cav 3 1  (Alomone Labs)


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    Structured Review

    Alomone Labs cav 3 1
    Ca currents in wt and <t>Cav3.2</t> KO ventricular cardiomyocytes. ( A ) Original traces of Ca currents of a typical wt and Cav3.2 KO myocyte elicited by the pulse protocol displayed on top. ( B ) Current density–voltage relationships of wt (n = 20) and Cav3.2 KO (n = 20) myocytes. Data are expressed as means ± SEM. The current density–voltage relations hardly revealed any T-type Ca channel activity (expected to be maximal at −45 mV) but did reveal significant L-type Ca channel activity (peaking at +5 mV), which was similar in wt and Cav3.2 KO myocytes ( p = 0.67 at +5 mV, unpaired Student’s t -test). Capacitance values of the examined myocytes were 184 ± 13 pF for wt and 169 ± 11 pF for Cav3.2 KO ( p = 0.37). ( C ) The effect of the external application of 100 nM isoprenaline (ISO) on ICaT in a wt myocyte. From a holding potential of −95 mV, depolarizing voltage steps to −45 mV were applied every 3 s to elicit the currents. The arrows indicate the beginning and end of ISO application. Current peaks were finally plotted against time. ( D ) ICaT peaks before, during application after the steady-state was reached, and after the washout of ISO in wt (top) and Cav3.2 KO (bottom) myocytes. There was no significant difference between wt and Cav3.2 KO under control conditions ( p = 0.81, unpaired Student’s t -test) or in the presence of ISO ( p = 0.54). Data are expressed as means ± SEM. Each data point represents a single cell. ** p
    Cav 3 1, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice"

    Article Title: Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice

    Journal: Membranes

    doi: 10.3390/membranes12060566

    Ca currents in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Original traces of Ca currents of a typical wt and Cav3.2 KO myocyte elicited by the pulse protocol displayed on top. ( B ) Current density–voltage relationships of wt (n = 20) and Cav3.2 KO (n = 20) myocytes. Data are expressed as means ± SEM. The current density–voltage relations hardly revealed any T-type Ca channel activity (expected to be maximal at −45 mV) but did reveal significant L-type Ca channel activity (peaking at +5 mV), which was similar in wt and Cav3.2 KO myocytes ( p = 0.67 at +5 mV, unpaired Student’s t -test). Capacitance values of the examined myocytes were 184 ± 13 pF for wt and 169 ± 11 pF for Cav3.2 KO ( p = 0.37). ( C ) The effect of the external application of 100 nM isoprenaline (ISO) on ICaT in a wt myocyte. From a holding potential of −95 mV, depolarizing voltage steps to −45 mV were applied every 3 s to elicit the currents. The arrows indicate the beginning and end of ISO application. Current peaks were finally plotted against time. ( D ) ICaT peaks before, during application after the steady-state was reached, and after the washout of ISO in wt (top) and Cav3.2 KO (bottom) myocytes. There was no significant difference between wt and Cav3.2 KO under control conditions ( p = 0.81, unpaired Student’s t -test) or in the presence of ISO ( p = 0.54). Data are expressed as means ± SEM. Each data point represents a single cell. ** p
    Figure Legend Snippet: Ca currents in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Original traces of Ca currents of a typical wt and Cav3.2 KO myocyte elicited by the pulse protocol displayed on top. ( B ) Current density–voltage relationships of wt (n = 20) and Cav3.2 KO (n = 20) myocytes. Data are expressed as means ± SEM. The current density–voltage relations hardly revealed any T-type Ca channel activity (expected to be maximal at −45 mV) but did reveal significant L-type Ca channel activity (peaking at +5 mV), which was similar in wt and Cav3.2 KO myocytes ( p = 0.67 at +5 mV, unpaired Student’s t -test). Capacitance values of the examined myocytes were 184 ± 13 pF for wt and 169 ± 11 pF for Cav3.2 KO ( p = 0.37). ( C ) The effect of the external application of 100 nM isoprenaline (ISO) on ICaT in a wt myocyte. From a holding potential of −95 mV, depolarizing voltage steps to −45 mV were applied every 3 s to elicit the currents. The arrows indicate the beginning and end of ISO application. Current peaks were finally plotted against time. ( D ) ICaT peaks before, during application after the steady-state was reached, and after the washout of ISO in wt (top) and Cav3.2 KO (bottom) myocytes. There was no significant difference between wt and Cav3.2 KO under control conditions ( p = 0.81, unpaired Student’s t -test) or in the presence of ISO ( p = 0.54). Data are expressed as means ± SEM. Each data point represents a single cell. ** p

    Techniques Used: Activity Assay

    Electrically induced and caffeine-induced intracellular Ca transients in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Left: Representative time courses of Fluo-4 fluorescence reporting rises in cytosolic Ca concentration during electrical field stimulation at 0.1 Hz frequency in a single wt and Cav3.2 KO myocyte. The orange lines represent fits of the data with a single exponential function. Right: Comparison of mean Ca peak fluorescence relative to baseline (F/F0) between wt and Cav3.2 KO myocytes. Each data point represents a single cell, and values are expressed as means ± SEM (n= 68 for wt and 59 for Cav3.2 KO myocytes). * p
    Figure Legend Snippet: Electrically induced and caffeine-induced intracellular Ca transients in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Left: Representative time courses of Fluo-4 fluorescence reporting rises in cytosolic Ca concentration during electrical field stimulation at 0.1 Hz frequency in a single wt and Cav3.2 KO myocyte. The orange lines represent fits of the data with a single exponential function. Right: Comparison of mean Ca peak fluorescence relative to baseline (F/F0) between wt and Cav3.2 KO myocytes. Each data point represents a single cell, and values are expressed as means ± SEM (n= 68 for wt and 59 for Cav3.2 KO myocytes). * p

