anti cav1 2 cacna1c antibody  (Alomone Labs)


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    Structured Review

    Alomone Labs anti cav1 2 cacna1c antibody
    <t>Cav1.2</t> maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The <t>CACNA1C</t> overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin <t>antibody.</t> P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p
    Anti Cav1 2 Cacna1c Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti cav1 2 cacna1c antibody - by Bioz Stars, 2022-12
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    Images

    1) Product Images from "Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma"

    Article Title: Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

    Journal: Cell & Bioscience

    doi: 10.1186/s13578-022-00873-9

    Cav1.2 maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The CACNA1C overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin antibody. P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p
    Figure Legend Snippet: Cav1.2 maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The CACNA1C overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin antibody. P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p

    Techniques Used: Activity Assay, Generated, Over Expression, Staining, Cell Culture, Immunohistochemistry, Western Blot, Expressing

    Cav1.2-dependent Ca 2+ /NFATc1 signaling increased the proliferation of AM cells. A – D Representative CACNA1C expression in AM cells indicated by arrowhead. CACNA1C was intensely expressed in the plasma membrane in the vehicle group. And it was broadly expressed in the plasma membrane, cytoplasm and nucleus in overexpression group. CACNA1C negatively expressed in knockdown group compared to the scramble. E – H The nuclear translocation of NFATc1 was observed in the overexpression group compared to the vehicle. NFATc1 was negatively expressed in the knockdown group compared to the scramble. I – L Representative confocal images of Ki67 staining of AM cells among the vehicle, overexpression, scramble, and siRNA groups. Nuclear were stained with TO-PRO-3 (TP3). M Percentages of CACNA1C + and NFATc1 + cells were quantified from immunostained images (N = 5 per group, biological replication). N Relative mRNA expression of CACNA1C , MKI67 , and NFATC1 between vehicle and CACNA1C overexpression, or scramble and siRNA group. O Western blot assay of AM cells with CACNA1C, PCNA, Cyclin D1, and GAPDH antibodies. P Western blot assay of nucleus and cytoplasm fractionated AM cells with NFATc1, Histone H3, and GAPDH antibodies. Scale bar: A–D, 50 μm; E–L, 100 μm. Quantitative data are presented as the mean ± SD. ** p
    Figure Legend Snippet: Cav1.2-dependent Ca 2+ /NFATc1 signaling increased the proliferation of AM cells. A – D Representative CACNA1C expression in AM cells indicated by arrowhead. CACNA1C was intensely expressed in the plasma membrane in the vehicle group. And it was broadly expressed in the plasma membrane, cytoplasm and nucleus in overexpression group. CACNA1C negatively expressed in knockdown group compared to the scramble. E – H The nuclear translocation of NFATc1 was observed in the overexpression group compared to the vehicle. NFATc1 was negatively expressed in the knockdown group compared to the scramble. I – L Representative confocal images of Ki67 staining of AM cells among the vehicle, overexpression, scramble, and siRNA groups. Nuclear were stained with TO-PRO-3 (TP3). M Percentages of CACNA1C + and NFATc1 + cells were quantified from immunostained images (N = 5 per group, biological replication). N Relative mRNA expression of CACNA1C , MKI67 , and NFATC1 between vehicle and CACNA1C overexpression, or scramble and siRNA group. O Western blot assay of AM cells with CACNA1C, PCNA, Cyclin D1, and GAPDH antibodies. P Western blot assay of nucleus and cytoplasm fractionated AM cells with NFATc1, Histone H3, and GAPDH antibodies. Scale bar: A–D, 50 μm; E–L, 100 μm. Quantitative data are presented as the mean ± SD. ** p

    Techniques Used: Expressing, Over Expression, Translocation Assay, Staining, Western Blot

    Schematic summary. Cav1.2 is dominantly expressed in ameloblastoma cells compared to the OKC. The Cav1.2-dependent Ca 2+ influx increases the proliferation of ameloblastoma cells by the accumulation of nucleic NFATc1, while intracellular Ca 2+ enhances Wnt/β-catenin signaling activity and the maintenance of the stemness of the ameloblastoma cells
    Figure Legend Snippet: Schematic summary. Cav1.2 is dominantly expressed in ameloblastoma cells compared to the OKC. The Cav1.2-dependent Ca 2+ influx increases the proliferation of ameloblastoma cells by the accumulation of nucleic NFATc1, while intracellular Ca 2+ enhances Wnt/β-catenin signaling activity and the maintenance of the stemness of the ameloblastoma cells

    Techniques Used: Activity Assay

    2) Product Images from "Epipharyngeal Abrasive Therapy Down-regulates the Expression of Cav1.2: A Key Molecule in Influenza Virus Entry"

    Article Title: Epipharyngeal Abrasive Therapy Down-regulates the Expression of Cav1.2: A Key Molecule in Influenza Virus Entry

    Journal: In Vivo

    doi: 10.21873/invivo.12967

    Protein expression patterns of Cav1.2 in patient tissue samples without and with epipharyngeal abrasive therapy (EAT). (A) Cav1.2 expression in the epipharynx of the EAT-treated and non-treated groups. (B) Immunohistochemical (IHC) scores for Cav1.2 expression on the epipharyngeal mucosa of the EAT-treated (n = 11) and non-treated groups (n = 7). **Significantly different at p
    Figure Legend Snippet: Protein expression patterns of Cav1.2 in patient tissue samples without and with epipharyngeal abrasive therapy (EAT). (A) Cav1.2 expression in the epipharynx of the EAT-treated and non-treated groups. (B) Immunohistochemical (IHC) scores for Cav1.2 expression on the epipharyngeal mucosa of the EAT-treated (n = 11) and non-treated groups (n = 7). **Significantly different at p

