induced by microinjection of histamine into the STN. Overexpression of the HCN2 channel in STN not only decreased the turnings, reduced removal time, and enlarged bilateral stride length of PD rats, but also improved the histamine-induced amelioration in these motor behaviors. Data are represented as mean ± SEM. *** P

    Article Snippet: The membranes were then incubated overnight at 4°C with primary antibodies as follows: rabbit anti-HCN1 (1:500, Alomone Labs), rabbit anti-HCN2 (1:200, Alomone Labs), rabbit anti-HCN3 (1:200, Alomone Labs), or rabbit anti-HCN4 (1:300, Alomone Labs) (clone number provided earlier).

    Techniques: shRNA, Expressing, Over Expression, Injection

    HCN3 channel expression in mitochondria isolated from renal cortex and HEK293 cells. ( a ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 with polyclonal antibodies detected only HCN2 (~94 kDa) and HCN3 (~86 kDa) in renal mitochondria. α-tubulin (~50 kDa) and voltage dependent anion channel (VDAC, ~31 kDa) were used as negative and positive controls of mitochondria abundance, respectively. ( b ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M) of control HEK293 cells. ( c ) Immunoblotting of HEK293 cells transfected with HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M). Only HCN3 (86 kDa) and HCN4 (160 kDa) were observed in HEK293 mitochondria. Immunogold electron microscopy localization of HCN3 (arrows) in the inner mitochondrial membrane of mitochondria from ( d ) rat (renal cortex) and ( e ) human kidney. ( f ) Negative control was performed in the absence of the primary antibody.

    Journal: International Journal of Molecular Sciences

    Article Title: Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels

    doi: 10.3390/ijms20204995

    Figure Lengend Snippet: HCN3 channel expression in mitochondria isolated from renal cortex and HEK293 cells. ( a ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 with polyclonal antibodies detected only HCN2 (~94 kDa) and HCN3 (~86 kDa) in renal mitochondria. α-tubulin (~50 kDa) and voltage dependent anion channel (VDAC, ~31 kDa) were used as negative and positive controls of mitochondria abundance, respectively. ( b ) Immunoblotting of HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M) of control HEK293 cells. ( c ) Immunoblotting of HEK293 cells transfected with HCN1, HCN2, HCN3 and HCN4 in supernatant (S) and mitochondria (M). Only HCN3 (86 kDa) and HCN4 (160 kDa) were observed in HEK293 mitochondria. Immunogold electron microscopy localization of HCN3 (arrows) in the inner mitochondrial membrane of mitochondria from ( d ) rat (renal cortex) and ( e ) human kidney. ( f ) Negative control was performed in the absence of the primary antibody.

    Article Snippet: Anti-HCN1, anti-HCN2, anti-HCN3 and anti-HCN4 were purchased from Alomone (Jerusalem, Israel). cOmplete™ Protease Inhibitor Cocktail Roche, Mexico.

    Techniques: Expressing, Isolation, Transfection, Electron Microscopy, Negative Control

    Respiratory parameters for control and HCN3 overexpressed in HEK293 cells. ( a ) Cellular routine respiration; ( b ) leak of respiration; ( c ) respiration associated to oxidative phosphorylation (P); ( d ) respiratory control index (RCI). Data is presented as mean ± SEM, n = 4–5. Unpaired t -test. *** p

    Journal: International Journal of Molecular Sciences

    Article Title: Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels

    doi: 10.3390/ijms20204995

    Figure Lengend Snippet: Respiratory parameters for control and HCN3 overexpressed in HEK293 cells. ( a ) Cellular routine respiration; ( b ) leak of respiration; ( c ) respiration associated to oxidative phosphorylation (P); ( d ) respiratory control index (RCI). Data is presented as mean ± SEM, n = 4–5. Unpaired t -test. *** p

    Article Snippet: Anti-HCN1, anti-HCN2, anti-HCN3 and anti-HCN4 were purchased from Alomone (Jerusalem, Israel). cOmplete™ Protease Inhibitor Cocktail Roche, Mexico.