    Techniques Used: Fluorescence, Concentration Assay

    Immunostaining of T-type Ca channels in ventricular cardiomyocytes isolated from adult wt mice. Cav3.1 ( top ) channel expression and localization was detected using a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, 1:500). Cav3.2 ( bottom ) was detected with the selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, 1:1000; left and right cell; or anti-Cav3.2 polyclonal, #PA5-106771, source: rabbit, Invitrogen, 1:200; middle cell). Secondary antibody: Alexa Fluor 488, #A11008, goat anti-rabbit, Invitrogen, 1:500.
    Figure Legend Snippet: Immunostaining of T-type Ca channels in ventricular cardiomyocytes isolated from adult wt mice. Cav3.1 ( top ) channel expression and localization was detected using a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, 1:500). Cav3.2 ( bottom ) was detected with the selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, 1:1000; left and right cell; or anti-Cav3.2 polyclonal, #PA5-106771, source: rabbit, Invitrogen, 1:200; middle cell). Secondary antibody: Alexa Fluor 488, #A11008, goat anti-rabbit, Invitrogen, 1:500.

    Techniques Used: Immunostaining, Isolation, Mouse Assay, Expressing

    2) Product Images from "Neuromedin B receptor stimulation of Cav3.2 T-type Ca2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity"

    Article Title: Neuromedin B receptor stimulation of Cav3.2 T-type Ca2+ channels in primary sensory neurons mediates peripheral pain hypersensitivity

    Journal: Theranostics

    doi: 10.7150/thno.62255

    Activation of NmbR stimulates recombinant Cav3.2 channels heterologously expressed in HEK293 cells. A, western blot analysis of NmbR in HEK293 cells transiently transfected with NmbR cDNA. Blots depicted are representative of three independent experiments. B, membrane localization of NmbR in transfected HEK293 cells. Alphabets a through c in the diagram indicate the differential interference contrast (DIC, a ), the EGFP fluorescent signals of NmbR ( b ), and the merged image ( c ), respectively. C, exemplary current traces show the effect of Nmb (100 nM) on Cav3.1 (α1G), Cav3.2 (α1H) and Cav3.3 (α1I) channel currents. Currents were elicited by a 100 ms depolarizing step pulse from the holding potential of -110 mV to -30 mV. D, summary data show the effect of 100 nM Nmb on Cav3.1 ( n = 10), Cav3.2 ( n = 9) and Cav3.3 ( n = 7) channel currents. ** p
    Figure Legend Snippet: Activation of NmbR stimulates recombinant Cav3.2 channels heterologously expressed in HEK293 cells. A, western blot analysis of NmbR in HEK293 cells transiently transfected with NmbR cDNA. Blots depicted are representative of three independent experiments. B, membrane localization of NmbR in transfected HEK293 cells. Alphabets a through c in the diagram indicate the differential interference contrast (DIC, a ), the EGFP fluorescent signals of NmbR ( b ), and the merged image ( c ), respectively. C, exemplary current traces show the effect of Nmb (100 nM) on Cav3.1 (α1G), Cav3.2 (α1H) and Cav3.3 (α1I) channel currents. Currents were elicited by a 100 ms depolarizing step pulse from the holding potential of -110 mV to -30 mV. D, summary data show the effect of 100 nM Nmb on Cav3.1 ( n = 10), Cav3.2 ( n = 9) and Cav3.3 ( n = 7) channel currents. ** p

    Techniques Used: Activation Assay, Recombinant, Western Blot, Transfection

    3) Product Images from "Transmitter and ion channel profiles of neurons in the primate abducens and trochlear nuclei"

    Article Title: Transmitter and ion channel profiles of neurons in the primate abducens and trochlear nuclei

    Journal: Brain Structure & Function

    doi: 10.1007/s00429-021-02315-7

    Low-voltage activated calcium channel family (Cav3) subunits in the abducens and trochlear nucleus. a Consecutive coronal paraffin sections through the abducens nucleus (nVI) ( a ) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (third panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (second panel) as reference. b, c Close-up of Cav subunit expression in nVI MIF (red arrowheads) and SIF motoneurons (MNs) (green arrows) and INTs (blue arrow). d Consecutive coronal paraffin sections through the trochlear nucleus (nVI) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (second panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (third panel) as reference. Thin dashed lines in d indicate the border of nIV and thick dashed lines indicate the boundary between the MIF and SIF MNs. e Close-up of Cav subunit expression in MIF (red arrowheads) and SIF MNs (green arrow) on different sections as those illustrated in d . Note the weak Cav3.1 expression along the membrane of some SIF MNs (left column, black star). Red dashed lines indicate the tentative position of the border delineating the dorsal cap of nIV. f Cerebellar Purkinje cells located on the same consecutive sections as nVI as controls for immunopositivity of the different Cav subunits. Scale bar indicates 100 μm in a, d, f and 50 μm in b, c, e
    Figure Legend Snippet: Low-voltage activated calcium channel family (Cav3) subunits in the abducens and trochlear nucleus. a Consecutive coronal paraffin sections through the abducens nucleus (nVI) ( a ) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (third panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (second panel) as reference. b, c Close-up of Cav subunit expression in nVI MIF (red arrowheads) and SIF motoneurons (MNs) (green arrows) and INTs (blue arrow). d Consecutive coronal paraffin sections through the trochlear nucleus (nVI) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (second panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (third panel) as reference. Thin dashed lines in d indicate the border of nIV and thick dashed lines indicate the boundary between the MIF and SIF MNs. e Close-up of Cav subunit expression in MIF (red arrowheads) and SIF MNs (green arrow) on different sections as those illustrated in d . Note the weak Cav3.1 expression along the membrane of some SIF MNs (left column, black star). Red dashed lines indicate the tentative position of the border delineating the dorsal cap of nIV. f Cerebellar Purkinje cells located on the same consecutive sections as nVI as controls for immunopositivity of the different Cav subunits. Scale bar indicates 100 μm in a, d, f and 50 μm in b, c, e