    Techniques Used: Expressing, Immunohistochemistry

    3) Product Images from "Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma"

    Article Title: Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

    Journal: Cell & Bioscience

    doi: 10.1186/s13578-022-00873-9

    Cav1.2 maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The CACNA1C overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin antibody. P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p
    Figure Legend Snippet: Cav1.2 maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The CACNA1C overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin antibody. P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p

    Techniques Used: Activity Assay, Generated, Over Expression, Staining, Cell Culture, Immunohistochemistry, Western Blot, Expressing

    Cav1.2-dependent Ca 2+ /NFATc1 signaling increased the proliferation of AM cells. A – D Representative CACNA1C expression in AM cells indicated by arrowhead. CACNA1C was intensely expressed in the plasma membrane in the vehicle group. And it was broadly expressed in the plasma membrane, cytoplasm and nucleus in overexpression group. CACNA1C negatively expressed in knockdown group compared to the scramble. E – H The nuclear translocation of NFATc1 was observed in the overexpression group compared to the vehicle. NFATc1 was negatively expressed in the knockdown group compared to the scramble. I – L Representative confocal images of Ki67 staining of AM cells among the vehicle, overexpression, scramble, and siRNA groups. Nuclear were stained with TO-PRO-3 (TP3). M Percentages of CACNA1C + and NFATc1 + cells were quantified from immunostained images (N = 5 per group, biological replication). N Relative mRNA expression of CACNA1C , MKI67 , and NFATC1 between vehicle and CACNA1C overexpression, or scramble and siRNA group. O Western blot assay of AM cells with CACNA1C, PCNA, Cyclin D1, and GAPDH antibodies. P Western blot assay of nucleus and cytoplasm fractionated AM cells with NFATc1, Histone H3, and GAPDH antibodies. Scale bar: A–D, 50 μm; E–L, 100 μm. Quantitative data are presented as the mean ± SD. ** p
    Figure Legend Snippet: Cav1.2-dependent Ca 2+ /NFATc1 signaling increased the proliferation of AM cells. A – D Representative CACNA1C expression in AM cells indicated by arrowhead. CACNA1C was intensely expressed in the plasma membrane in the vehicle group. And it was broadly expressed in the plasma membrane, cytoplasm and nucleus in overexpression group. CACNA1C negatively expressed in knockdown group compared to the scramble. E – H The nuclear translocation of NFATc1 was observed in the overexpression group compared to the vehicle. NFATc1 was negatively expressed in the knockdown group compared to the scramble. I – L Representative confocal images of Ki67 staining of AM cells among the vehicle, overexpression, scramble, and siRNA groups. Nuclear were stained with TO-PRO-3 (TP3). M Percentages of CACNA1C + and NFATc1 + cells were quantified from immunostained images (N = 5 per group, biological replication). N Relative mRNA expression of CACNA1C , MKI67 , and NFATC1 between vehicle and CACNA1C overexpression, or scramble and siRNA group. O Western blot assay of AM cells with CACNA1C, PCNA, Cyclin D1, and GAPDH antibodies. P Western blot assay of nucleus and cytoplasm fractionated AM cells with NFATc1, Histone H3, and GAPDH antibodies. Scale bar: A–D, 50 μm; E–L, 100 μm. Quantitative data are presented as the mean ± SD. ** p

    Techniques Used: Expressing, Over Expression, Translocation Assay, Staining, Western Blot

    Schematic summary. Cav1.2 is dominantly expressed in ameloblastoma cells compared to the OKC. The Cav1.2-dependent Ca 2+ influx increases the proliferation of ameloblastoma cells by the accumulation of nucleic NFATc1, while intracellular Ca 2+ enhances Wnt/β-catenin signaling activity and the maintenance of the stemness of the ameloblastoma cells
    Figure Legend Snippet: Schematic summary. Cav1.2 is dominantly expressed in ameloblastoma cells compared to the OKC. The Cav1.2-dependent Ca 2+ influx increases the proliferation of ameloblastoma cells by the accumulation of nucleic NFATc1, while intracellular Ca 2+ enhances Wnt/β-catenin signaling activity and the maintenance of the stemness of the ameloblastoma cells

    Techniques Used: Activity Assay

    4) Product Images from "Role and mechanism of REG2 depletion in insulin secretion augmented by glutathione peroxidase-1 overproduction"

    Article Title: Role and mechanism of REG2 depletion in insulin secretion augmented by glutathione peroxidase-1 overproduction