    Techniques:

    Effect of ZD7288 and carbonyl cyanide m-chlorophenylhydrazone (CCCP) on mitochondrial membrane potential (ΔΨm) in HEK293 cells (control) and HEK293 cells transfected with HCN3. ( a ) Visualization by Cytation 5 showing JC-1 red, JC-1 green and merge images of HEK293 cells. ( b ) The JC-1 fluorescence was quantified as the ratio of the red fluorescence (590 nm) to green fluorescence (525 nm) using Cytation 5 and the fluorescence was normalized with HEK293 cells (control) without inhibitor. ZD7288 (50 μM), CCCP (50 μM). Data are mean ± SEM, n = 4–8. *** p

    Journal: International Journal of Molecular Sciences

    Article Title: Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels

    doi: 10.3390/ijms20204995

    Figure Lengend Snippet: Effect of ZD7288 and carbonyl cyanide m-chlorophenylhydrazone (CCCP) on mitochondrial membrane potential (ΔΨm) in HEK293 cells (control) and HEK293 cells transfected with HCN3. ( a ) Visualization by Cytation 5 showing JC-1 red, JC-1 green and merge images of HEK293 cells. ( b ) The JC-1 fluorescence was quantified as the ratio of the red fluorescence (590 nm) to green fluorescence (525 nm) using Cytation 5 and the fluorescence was normalized with HEK293 cells (control) without inhibitor. ZD7288 (50 μM), CCCP (50 μM). Data are mean ± SEM, n = 4–8. *** p

    Article Snippet: Anti-HCN1, anti-HCN2, anti-HCN3 and anti-HCN4 were purchased from Alomone (Jerusalem, Israel). cOmplete™ Protease Inhibitor Cocktail Roche, Mexico.

    Techniques: Transfection, Fluorescence

    Inwardly potassium (K + ) currents recorded in isolated mitochondria from the renal cortex and HEK293 cells correspond to HCN3. ( a ) Fluorescence microscopy imaging from isolated mitochondria obtained from the renal cortex. Mitochondria were incubated for 10 min with 5 µM of the fluorescent indicator MitoTracker Green FM. Excitation was 490 nm and emission collected at 525 nm. By fluorescence microscopy it was possible to separate mitochondria from debris during patch clamp experiments. ( b ) Whole-mitochondria voltage clamp currents were recorded with 20 mV steps from −120 mV to +60 mV and a holding potential of 0 mV. Basal shows a representative family of HCN currents obtained from a single mitochondrion and the same family of currents after 2 min of incubation with 50 µM of the inhibitor ZD7288. ( c ) Currents obtained at −120 mV from different independent mitochondria under basal conditions and after addition of ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value. ( d ) HEK293T cells labeled with the fluorescent indicator MitoTracker Green FM. ( e ) Isolated mitochondria from HEK293 cells labeled with MitoTracker Green FM. ( f ) Family of currents obtained in whole-cell configuration and ( g ) in whole-mitochondria, under basal conditions and from cells overexpressing HCN1, HCN2 and HCN3. ( h ) Currents recorded at −120 mV from mitochondria isolated from HEK293 control cells (Basal) and cells overexpressing HCN1, HCN2, HCN3 and HCN3 + ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value.

    Journal: International Journal of Molecular Sciences

    Article Title: Novel Potassium Channels in Kidney Mitochondria: The Hyperpolarization-Activated and Cyclic Nucleotide-Gated HCN Channels

    doi: 10.3390/ijms20204995

    Figure Lengend Snippet: Inwardly potassium (K + ) currents recorded in isolated mitochondria from the renal cortex and HEK293 cells correspond to HCN3. ( a ) Fluorescence microscopy imaging from isolated mitochondria obtained from the renal cortex. Mitochondria were incubated for 10 min with 5 µM of the fluorescent indicator MitoTracker Green FM. Excitation was 490 nm and emission collected at 525 nm. By fluorescence microscopy it was possible to separate mitochondria from debris during patch clamp experiments. ( b ) Whole-mitochondria voltage clamp currents were recorded with 20 mV steps from −120 mV to +60 mV and a holding potential of 0 mV. Basal shows a representative family of HCN currents obtained from a single mitochondrion and the same family of currents after 2 min of incubation with 50 µM of the inhibitor ZD7288. ( c ) Currents obtained at −120 mV from different independent mitochondria under basal conditions and after addition of ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value. ( d ) HEK293T cells labeled with the fluorescent indicator MitoTracker Green FM. ( e ) Isolated mitochondria from HEK293 cells labeled with MitoTracker Green FM. ( f ) Family of currents obtained in whole-cell configuration and ( g ) in whole-mitochondria, under basal conditions and from cells overexpressing HCN1, HCN2 and HCN3. ( h ) Currents recorded at −120 mV from mitochondria isolated from HEK293 control cells (Basal) and cells overexpressing HCN1, HCN2, HCN3 and HCN3 + ZD7288. Each filled circle represents a single measurement and the horizontal line indicates the mean value.

    Article Snippet: Anti-HCN1, anti-HCN2, anti-HCN3 and anti-HCN4 were purchased from Alomone (Jerusalem, Israel). cOmplete™ Protease Inhibitor Cocktail Roche, Mexico.

    Techniques: Isolation, Fluorescence, Microscopy, Imaging, Incubation, Patch Clamp, Labeling