    Techniques Used: Immunolabeling, Immunostaining, Expressing

    4) Product Images from "Transmitter and ion channel profiles of neurons in the primate abducens and trochlear nuclei"

    Article Title: Transmitter and ion channel profiles of neurons in the primate abducens and trochlear nuclei

    Journal: Brain Structure & Function

    doi: 10.1007/s00429-021-02315-7

    Low-voltage activated calcium channel family (Cav3) subunits in the abducens and trochlear nucleus. a Consecutive coronal paraffin sections through the abducens nucleus (nVI) ( a ) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (third panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (second panel) as reference. b, c Close-up of Cav subunit expression in nVI MIF (red arrowheads) and SIF motoneurons (MNs) (green arrows) and INTs (blue arrow). d Consecutive coronal paraffin sections through the trochlear nucleus (nVI) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (second panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (third panel) as reference. Thin dashed lines in d indicate the border of nIV and thick dashed lines indicate the boundary between the MIF and SIF MNs. e Close-up of Cav subunit expression in MIF (red arrowheads) and SIF MNs (green arrow) on different sections as those illustrated in d . Note the weak Cav3.1 expression along the membrane of some SIF MNs (left column, black star). Red dashed lines indicate the tentative position of the border delineating the dorsal cap of nIV. f Cerebellar Purkinje cells located on the same consecutive sections as nVI as controls for immunopositivity of the different Cav subunits. Scale bar indicates 100 μm in a, d, f and 50 μm in b, c, e
    Figure Legend Snippet: Low-voltage activated calcium channel family (Cav3) subunits in the abducens and trochlear nucleus. a Consecutive coronal paraffin sections through the abducens nucleus (nVI) ( a ) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (third panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (second panel) as reference. b, c Close-up of Cav subunit expression in nVI MIF (red arrowheads) and SIF motoneurons (MNs) (green arrows) and INTs (blue arrow). d Consecutive coronal paraffin sections through the trochlear nucleus (nVI) depicting the immunolabeling for Cav3.1 (first panel), Cav3.2 (second panel) and Cav3.3 (fourth panel) subunits with combined immunostaining for ChAT (brown) and ACAN (black) (third panel) as reference. Thin dashed lines in d indicate the border of nIV and thick dashed lines indicate the boundary between the MIF and SIF MNs. e Close-up of Cav subunit expression in MIF (red arrowheads) and SIF MNs (green arrow) on different sections as those illustrated in d . Note the weak Cav3.1 expression along the membrane of some SIF MNs (left column, black star). Red dashed lines indicate the tentative position of the border delineating the dorsal cap of nIV. f Cerebellar Purkinje cells located on the same consecutive sections as nVI as controls for immunopositivity of the different Cav subunits. Scale bar indicates 100 μm in a, d, f and 50 μm in b, c, e

    Techniques Used: Immunolabeling, Immunostaining, Expressing

    5) Product Images from "TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes"

    Article Title: TRPC7 regulates the electrophysiological functions of embryonic stem cell-derived cardiomyocytes

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/s13287-021-02308-7

    Knockdown or overexpression of TRPC7 did not alter the expression of several important ion channels/pump in NRVMs. a – g Western blots showing the expression of a TRPC7, b HCN4, c Cav1.3, d IP3R1, e Cav3.1, f Cav3.2, g SERCA in NRVMs infected with different adenoviruses to knockdown or overexpress TRPC7. h – n Bar charts showing the quantification of each protein from a – g . To eliminate the loading bias, intensity of each target protein was normalized to that of its corresponding β-tubulin. TRPC7 was successfully knocked down or overexpressed in NRVMs but the change of TRPC7 expression did not alter the expression of HCN4, Cav1.3, IP3R1, Cav3.1, Cav3.2, and SERCA. Data were presented as mean ± SEM ( n = 4). * P
    Figure Legend Snippet: Knockdown or overexpression of TRPC7 did not alter the expression of several important ion channels/pump in NRVMs. a – g Western blots showing the expression of a TRPC7, b HCN4, c Cav1.3, d IP3R1, e Cav3.1, f Cav3.2, g SERCA in NRVMs infected with different adenoviruses to knockdown or overexpress TRPC7. h – n Bar charts showing the quantification of each protein from a – g . To eliminate the loading bias, intensity of each target protein was normalized to that of its corresponding β-tubulin. TRPC7 was successfully knocked down or overexpressed in NRVMs but the change of TRPC7 expression did not alter the expression of HCN4, Cav1.3, IP3R1, Cav3.1, Cav3.2, and SERCA. Data were presented as mean ± SEM ( n = 4). * P

    Techniques Used: Over Expression, Expressing, Western Blot, Infection

    6) Product Images from "Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression"

    Article Title: Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22073561

    Id2 regulates the activity of CaV3.1 promoter. The luciferase reporter gene was placed under the control of 0.8kb of the CaV3.1 promoter. The reporter gene was transected into neonatal rat cardiomyocytes to measure the luciferase activity upon Id2 overexpression (left) or Id2 siRNA knockdown (right). Bar graphs represent the mean of the relative activity of luciferase from the CaV3.1 luciferase reporter plasmid construct. The data were evaluated by one-way analysis of variance (ANOVA) followed by Tukey–Kramer’s post hoc test. Values are mean + s.e.m., *** p
    Figure Legend Snippet: Id2 regulates the activity of CaV3.1 promoter. The luciferase reporter gene was placed under the control of 0.8kb of the CaV3.1 promoter. The reporter gene was transected into neonatal rat cardiomyocytes to measure the luciferase activity upon Id2 overexpression (left) or Id2 siRNA knockdown (right). Bar graphs represent the mean of the relative activity of luciferase from the CaV3.1 luciferase reporter plasmid construct. The data were evaluated by one-way analysis of variance (ANOVA) followed by Tukey–Kramer’s post hoc test. Values are mean + s.e.m., *** p