    Journal: Redox Biology

    doi: 10.1016/j.redox.2022.102457

    Evidences for a ligand-receptor binding between REG2 and CaV1.2. Western blot analysis of CaV1.2 protein produced by beta TC3 cells (50 μg protein per lane) transfected with pcDNA v ector and pcDNA-CaV1.2 plasmid (A), co-immunoprecipitation of CaV1.2 protein with REG2: the lysates (500 μg protein per sample) of beta - TC3 cells transfected with pcDNA-CaV1.2 plasmid were incubated with REG2 protein (2 μg) and REG2 antibody (1 μg) and the precipitates were collected by protein G beads and immunoblotted against CaV1.2 antibody (B), co-immunoprecipitation of REG2 with glycosylated verse deglycosylated CaV1.2 in lysates of Min6 cells transfected with pcDNA-CaV1.2 plasmid: cell lysates (1 mg protein per sample) were treated with or without PNGase F (20 μl, 10,000 units) and incubated with REG2 protein (2 μg) and REG2 antibody (1 μg); the precipitates were collected by protein G beads and immunoblotted against CaV1.2 antibody; and the CaV1.2 α1c subunit was detected only in the precipitated cell lysates without deglycosylation (C), the putative ligand-receptor binding of alkaline phosphatase (AP)-conjugated REG2 (AP-REG2) vs. AP-REG2 M1 and AP (1 μg/ml) overexpressed and secreted by HEK293T cells to CaV1.2 on the surface of beta TC3 cells transfected with pcDNA vector or pcDNA-CaV1.2 plasmid in the presence or absence of CaV1.2 antibody (1 μg/ml) or REG2 (1 μg/ml), and the extent of binding was shown by the retained AP activity on cell surface and quantitated (the right box) by the shading/dark pixels using software Image J (D), co-immunofluorescence of green fluorescence protein (GFP)-conjugated REG2 (GFP-REG2) vs. GFP-REG2 and GFP (1 μg/ml) overexpressed and secreted by HEK293T cells with mCherry-CaV1.2 on the surface of beta TC3 cells transfected with pmCherry vector or pcmCherry-CaV1.2 plasmid for 48 h, and the relative percentage of yellow fluorescence area (% of GFP positive cells in mCherry positive cells) was scored using MetaMorph image analysis software (E ) . In panels A, B, and C, the images were representative of 4 independent experiments. In panels of D and E, scale bar = 10 μm; values are mean ± SE from four independent experiments; p
    Figure Legend Snippet: Evidences for a ligand-receptor binding between REG2 and CaV1.2. Western blot analysis of CaV1.2 protein produced by beta TC3 cells (50 μg protein per lane) transfected with pcDNA v ector and pcDNA-CaV1.2 plasmid (A), co-immunoprecipitation of CaV1.2 protein with REG2: the lysates (500 μg protein per sample) of beta - TC3 cells transfected with pcDNA-CaV1.2 plasmid were incubated with REG2 protein (2 μg) and REG2 antibody (1 μg) and the precipitates were collected by protein G beads and immunoblotted against CaV1.2 antibody (B), co-immunoprecipitation of REG2 with glycosylated verse deglycosylated CaV1.2 in lysates of Min6 cells transfected with pcDNA-CaV1.2 plasmid: cell lysates (1 mg protein per sample) were treated with or without PNGase F (20 μl, 10,000 units) and incubated with REG2 protein (2 μg) and REG2 antibody (1 μg); the precipitates were collected by protein G beads and immunoblotted against CaV1.2 antibody; and the CaV1.2 α1c subunit was detected only in the precipitated cell lysates without deglycosylation (C), the putative ligand-receptor binding of alkaline phosphatase (AP)-conjugated REG2 (AP-REG2) vs. AP-REG2 M1 and AP (1 μg/ml) overexpressed and secreted by HEK293T cells to CaV1.2 on the surface of beta TC3 cells transfected with pcDNA vector or pcDNA-CaV1.2 plasmid in the presence or absence of CaV1.2 antibody (1 μg/ml) or REG2 (1 μg/ml), and the extent of binding was shown by the retained AP activity on cell surface and quantitated (the right box) by the shading/dark pixels using software Image J (D), co-immunofluorescence of green fluorescence protein (GFP)-conjugated REG2 (GFP-REG2) vs. GFP-REG2 and GFP (1 μg/ml) overexpressed and secreted by HEK293T cells with mCherry-CaV1.2 on the surface of beta TC3 cells transfected with pmCherry vector or pcmCherry-CaV1.2 plasmid for 48 h, and the relative percentage of yellow fluorescence area (% of GFP positive cells in mCherry positive cells) was scored using MetaMorph image analysis software (E ) . In panels A, B, and C, the images were representative of 4 independent experiments. In panels of D and E, scale bar = 10 μm; values are mean ± SE from four independent experiments; p

    Techniques Used: Binding Assay, Western Blot, Produced, Transfection, Plasmid Preparation, Immunoprecipitation, Incubation, Activity Assay, Software, Immunofluorescence, Fluorescence

    5) Product Images from "HDAC Inhibition Regulates Cardiac Function by Increasing Myofilament Calcium Sensitivity and Decreasing Diastolic Tension"

    Article Title: HDAC Inhibition Regulates Cardiac Function by Increasing Myofilament Calcium Sensitivity and Decreasing Diastolic Tension

    Journal: Pharmaceutics

    doi: 10.3390/pharmaceutics14071509

    Effect of acute SAHA treatment on abundance of calcium handling proteins. Western Blots ( A ) of right atrium trabeculae after being treated with vehicle or SAHA. There was no change in protein abundance with SAHA treatment for ( B ) phosphorylated calcium/calmodulin-dependent protein kinase (pCaMKII T286), ( C ) CaMKII, ( D ) sarcoendoplasmic reticulum calcium transport ATPase (SERCA), ( E ) sodium–calcium exchanger 1 (NCX1), ( F ) ryanodine receptor (Ryr), ( G ) Ryr serine 2808, ( H ) Cav1.2, ( I ) Cav1.2 150 kDa, and ( J ) Cav1.2 75 kDa; n = 7–8 samples per protein from 8 patients. All analysis was performed using a two-sided Student’s t -test. NS stands for not significant. Data shown are means ± SEM.
    Figure Legend Snippet: Effect of acute SAHA treatment on abundance of calcium handling proteins. Western Blots ( A ) of right atrium trabeculae after being treated with vehicle or SAHA. There was no change in protein abundance with SAHA treatment for ( B ) phosphorylated calcium/calmodulin-dependent protein kinase (pCaMKII T286), ( C ) CaMKII, ( D ) sarcoendoplasmic reticulum calcium transport ATPase (SERCA), ( E ) sodium–calcium exchanger 1 (NCX1), ( F ) ryanodine receptor (Ryr), ( G ) Ryr serine 2808, ( H ) Cav1.2, ( I ) Cav1.2 150 kDa, and ( J ) Cav1.2 75 kDa; n = 7–8 samples per protein from 8 patients. All analysis was performed using a two-sided Student’s t -test. NS stands for not significant. Data shown are means ± SEM.