    Techniques Used: Activity Assay, Luciferase, Over Expression, Plasmid Preparation, Construct

    Id2 expressing transgenic mice prevents the aldosterone-stimulated expression of CaV3.1 voltage-gated calcium channels in vivo. WT or cardiomyocyte-specific Id2 expressing transgenic B6D2F1/Slc mice were stimulated with Aldosterone (60 mg/Kg/day) or Saline solution for 1 week by implanting subcutaneously osmotic pumps. ( A ) Representative pictures of western blot experiments showing the Id2 protein (upper) and GAPDH protein (lower) expression levels from the heart of WT mice treated with saline solution or aldosterone. The bar graph is the mean of Id2 expression ( n = 4). ( B ) Pictures of western blotting experiments showing the Id2 protein (upper) and GAPDH protein (lower) expression levels in the heart of B6D2F1/Slc WT and two cardiomyocyte-specific Id2 expressing transgenic (Tg) mice. ( C ) Pictures of western blotting experiments showing CaV3.1 (upper) and tubulin (lower) proteins expression levels in WT or Id2 transgenic mice treated with saline solution or aldosterone. Graph is are the mean expression of CaV3.1 and tubulin expression ( n = 4). The data were evaluated by one-way analysis of variance (ANOVA) followed by Tukey–Kramer’s post hoc test or by unpaired two-tailed Student’s t -test. Bars and error bars indicate the mean ± s.e.m., ** p
    Figure Legend Snippet: Id2 expressing transgenic mice prevents the aldosterone-stimulated expression of CaV3.1 voltage-gated calcium channels in vivo. WT or cardiomyocyte-specific Id2 expressing transgenic B6D2F1/Slc mice were stimulated with Aldosterone (60 mg/Kg/day) or Saline solution for 1 week by implanting subcutaneously osmotic pumps. ( A ) Representative pictures of western blot experiments showing the Id2 protein (upper) and GAPDH protein (lower) expression levels from the heart of WT mice treated with saline solution or aldosterone. The bar graph is the mean of Id2 expression ( n = 4). ( B ) Pictures of western blotting experiments showing the Id2 protein (upper) and GAPDH protein (lower) expression levels in the heart of B6D2F1/Slc WT and two cardiomyocyte-specific Id2 expressing transgenic (Tg) mice. ( C ) Pictures of western blotting experiments showing CaV3.1 (upper) and tubulin (lower) proteins expression levels in WT or Id2 transgenic mice treated with saline solution or aldosterone. Graph is are the mean expression of CaV3.1 and tubulin expression ( n = 4). The data were evaluated by one-way analysis of variance (ANOVA) followed by Tukey–Kramer’s post hoc test or by unpaired two-tailed Student’s t -test. Bars and error bars indicate the mean ± s.e.m., ** p

    Techniques Used: Expressing, Transgenic Assay, Mouse Assay, In Vivo, Western Blot, Two Tailed Test

    Manipulation of Id2′s expression altered of voltage-gated calcium channel expression in neonatal rat ventricular cardiomyocytes and prevented aldosterone-stimulated increased. ( A ) 2, CaV3.1, and CaV3.2 were measured by RT-qPCR in neonatal rat ventricular cardiomyocytes treated and non-treated with 1 µmol/L Aldo for 24 h upon Id2 overexpression. Bar graphs shows the mean expression of CaV1.2 mRNA (left), CaV3.1 mRNA (middle), and CaV3.2 (right) ( n = 5). ( B ) The mRNA expression of CaV1.2, CaV3.1, and CaV3.2 were measured by real-time qPCR in neonatal rat ventricular cardiomyocytes treated with Id2 siRNA-2, siRNA-5 or Luciferase1 siRNA for 48 h. Bar graphs shows the mean expression of CaV1.2 mRNA (left), CaV3.1 mRNA (middle), and CaV3.2 (right) ( n = 3). The data were evaluated by one-way analysis of variance (ANOVA) followed by Tukey–Kramer’s post hoc test. Data are the mean ± s.e.m, * p
    Figure Legend Snippet: Manipulation of Id2′s expression altered of voltage-gated calcium channel expression in neonatal rat ventricular cardiomyocytes and prevented aldosterone-stimulated increased. ( A ) 2, CaV3.1, and CaV3.2 were measured by RT-qPCR in neonatal rat ventricular cardiomyocytes treated and non-treated with 1 µmol/L Aldo for 24 h upon Id2 overexpression. Bar graphs shows the mean expression of CaV1.2 mRNA (left), CaV3.1 mRNA (middle), and CaV3.2 (right) ( n = 5). ( B ) The mRNA expression of CaV1.2, CaV3.1, and CaV3.2 were measured by real-time qPCR in neonatal rat ventricular cardiomyocytes treated with Id2 siRNA-2, siRNA-5 or Luciferase1 siRNA for 48 h. Bar graphs shows the mean expression of CaV1.2 mRNA (left), CaV3.1 mRNA (middle), and CaV3.2 (right) ( n = 3). The data were evaluated by one-way analysis of variance (ANOVA) followed by Tukey–Kramer’s post hoc test. Data are the mean ± s.e.m, * p

    Techniques Used: Expressing, Quantitative RT-PCR, Over Expression, Real-time Polymerase Chain Reaction

    7) Product Images from "Bursting firing in ventromedial hypothalamic neurons exerts dual control of anxiety-like behavior and energy expenditure"

    Article Title: Bursting firing in ventromedial hypothalamic neurons exerts dual control of anxiety-like behavior and energy expenditure

    Journal: bioRxiv

    doi: 10.1101/2020.12.20.423695

    Knockdown of Cav3.1 in dmVMH decreased burst firing, and rescued anxiety-like behavior and metabolic alteration induced by chronic stress. (a) Schematic of Cav3.1 shRNA construct and injection of shRNA-expressing lenti-viral vector into dmVMH to interfere with Cav 3.1 expression. (b) Representative images of dmVMH Cav 3.1 immunostaining in chronic stress and RNAi (under chronic stress) animals (left). Proportion of burst firing neurons decreased in RNAi group (2/13, 15.38%) compared with stress group (7/17, 41.18%) (right). Scale bar is 100 μm. (c) Time spent in central area and number of entries into central area of open field in control, chronic stress, and RNAi groups. Residence time: control (n = 8) versus chronic stress group (n = 8), P = 0.0068; chronic stress versus RNAi group (n = 7), P = 0.0017. Number of entries: control versus chronic stress group, P = 0.4830; chronic stress versus RNAi group, P = 0.8437 (unpaired Student’s t -test). (d) Time spent in open arm and number of entries into open arm of elevated plus-maze in control, chronic stress, and RNAi groups. Residence time: control versus chronic stress group, P = 0.0009; chronic stress versus RNAi group, P = 0.0379. Number of entries: control versus chronic stress group, P
    Figure Legend Snippet: Knockdown of Cav3.1 in dmVMH decreased burst firing, and rescued anxiety-like behavior and metabolic alteration induced by chronic stress. (a) Schematic of Cav3.1 shRNA construct and injection of shRNA-expressing lenti-viral vector into dmVMH to interfere with Cav 3.1 expression. (b) Representative images of dmVMH Cav 3.1 immunostaining in chronic stress and RNAi (under chronic stress) animals (left). Proportion of burst firing neurons decreased in RNAi group (2/13, 15.38%) compared with stress group (7/17, 41.18%) (right). Scale bar is 100 μm. (c) Time spent in central area and number of entries into central area of open field in control, chronic stress, and RNAi groups. Residence time: control (n = 8) versus chronic stress group (n = 8), P = 0.0068; chronic stress versus RNAi group (n = 7), P = 0.0017. Number of entries: control versus chronic stress group, P = 0.4830; chronic stress versus RNAi group, P = 0.8437 (unpaired Student’s t -test). (d) Time spent in open arm and number of entries into open arm of elevated plus-maze in control, chronic stress, and RNAi groups. Residence time: control versus chronic stress group, P = 0.0009; chronic stress versus RNAi group, P = 0.0379. Number of entries: control versus chronic stress group, P

    Techniques Used: shRNA, Construct, Injection, Expressing, Plasmid Preparation, Immunostaining