    Techniques Used: Western Blot

    6) Product Images from "Virus-induced inhibition of cardiac pacemaker channel HCN4 triggers bradycardia in human-induced stem cell system"

    Article Title: Virus-induced inhibition of cardiac pacemaker channel HCN4 triggers bradycardia in human-induced stem cell system

    Journal: Cellular and Molecular Life Sciences

    doi: 10.1007/s00018-022-04435-7

    Immunofluorescence staining and analysis under basal conditions (control) and after 5 days of CVB3 expression (CVB3) in pacemaker-like cells. a Immunofluorescence staining of pacemaker-like cells with antibodies against N-Cadherin (membrane marker) and either anti-HCN4 (top panel), anti-Nav1.5 (middle panel) and anti-Cav1.2 (bottom panel). The distributions were visualized via linescan. b Quantitative distribution analysis of N-Cadherin ( n = 30), HCN4 ( n = 30), Nav1.5 ( n = 5) and Cav1.2 ( n = 5). The localization of all targets in the membrane and the cytoplasmatic fraction was monitored and put into a ratiometric dependence (*** p
    Figure Legend Snippet: Immunofluorescence staining and analysis under basal conditions (control) and after 5 days of CVB3 expression (CVB3) in pacemaker-like cells. a Immunofluorescence staining of pacemaker-like cells with antibodies against N-Cadherin (membrane marker) and either anti-HCN4 (top panel), anti-Nav1.5 (middle panel) and anti-Cav1.2 (bottom panel). The distributions were visualized via linescan. b Quantitative distribution analysis of N-Cadherin ( n = 30), HCN4 ( n = 30), Nav1.5 ( n = 5) and Cav1.2 ( n = 5). The localization of all targets in the membrane and the cytoplasmatic fraction was monitored and put into a ratiometric dependence (*** p

    Techniques Used: Immunofluorescence, Staining, Expressing, Marker

    a Differentiated hiPSC-derived pacemaker cells express the SAN channel HCN4 and the cardiac channels Nav1.5 and Cav1.2. b Immunofluorescence staining of hiPSC-derived ventricular-like cells and hiPSC-derived pacemaker-like cells against connexin 43 (magenta), connexin 40 (red) and connexin 45 (green). Single channel pictures. c Schematic interaction between CVB3 and hiPSC-derived pacemaker cells concerning HCN4 transport and function as it was observed in this study. Not only is CVB3 a player in general HCN4 expression but mainly disturbs HCN4 recycling via Rab7-dependent autophagy combined with elevated autophagosome formation, leading to the loss of HCN4 function
    Figure Legend Snippet: a Differentiated hiPSC-derived pacemaker cells express the SAN channel HCN4 and the cardiac channels Nav1.5 and Cav1.2. b Immunofluorescence staining of hiPSC-derived ventricular-like cells and hiPSC-derived pacemaker-like cells against connexin 43 (magenta), connexin 40 (red) and connexin 45 (green). Single channel pictures. c Schematic interaction between CVB3 and hiPSC-derived pacemaker cells concerning HCN4 transport and function as it was observed in this study. Not only is CVB3 a player in general HCN4 expression but mainly disturbs HCN4 recycling via Rab7-dependent autophagy combined with elevated autophagosome formation, leading to the loss of HCN4 function

    Techniques Used: Derivative Assay, Immunofluorescence, Staining, Expressing

    7) Product Images from "Inhibition of L‐type voltage‐gated calcium channel‐mediated Ca2+ influx suppresses the collective migration and invasion of ameloblastoma, et al. Inhibition of L‐type voltage‐gated calcium channel‐mediated Ca2+ influx suppresses the collective migration and invasion of ameloblastoma"

    Article Title: Inhibition of L‐type voltage‐gated calcium channel‐mediated Ca2+ influx suppresses the collective migration and invasion of ameloblastoma, et al. Inhibition of L‐type voltage‐gated calcium channel‐mediated Ca2+ influx suppresses the collective migration and invasion of ameloblastoma

    Journal: Cell Proliferation

    doi: 10.1111/cpr.13305

    Cav1.2 is expressed and active in immortalized human AM cell line, AM‐1. (A) Immunofluorescence staining of AM‐1 cells for Actin and Cav1.2. Nuclei were counterstained with TO‐PRO‐3 (TP3). (B–E) A green fluorescent protein‐based Ca 2+ indicator (GCaMP7)‐overexpressed AM‐1 cells were stimulated by calcium chloride or BAY K‐8644 with or without verapamil (VPM). Time‐lapse images (B; Video S1 ), time‐dependent GFP intensity (C), and fold change of intensity (D, maximum vs. baseline) after calcium chloride treatment with or without VPM. (E) Time‐dependent GFP intensity after BAY K‐8644 treatment with or without VPM. ** p
    Figure Legend Snippet: Cav1.2 is expressed and active in immortalized human AM cell line, AM‐1. (A) Immunofluorescence staining of AM‐1 cells for Actin and Cav1.2. Nuclei were counterstained with TO‐PRO‐3 (TP3). (B–E) A green fluorescent protein‐based Ca 2+ indicator (GCaMP7)‐overexpressed AM‐1 cells were stimulated by calcium chloride or BAY K‐8644 with or without verapamil (VPM). Time‐lapse images (B; Video S1 ), time‐dependent GFP intensity (C), and fold change of intensity (D, maximum vs. baseline) after calcium chloride treatment with or without VPM. (E) Time‐dependent GFP intensity after BAY K‐8644 treatment with or without VPM. ** p

    Techniques Used: Immunofluorescence, Staining

    Verapamil suppressed function of Cav1.2 and collective invasion of primary ameloblastoma cells. (A) Immunofluorescence staining of primary AM cells for actin and Cav1.2. (B–D) GCaMP7‐overexpressed primary AM cells were stimulated by calcium chloride (Ca 2+ ) with or without verapamil (VPM). Time‐lapse images (B; Video S6 ), time‐dependent GFP intensity (C), and fold change of intensity (D, maximum vs. baseline) after calcium chloride treatment with or without VPM. (E and F) Primary AM spheroids embed into collagen gel were cultured with or without Ca 2+ or VPM for 72 h. Cleared whole‐mount staining images for E‐cadherin. Nuclei were counterstained with TO‐PRO‐3 (TP3). Collective invasion of each spheroid was quantified by distance (F) of extrusions. ** p
    Figure Legend Snippet: Verapamil suppressed function of Cav1.2 and collective invasion of primary ameloblastoma cells. (A) Immunofluorescence staining of primary AM cells for actin and Cav1.2. (B–D) GCaMP7‐overexpressed primary AM cells were stimulated by calcium chloride (Ca 2+ ) with or without verapamil (VPM). Time‐lapse images (B; Video S6 ), time‐dependent GFP intensity (C), and fold change of intensity (D, maximum vs. baseline) after calcium chloride treatment with or without VPM. (E and F) Primary AM spheroids embed into collagen gel were cultured with or without Ca 2+ or VPM for 72 h. Cleared whole‐mount staining images for E‐cadherin. Nuclei were counterstained with TO‐PRO‐3 (TP3). Collective invasion of each spheroid was quantified by distance (F) of extrusions. ** p

    Techniques Used: Immunofluorescence, Staining, Cell Culture

    Transcriptomic comparison between ameloblastomas (AMs) and odontogenic keratocysts (OKCs) revealed high expression of Cav1.2 in AMs. (A) Enriched gene ontology terms on upregulated differentially expressed genes (DEGs) in AMs compared with OKCs. Calcium‐related GO terms are specifically labelled. (B) DEGs are visualized using volcano plot, and the DEGs encoding calcium voltage‐gated channel alpha1 subunits are specifically labelled. A horizonal dashed line indicate p = 0.05 and vertical dashed lines mark fold change = −4 and 4, respectively. Significant DEGs ( p
    Figure Legend Snippet: Transcriptomic comparison between ameloblastomas (AMs) and odontogenic keratocysts (OKCs) revealed high expression of Cav1.2 in AMs. (A) Enriched gene ontology terms on upregulated differentially expressed genes (DEGs) in AMs compared with OKCs. Calcium‐related GO terms are specifically labelled. (B) DEGs are visualized using volcano plot, and the DEGs encoding calcium voltage‐gated channel alpha1 subunits are specifically labelled. A horizonal dashed line indicate p = 0.05 and vertical dashed lines mark fold change = −4 and 4, respectively. Significant DEGs ( p

    Techniques Used: Affinity Magnetic Separation, Expressing

    Verapamil suppressed in vivo expansion and invasion of AM‐1 spheroids. (A) Timeline for AM‐1 cell line‐based orthotopic xenograft mouse model. (B) Extraction sites of first right molars in micro‐CT data were set as region of interest and bone volume to total volume (BV/TV) was measured ( n = 7). (C) Micro‐CT images, haematoxylin and eosin staining (HE), and immunofluorescence staining for human leukocyte antigen (HLA) of maxillae of xenograft mouse models. (D and E) Immunohistochemistry staining for cytokeratin 14 (KRT14), CACNA1C, and P‐cadherin. Nuclei were counterstained with TO‐PRO‐3 (TP3). Scale bars, C, HE, 500 μm; HLA, 100 μm; D, 100 μm; E, 50 μm. ** p
    Figure Legend Snippet: Verapamil suppressed in vivo expansion and invasion of AM‐1 spheroids. (A) Timeline for AM‐1 cell line‐based orthotopic xenograft mouse model. (B) Extraction sites of first right molars in micro‐CT data were set as region of interest and bone volume to total volume (BV/TV) was measured ( n = 7). (C) Micro‐CT images, haematoxylin and eosin staining (HE), and immunofluorescence staining for human leukocyte antigen (HLA) of maxillae of xenograft mouse models. (D and E) Immunohistochemistry staining for cytokeratin 14 (KRT14), CACNA1C, and P‐cadherin. Nuclei were counterstained with TO‐PRO‐3 (TP3). Scale bars, C, HE, 500 μm; HLA, 100 μm; D, 100 μm; E, 50 μm. ** p

    Techniques Used: In Vivo, Micro-CT, Staining, Immunofluorescence, Immunohistochemistry