    T-VGCC mediated enhancement of burst firing in dmVMH neurons under chronic stress. (a) Schematic of structure of T-VGCC located on cell membrane (left top). Representative immunofluorescence showing Cav 3.1 (left bottom), Cav 3.2 (right top), and Cav 3.3 (right bottom) expression in dmVMH, respectively, with stronger Cav3.1 expression observed. Scale bar is 200 μm. (b) Quantification of Cav 3.1, Cav 3.2, and Cav 3.3 expression in dmVMH tissue between control (n = 5 mice) and chronic stress groups (n = 6 mice). Expression of Cav 3.1 was significantly up-regulated under chronic stress conditions (unpaired Student’s t -test, P = 0.0232). (c) Single-cell qRT-PCR analysis of Cav 3.1, Cav 3.2, and Cav 3.3 expression in dmVMH neurons between control (n = 16 cells) and chronic stress groups (n = 14 cells). Expression of Cav 3.1 was significantly up-regulated under chronic stress conditions (unpaired Student’s t -test, P = 0.0390). (d) Evoked burst firing trace of dmVMH neurons without and with T-VGCC antagonist (mibefradil, 10 μM), 10 pA current injection was given in cosine waveform. (e) Effects of mibefradil on onset time and RMP of dmVMH neurons from wild-type (n = 15) and chronic stress groups (n = 13). Significant differences were observed in both onset time and RMP (paired Student’s t- test, P = 0.0388 and P = 0.0395) in the stress group, whereas the control group demonstrated obvious changes in RMP but not onset time (paired Student’s t -test, P = 0.0275 and P = 0.3125). (f) Single-cell qRT-PCR analysis of Cav 3.1 expression among three neuronal subtypes in dmVMH. Upper: burst firing neurons (n = 11) showed higher Cav 3.1 expression than other two subtypes (unpaired Student’s t -test, P = 0.0133 compared with silent neurons (n = 7), P = 0.0139 compared with tonic-firing neurons (n = 12)); bottom: Cav 3.1 expression in burst firing subtype showed significant differences between control and chronic-stress groups (unpaired Student’s t -test, silent: control, n = 3, stress, n = 3, P = 0.5574; tonic-firing: control, n = 7, stress, n = 5, P = 0.9339; bursting: control, n = 5, stress, n = 6, P = 0.0165). (g) Effects of mibefradil on suprathreshold and subthreshold activity in dmVMH burst firing neurons in control (n = 5) and chronic stress groups (n = 7). Mibefradil inhibited T-VGCC and caused a right frequency-current curve shift (two-way ANOVA, control, P = 0.2140, F (1, 8) = 1.854; stress, P = 0.0077, F (1, 12) = 10.22); lower, mibefradil application exerted no obvious influence on current-voltage curve of burst neurons (two-way ANOVA, control, P = 0.8188, F (1, 10) = 0.0573; stress, P = 0.4487, F (1, 10) = 0.6218). (h) Obvious differences were observed in suprathreshold activity (two-way ANOVA, P = 0.0047, F (1, 110) = 20.53), but not in subthreshold (two-way ANOVA, P = 0.9913, F (1, 33) = 4.958) membrane potential of dmVMH burst firing neurons between control (n = 5) and chronic stress groups (n = 7) after application of mibefradil. Data are means ± SEM. * P
    Figure Legend Snippet: T-VGCC mediated enhancement of burst firing in dmVMH neurons under chronic stress. (a) Schematic of structure of T-VGCC located on cell membrane (left top). Representative immunofluorescence showing Cav 3.1 (left bottom), Cav 3.2 (right top), and Cav 3.3 (right bottom) expression in dmVMH, respectively, with stronger Cav3.1 expression observed. Scale bar is 200 μm. (b) Quantification of Cav 3.1, Cav 3.2, and Cav 3.3 expression in dmVMH tissue between control (n = 5 mice) and chronic stress groups (n = 6 mice). Expression of Cav 3.1 was significantly up-regulated under chronic stress conditions (unpaired Student’s t -test, P = 0.0232). (c) Single-cell qRT-PCR analysis of Cav 3.1, Cav 3.2, and Cav 3.3 expression in dmVMH neurons between control (n = 16 cells) and chronic stress groups (n = 14 cells). Expression of Cav 3.1 was significantly up-regulated under chronic stress conditions (unpaired Student’s t -test, P = 0.0390). (d) Evoked burst firing trace of dmVMH neurons without and with T-VGCC antagonist (mibefradil, 10 μM), 10 pA current injection was given in cosine waveform. (e) Effects of mibefradil on onset time and RMP of dmVMH neurons from wild-type (n = 15) and chronic stress groups (n = 13). Significant differences were observed in both onset time and RMP (paired Student’s t- test, P = 0.0388 and P = 0.0395) in the stress group, whereas the control group demonstrated obvious changes in RMP but not onset time (paired Student’s t -test, P = 0.0275 and P = 0.3125). (f) Single-cell qRT-PCR analysis of Cav 3.1 expression among three neuronal subtypes in dmVMH. Upper: burst firing neurons (n = 11) showed higher Cav 3.1 expression than other two subtypes (unpaired Student’s t -test, P = 0.0133 compared with silent neurons (n = 7), P = 0.0139 compared with tonic-firing neurons (n = 12)); bottom: Cav 3.1 expression in burst firing subtype showed significant differences between control and chronic-stress groups (unpaired Student’s t -test, silent: control, n = 3, stress, n = 3, P = 0.5574; tonic-firing: control, n = 7, stress, n = 5, P = 0.9339; bursting: control, n = 5, stress, n = 6, P = 0.0165). (g) Effects of mibefradil on suprathreshold and subthreshold activity in dmVMH burst firing neurons in control (n = 5) and chronic stress groups (n = 7). Mibefradil inhibited T-VGCC and caused a right frequency-current curve shift (two-way ANOVA, control, P = 0.2140, F (1, 8) = 1.854; stress, P = 0.0077, F (1, 12) = 10.22); lower, mibefradil application exerted no obvious influence on current-voltage curve of burst neurons (two-way ANOVA, control, P = 0.8188, F (1, 10) = 0.0573; stress, P = 0.4487, F (1, 10) = 0.6218). (h) Obvious differences were observed in suprathreshold activity (two-way ANOVA, P = 0.0047, F (1, 110) = 20.53), but not in subthreshold (two-way ANOVA, P = 0.9913, F (1, 33) = 4.958) membrane potential of dmVMH burst firing neurons between control (n = 5) and chronic stress groups (n = 7) after application of mibefradil. Data are means ± SEM. * P

    Techniques Used: Immunofluorescence, Expressing, Mouse Assay, Quantitative RT-PCR, Injection, Activity Assay

    8) Product Images from "TAF1-gene editing alters the morphology and function of the cerebellum"

    Article Title: TAF1-gene editing alters the morphology and function of the cerebellum

    Journal: Neurobiology of disease

    doi: 10.1016/j.nbd.2019.104539

    TAF1 gene editing leads to a downregulation of the CaV3.1 voltage-gated calcium channel. ( A ) Representative photomicrographs of cerebellar slices from animals injected with (vehicle) or control or TAF1 gRNAs stained with an antibody against CaV3.1. Nuclei stained with DAPI. ( B ) Quantification of fluorescence intensity for the CaV3.1 immunohistochemistry. Scale bar = 200 μm. The experiments were performed in a blinded fashion. Data are shown as mean ± S.E.M. from 3 different fields from 3 animals per experimental condition (i.e. a total of nine fields per group). *p
    Figure Legend Snippet: TAF1 gene editing leads to a downregulation of the CaV3.1 voltage-gated calcium channel. ( A ) Representative photomicrographs of cerebellar slices from animals injected with (vehicle) or control or TAF1 gRNAs stained with an antibody against CaV3.1. Nuclei stained with DAPI. ( B ) Quantification of fluorescence intensity for the CaV3.1 immunohistochemistry. Scale bar = 200 μm. The experiments were performed in a blinded fashion. Data are shown as mean ± S.E.M. from 3 different fields from 3 animals per experimental condition (i.e. a total of nine fields per group). *p

    Techniques Used: Injection, Staining, Fluorescence, Immunohistochemistry

    9) Product Images from "Transcriptome analysis of PDGFRα+ cells identifies T-type Ca2+ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia"

    Article Title: Transcriptome analysis of PDGFRα+ cells identifies T-type Ca2+ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0182265