    8) Product Images from "Cardiac Fibroblasts Promote Ferroptosis in Atrial Fibrillation by Secreting Exo-miR-23a-3p Targeting SLC7A11"

    Article Title: Cardiac Fibroblasts Promote Ferroptosis in Atrial Fibrillation by Secreting Exo-miR-23a-3p Targeting SLC7A11

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/3961495

    Canines electrophysiological examination by programmed stimulation and the expression of ion channel. (a) Canines electrocardiogram during programmed stimulation. In Sham group, the state at which atrial fibrillation (AF) was not reached. In Pacing group, the state at which AF was reached and the AF sustained more than 5 seconds. Compared with Pacing group, AF susceptibility attenuated by GW4869 injection because most irregular rhythm shortens than 5 seconds. (b) Effective refractory period of different parts of the atrium. GW4869 increased the ERP of RSPV and LIPV in Pacing group. ( n =6). (c) Difference in AF inducibility, shown by the number of episodes. ( n =6). (d) Difference in mean AF durations. ( n =6). (e, f) Representative gel bands depicting KCa3.1 and Cav1.2 protein expression using specific antibodies. GAPDH was used as the loading control. ( n =5). (g) Total iron level in atrial tissue. ( n =3). (h) MDA level in atrial tissue. ( n =3). Data are presented as the mean ± SD. Statistical significance was determined using one-way ANOVA with a post hoc Dunnett test. ∗ P
    Figure Legend Snippet: Canines electrophysiological examination by programmed stimulation and the expression of ion channel. (a) Canines electrocardiogram during programmed stimulation. In Sham group, the state at which atrial fibrillation (AF) was not reached. In Pacing group, the state at which AF was reached and the AF sustained more than 5 seconds. Compared with Pacing group, AF susceptibility attenuated by GW4869 injection because most irregular rhythm shortens than 5 seconds. (b) Effective refractory period of different parts of the atrium. GW4869 increased the ERP of RSPV and LIPV in Pacing group. ( n =6). (c) Difference in AF inducibility, shown by the number of episodes. ( n =6). (d) Difference in mean AF durations. ( n =6). (e, f) Representative gel bands depicting KCa3.1 and Cav1.2 protein expression using specific antibodies. GAPDH was used as the loading control. ( n =5). (g) Total iron level in atrial tissue. ( n =3). (h) MDA level in atrial tissue. ( n =3). Data are presented as the mean ± SD. Statistical significance was determined using one-way ANOVA with a post hoc Dunnett test. ∗ P

    Techniques Used: Expressing, Injection, Multiple Displacement Amplification

    9) Product Images from "Alterations of the Sympathoadrenal Axis Related to the Development of Alzheimer’s Disease in the 3xTg Mouse Model"

    Article Title: Alterations of the Sympathoadrenal Axis Related to the Development of Alzheimer’s Disease in the 3xTg Mouse Model

    Journal: Biology

    doi: 10.3390/biology11040511

    Analysis of mRNA levels and the expression of different VDCC subtypes in adrenal medullae of WT and 3xTg mice over 12 m age. ( A ) Normalized mRNA levels of different VDCCs in adrenal medullae from WT and 3xTg mice > 12 m. Both medullas of the same mouse were homogenized, so each dot represents an individual mouse. ( B ) Representative image of WT and 3xTg adrenal medulla stained with anti-Cav1.3 (top) and anti Cav2.1 (bottom) + DAPI (nuclei). ( C ) IntDen quantification of calcium channel expression. Each dot represents an image analyzed, and the bars represent mean ± SEM. A Student’s t -test was used to statistically compare the WT and 3xTg groups. ** p
    Figure Legend Snippet: Analysis of mRNA levels and the expression of different VDCC subtypes in adrenal medullae of WT and 3xTg mice over 12 m age. ( A ) Normalized mRNA levels of different VDCCs in adrenal medullae from WT and 3xTg mice > 12 m. Both medullas of the same mouse were homogenized, so each dot represents an individual mouse. ( B ) Representative image of WT and 3xTg adrenal medulla stained with anti-Cav1.3 (top) and anti Cav2.1 (bottom) + DAPI (nuclei). ( C ) IntDen quantification of calcium channel expression. Each dot represents an image analyzed, and the bars represent mean ± SEM. A Student’s t -test was used to statistically compare the WT and 3xTg groups. ** p

    Techniques Used: Expressing, Mouse Assay, Staining

    10) Product Images from "Piezo1 Participated in Decreased L-Type Calcium Current Induced by High Hydrostatic Pressure via. CaM/Src/Pitx2 Activation in Atrial Myocytes"

    Article Title: Piezo1 Participated in Decreased L-Type Calcium Current Induced by High Hydrostatic Pressure via. CaM/Src/Pitx2 Activation in Atrial Myocytes

    Journal: Frontiers in Cardiovascular Medicine

    doi: 10.3389/fcvm.2022.842885

    Protein expression levels of Cav1.2, Piezo1, CaM, and Src in human LAA tissues. (A) Representative western blots and densitometric analysis of Cav1.2 and Piezo1 proteins in LA tissues of AF patients and those with SR. (B) Representative western blots and densitometric analysis of CaM and Src protein in LA tissues of AF patients and those with SR. GAPDH was the internal control. ** p
    Figure Legend Snippet: Protein expression levels of Cav1.2, Piezo1, CaM, and Src in human LAA tissues. (A) Representative western blots and densitometric analysis of Cav1.2 and Piezo1 proteins in LA tissues of AF patients and those with SR. (B) Representative western blots and densitometric analysis of CaM and Src protein in LA tissues of AF patients and those with SR. GAPDH was the internal control. ** p