    Induced expression of Cacna1g mRNAs and protein in hypertrophic smooth muscle. (A) Expression of Cacna1g exons with alternative transcriptional start sites (ATSS) and/or alternative spliced sites (ASS) in sham operation (SO) and partial obstruction (PO) examined by RT-PCR. NTC is non-template control. (B) Detection of Cacna1g mRNAs in isolated eGFP high and eGFP low PDGFRα + cells from sham operation and partial obstruction opertaion by RT-PCR. PCR products were analyzed with a DNA size marker on 1.5% agarose gels. Note expression of Cacna1g is increased in eGFP high and eGFP low PDGFRα + cells. (C) Quantification of Cacna1g mRNAs by qPCR. * p ≤ 0 . 05 and ** p ≤ 0 . 01 , SO versus PO. (D) Western blot analysis using N-terminal and C-terminal CACNA1G antibodies (CACNA1G-N and CACNA1G-C), showing that the protein has significantly higher expression levels in hypertrophic tissue induced by partial obstruction. (E) Detection of serosal PDGFRα + cells expressing CACNA1G in partial obstruction models by CACNA1G-C antibody. Scale bars are 50 μm (F) Confocal cross section images of serosal PDGFRα + cells in sham operation and partial obstruction screened with CACNA1G-N and CACNA1G-C antibodies co-labeled with PDGFRA and PDGFRB antibodies. Scale bars are 50 μm.
    Figure Legend Snippet: Induced expression of Cacna1g mRNAs and protein in hypertrophic smooth muscle. (A) Expression of Cacna1g exons with alternative transcriptional start sites (ATSS) and/or alternative spliced sites (ASS) in sham operation (SO) and partial obstruction (PO) examined by RT-PCR. NTC is non-template control. (B) Detection of Cacna1g mRNAs in isolated eGFP high and eGFP low PDGFRα + cells from sham operation and partial obstruction opertaion by RT-PCR. PCR products were analyzed with a DNA size marker on 1.5% agarose gels. Note expression of Cacna1g is increased in eGFP high and eGFP low PDGFRα + cells. (C) Quantification of Cacna1g mRNAs by qPCR. * p ≤ 0 . 05 and ** p ≤ 0 . 01 , SO versus PO. (D) Western blot analysis using N-terminal and C-terminal CACNA1G antibodies (CACNA1G-N and CACNA1G-C), showing that the protein has significantly higher expression levels in hypertrophic tissue induced by partial obstruction. (E) Detection of serosal PDGFRα + cells expressing CACNA1G in partial obstruction models by CACNA1G-C antibody. Scale bars are 50 μm (F) Confocal cross section images of serosal PDGFRα + cells in sham operation and partial obstruction screened with CACNA1G-N and CACNA1G-C antibodies co-labeled with PDGFRA and PDGFRB antibodies. Scale bars are 50 μm.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Isolation, Polymerase Chain Reaction, Marker, Real-time Polymerase Chain Reaction, Western Blot, Labeling

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    Alomone Labs cav 3 1
    Ca currents in wt and <t>Cav3.2</t> KO ventricular cardiomyocytes. ( A ) Original traces of Ca currents of a typical wt and Cav3.2 KO myocyte elicited by the pulse protocol displayed on top. ( B ) Current density–voltage relationships of wt (n = 20) and Cav3.2 KO (n = 20) myocytes. Data are expressed as means ± SEM. The current density–voltage relations hardly revealed any T-type Ca channel activity (expected to be maximal at −45 mV) but did reveal significant L-type Ca channel activity (peaking at +5 mV), which was similar in wt and Cav3.2 KO myocytes ( p = 0.67 at +5 mV, unpaired Student’s t -test). Capacitance values of the examined myocytes were 184 ± 13 pF for wt and 169 ± 11 pF for Cav3.2 KO ( p = 0.37). ( C ) The effect of the external application of 100 nM isoprenaline (ISO) on ICaT in a wt myocyte. From a holding potential of −95 mV, depolarizing voltage steps to −45 mV were applied every 3 s to elicit the currents. The arrows indicate the beginning and end of ISO application. Current peaks were finally plotted against time. ( D ) ICaT peaks before, during application after the steady-state was reached, and after the washout of ISO in wt (top) and Cav3.2 KO (bottom) myocytes. There was no significant difference between wt and Cav3.2 KO under control conditions ( p = 0.81, unpaired Student’s t -test) or in the presence of ISO ( p = 0.54). Data are expressed as means ± SEM. Each data point represents a single cell. ** p
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    Ca currents in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Original traces of Ca currents of a typical wt and Cav3.2 KO myocyte elicited by the pulse protocol displayed on top. ( B ) Current density–voltage relationships of wt (n = 20) and Cav3.2 KO (n = 20) myocytes. Data are expressed as means ± SEM. The current density–voltage relations hardly revealed any T-type Ca channel activity (expected to be maximal at −45 mV) but did reveal significant L-type Ca channel activity (peaking at +5 mV), which was similar in wt and Cav3.2 KO myocytes ( p = 0.67 at +5 mV, unpaired Student’s t -test). Capacitance values of the examined myocytes were 184 ± 13 pF for wt and 169 ± 11 pF for Cav3.2 KO ( p = 0.37). ( C ) The effect of the external application of 100 nM isoprenaline (ISO) on ICaT in a wt myocyte. From a holding potential of −95 mV, depolarizing voltage steps to −45 mV were applied every 3 s to elicit the currents. The arrows indicate the beginning and end of ISO application. Current peaks were finally plotted against time. ( D ) ICaT peaks before, during application after the steady-state was reached, and after the washout of ISO in wt (top) and Cav3.2 KO (bottom) myocytes. There was no significant difference between wt and Cav3.2 KO under control conditions ( p = 0.81, unpaired Student’s t -test) or in the presence of ISO ( p = 0.54). Data are expressed as means ± SEM. Each data point represents a single cell. ** p