    Techniques Used: Expressing, Chick Chorioallantoic Membrane Assay, Western Blot

    11) Product Images from "L-Type Calcium Channels Contribute to Ethanol-Induced Aberrant Tangential Migration of Primordial Cortical GABAergic Interneurons in the Embryonic Medial Prefrontal Cortex"

    Article Title: L-Type Calcium Channels Contribute to Ethanol-Induced Aberrant Tangential Migration of Primordial Cortical GABAergic Interneurons in the Embryonic Medial Prefrontal Cortex

    Journal: eNeuro

    doi: 10.1523/ENEURO.0359-21.2021

    Cav1.2 is expressed in the embryonic mPFC. A , Representative images of histologic sections from Nkx2.1/Ai14 E16.5 mouse brain ( A1 ) immunostained for Cav1.2 ( A2 ) and overlayed with images of DAPI counterstaining and Nkx2.1/tdTomato-fluorescent GINs ( A3 ). Images were captured at 10× magnification on a spinning disk confocal microscope. B , Representative images at 40× magnification. These images are magnified images of the area demarcated by the white box in A1–A3 . C , Representative images of no primary antibody negative control of Cav1.2 staining.
    Figure Legend Snippet: Cav1.2 is expressed in the embryonic mPFC. A , Representative images of histologic sections from Nkx2.1/Ai14 E16.5 mouse brain ( A1 ) immunostained for Cav1.2 ( A2 ) and overlayed with images of DAPI counterstaining and Nkx2.1/tdTomato-fluorescent GINs ( A3 ). Images were captured at 10× magnification on a spinning disk confocal microscope. B , Representative images at 40× magnification. These images are magnified images of the area demarcated by the white box in A1–A3 . C , Representative images of no primary antibody negative control of Cav1.2 staining.

    Techniques Used: Microscopy, Negative Control, Staining

    Prenatal ethanol exposure does not alter Cav1.2 expression. A , Representative images of Cav1.2 staining overlayed with DAPI and Nkx2.1 in the mPFC of control ( A1 ) and ethanol-fed ( A2 ) E16.5 mouse brain. B , Quantification of fluorescence intensity ratio of Cav1.2 to Nkx2.1 in the mPFC of control and ethanol-treated mice. Unpaired t test. For statistical details, see Results.
    Figure Legend Snippet: Prenatal ethanol exposure does not alter Cav1.2 expression. A , Representative images of Cav1.2 staining overlayed with DAPI and Nkx2.1 in the mPFC of control ( A1 ) and ethanol-fed ( A2 ) E16.5 mouse brain. B , Quantification of fluorescence intensity ratio of Cav1.2 to Nkx2.1 in the mPFC of control and ethanol-treated mice. Unpaired t test. For statistical details, see Results.

    Techniques Used: Expressing, Staining, Fluorescence, Mouse Assay

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    Alomone Labs anti cav1 2 cacna1c antibody
    <t>Cav1.2</t> maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The <t>CACNA1C</t> overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin <t>antibody.</t> P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p
    Anti Cav1 2 Cacna1c Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cav1.2 maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The CACNA1C overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin antibody. P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p

    Journal: Cell & Bioscience

    Article Title: Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

    doi: 10.1186/s13578-022-00873-9

    Figure Lengend Snippet: Cav1.2 maintained Wnt/β-catenin signaling activity in AM tumoroids. A – C Bright field images of an AM tumoroid generated from a single cell. D The organoid forming efficiency was evaluated as a percentage of the number of tumoroids in each well. The CACNA1C overexpression effectively retained the organoid forming efficiency compared to vehicle and VPM treatment group. E – G Hematoxylin and eosin staining of paraffin sections of AM tumoroids. Spherical shaped AM tumoroids were observed in vehicle and VPM treatment group. Budding-like structures expended from CACNA1C-overexpressed AM tumoroids. H Quantification of the size of 14 days and 21 days cultured AM tumoroids. I – K Immunohistochemistry staining of β-catenin in an AM tumoroid. β-catenin was primary found in the plasma membrane. The nuclear accumulation of β-catenin was dominantly observed in the overexpression group compared to the vehicle and VPM treatment groups. L – M Immunohistochemistry staining of CK10 and CACNA1C. The white rectangle indicates the CK10 positive differentiated AM cells in the vehicle and VPM treatment groups. Nuclei were counterstained by TO-PRO-3 (TP3). O Western blot assay of nucleus and cytoplasm fractionated AM tumoroids with β-catenin antibody. P The relative mRNA expression of WNT3A, AXIN2, CTNNB1 , and LGR5 in CACNA1C-overexpressed and VPM treated tumoroids. Scale bar: A–C, 300 μm; E–G, I–K, L–M, 100 μm. Data are presented as the mean ± SD of triplicate experiments. * p

    Article Snippet: Rabbit anti-CACNA1C (1:200, Alomone Labs, ACC-003), mouse anti-CK14 (1:500, Abcam, ab7800), mouse anti-CK10 (1:500, Invitrogen, MA5-13705), mouse anti-E-cadherin (1:500, BD Biosciences, AF748), rabbit anti-MMP-9 (1:200, Merck, AB19016), rabbit anti-LGR5 (1:200, Abcam, ab75732), mouse anti-Ki67 (1:200, Abcam, ab16667), mouse anti-PCNA (1:500, Abcam, ab29), mouse anti-NFATc1 (1:200, Santa Cruz, SC-7294), and mouse anti-β-catenin (1:500, Santa Cruz, SC-7963).