    Journal: Membranes

    Article Title: Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice

    doi: 10.3390/membranes12060566

    Figure Lengend Snippet: Ca currents in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Original traces of Ca currents of a typical wt and Cav3.2 KO myocyte elicited by the pulse protocol displayed on top. ( B ) Current density–voltage relationships of wt (n = 20) and Cav3.2 KO (n = 20) myocytes. Data are expressed as means ± SEM. The current density–voltage relations hardly revealed any T-type Ca channel activity (expected to be maximal at −45 mV) but did reveal significant L-type Ca channel activity (peaking at +5 mV), which was similar in wt and Cav3.2 KO myocytes ( p = 0.67 at +5 mV, unpaired Student’s t -test). Capacitance values of the examined myocytes were 184 ± 13 pF for wt and 169 ± 11 pF for Cav3.2 KO ( p = 0.37). ( C ) The effect of the external application of 100 nM isoprenaline (ISO) on ICaT in a wt myocyte. From a holding potential of −95 mV, depolarizing voltage steps to −45 mV were applied every 3 s to elicit the currents. The arrows indicate the beginning and end of ISO application. Current peaks were finally plotted against time. ( D ) ICaT peaks before, during application after the steady-state was reached, and after the washout of ISO in wt (top) and Cav3.2 KO (bottom) myocytes. There was no significant difference between wt and Cav3.2 KO under control conditions ( p = 0.81, unpaired Student’s t -test) or in the presence of ISO ( p = 0.54). Data are expressed as means ± SEM. Each data point represents a single cell. ** p

    Article Snippet: This was followed by blocking with 10% goat serum (Sigma-Aldrich, Vienna, Austria) and 0.01% azide (Sigma-Aldrich, Vienna, Austria) in PBS for 2 h. Subsequently, the cells were incubated with a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, Jerusalem, Israel, 1:500) or with one of two selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, Jerusalem, Israel, 1:1000; anti-Cav3.2 polyclonal antibody, #PA5-106771, source: rabbit, Invitrogen, Paisley, England, 1:200) at 4 °C overnight.

    Techniques: Activity Assay

    Electrically induced and caffeine-induced intracellular Ca transients in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Left: Representative time courses of Fluo-4 fluorescence reporting rises in cytosolic Ca concentration during electrical field stimulation at 0.1 Hz frequency in a single wt and Cav3.2 KO myocyte. The orange lines represent fits of the data with a single exponential function. Right: Comparison of mean Ca peak fluorescence relative to baseline (F/F0) between wt and Cav3.2 KO myocytes. Each data point represents a single cell, and values are expressed as means ± SEM (n= 68 for wt and 59 for Cav3.2 KO myocytes). * p

    Journal: Membranes

    Article Title: Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice

    doi: 10.3390/membranes12060566

    Figure Lengend Snippet: Electrically induced and caffeine-induced intracellular Ca transients in wt and Cav3.2 KO ventricular cardiomyocytes. ( A ) Left: Representative time courses of Fluo-4 fluorescence reporting rises in cytosolic Ca concentration during electrical field stimulation at 0.1 Hz frequency in a single wt and Cav3.2 KO myocyte. The orange lines represent fits of the data with a single exponential function. Right: Comparison of mean Ca peak fluorescence relative to baseline (F/F0) between wt and Cav3.2 KO myocytes. Each data point represents a single cell, and values are expressed as means ± SEM (n= 68 for wt and 59 for Cav3.2 KO myocytes). * p

    Article Snippet: This was followed by blocking with 10% goat serum (Sigma-Aldrich, Vienna, Austria) and 0.01% azide (Sigma-Aldrich, Vienna, Austria) in PBS for 2 h. Subsequently, the cells were incubated with a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, Jerusalem, Israel, 1:500) or with one of two selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, Jerusalem, Israel, 1:1000; anti-Cav3.2 polyclonal antibody, #PA5-106771, source: rabbit, Invitrogen, Paisley, England, 1:200) at 4 °C overnight.

    Techniques: Fluorescence, Concentration Assay

    Immunostaining of T-type Ca channels in ventricular cardiomyocytes isolated from adult wt mice. Cav3.1 ( top ) channel expression and localization was detected using a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, 1:500). Cav3.2 ( bottom ) was detected with the selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, 1:1000; left and right cell; or anti-Cav3.2 polyclonal, #PA5-106771, source: rabbit, Invitrogen, 1:200; middle cell). Secondary antibody: Alexa Fluor 488, #A11008, goat anti-rabbit, Invitrogen, 1:500.

    Journal: Membranes

    Article Title: Evidence for a Physiological Role of T-Type Ca Channels in Ventricular Cardiomyocytes of Adult Mice

    doi: 10.3390/membranes12060566

    Figure Lengend Snippet: Immunostaining of T-type Ca channels in ventricular cardiomyocytes isolated from adult wt mice. Cav3.1 ( top ) channel expression and localization was detected using a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, 1:500). Cav3.2 ( bottom ) was detected with the selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, 1:1000; left and right cell; or anti-Cav3.2 polyclonal, #PA5-106771, source: rabbit, Invitrogen, 1:200; middle cell). Secondary antibody: Alexa Fluor 488, #A11008, goat anti-rabbit, Invitrogen, 1:500.

    Article Snippet: This was followed by blocking with 10% goat serum (Sigma-Aldrich, Vienna, Austria) and 0.01% azide (Sigma-Aldrich, Vienna, Austria) in PBS for 2 h. Subsequently, the cells were incubated with a selective anti-Cav3.1 antibody (anti-CACNA1G, #ACC-021, source: rabbit, Alomone Labs, Jerusalem, Israel, 1:500) or with one of two selective anti-Cav3.2 antibodies (anti-CACNA1H, #ACC-025, source: rabbit, Alomone Labs, Jerusalem, Israel, 1:1000; anti-Cav3.2 polyclonal antibody, #PA5-106771, source: rabbit, Invitrogen, Paisley, England, 1:200) at 4 °C overnight.

    Techniques: Immunostaining, Isolation, Mouse Assay, Expressing