    Techniques: Activity Assay, Generated, Over Expression, Staining, Cell Culture, Immunohistochemistry, Western Blot, Expressing

    Cav1.2-dependent Ca 2+ /NFATc1 signaling increased the proliferation of AM cells. A – D Representative CACNA1C expression in AM cells indicated by arrowhead. CACNA1C was intensely expressed in the plasma membrane in the vehicle group. And it was broadly expressed in the plasma membrane, cytoplasm and nucleus in overexpression group. CACNA1C negatively expressed in knockdown group compared to the scramble. E – H The nuclear translocation of NFATc1 was observed in the overexpression group compared to the vehicle. NFATc1 was negatively expressed in the knockdown group compared to the scramble. I – L Representative confocal images of Ki67 staining of AM cells among the vehicle, overexpression, scramble, and siRNA groups. Nuclear were stained with TO-PRO-3 (TP3). M Percentages of CACNA1C + and NFATc1 + cells were quantified from immunostained images (N = 5 per group, biological replication). N Relative mRNA expression of CACNA1C , MKI67 , and NFATC1 between vehicle and CACNA1C overexpression, or scramble and siRNA group. O Western blot assay of AM cells with CACNA1C, PCNA, Cyclin D1, and GAPDH antibodies. P Western blot assay of nucleus and cytoplasm fractionated AM cells with NFATc1, Histone H3, and GAPDH antibodies. Scale bar: A–D, 50 μm; E–L, 100 μm. Quantitative data are presented as the mean ± SD. ** p

    Journal: Cell & Bioscience

    Article Title: Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

    doi: 10.1186/s13578-022-00873-9

    Figure Lengend Snippet: Cav1.2-dependent Ca 2+ /NFATc1 signaling increased the proliferation of AM cells. A – D Representative CACNA1C expression in AM cells indicated by arrowhead. CACNA1C was intensely expressed in the plasma membrane in the vehicle group. And it was broadly expressed in the plasma membrane, cytoplasm and nucleus in overexpression group. CACNA1C negatively expressed in knockdown group compared to the scramble. E – H The nuclear translocation of NFATc1 was observed in the overexpression group compared to the vehicle. NFATc1 was negatively expressed in the knockdown group compared to the scramble. I – L Representative confocal images of Ki67 staining of AM cells among the vehicle, overexpression, scramble, and siRNA groups. Nuclear were stained with TO-PRO-3 (TP3). M Percentages of CACNA1C + and NFATc1 + cells were quantified from immunostained images (N = 5 per group, biological replication). N Relative mRNA expression of CACNA1C , MKI67 , and NFATC1 between vehicle and CACNA1C overexpression, or scramble and siRNA group. O Western blot assay of AM cells with CACNA1C, PCNA, Cyclin D1, and GAPDH antibodies. P Western blot assay of nucleus and cytoplasm fractionated AM cells with NFATc1, Histone H3, and GAPDH antibodies. Scale bar: A–D, 50 μm; E–L, 100 μm. Quantitative data are presented as the mean ± SD. ** p

    Article Snippet: Rabbit anti-CACNA1C (1:200, Alomone Labs, ACC-003), mouse anti-CK14 (1:500, Abcam, ab7800), mouse anti-CK10 (1:500, Invitrogen, MA5-13705), mouse anti-E-cadherin (1:500, BD Biosciences, AF748), rabbit anti-MMP-9 (1:200, Merck, AB19016), rabbit anti-LGR5 (1:200, Abcam, ab75732), mouse anti-Ki67 (1:200, Abcam, ab16667), mouse anti-PCNA (1:500, Abcam, ab29), mouse anti-NFATc1 (1:200, Santa Cruz, SC-7294), and mouse anti-β-catenin (1:500, Santa Cruz, SC-7963).

    Techniques: Expressing, Over Expression, Translocation Assay, Staining, Western Blot

    Schematic summary. Cav1.2 is dominantly expressed in ameloblastoma cells compared to the OKC. The Cav1.2-dependent Ca 2+ influx increases the proliferation of ameloblastoma cells by the accumulation of nucleic NFATc1, while intracellular Ca 2+ enhances Wnt/β-catenin signaling activity and the maintenance of the stemness of the ameloblastoma cells

    Journal: Cell & Bioscience

    Article Title: Unraveled roles of Cav1.2 in proliferation and stemness of ameloblastoma

    doi: 10.1186/s13578-022-00873-9

    Figure Lengend Snippet: Schematic summary. Cav1.2 is dominantly expressed in ameloblastoma cells compared to the OKC. The Cav1.2-dependent Ca 2+ influx increases the proliferation of ameloblastoma cells by the accumulation of nucleic NFATc1, while intracellular Ca 2+ enhances Wnt/β-catenin signaling activity and the maintenance of the stemness of the ameloblastoma cells

    Article Snippet: Rabbit anti-CACNA1C (1:200, Alomone Labs, ACC-003), mouse anti-CK14 (1:500, Abcam, ab7800), mouse anti-CK10 (1:500, Invitrogen, MA5-13705), mouse anti-E-cadherin (1:500, BD Biosciences, AF748), rabbit anti-MMP-9 (1:200, Merck, AB19016), rabbit anti-LGR5 (1:200, Abcam, ab75732), mouse anti-Ki67 (1:200, Abcam, ab16667), mouse anti-PCNA (1:500, Abcam, ab29), mouse anti-NFATc1 (1:200, Santa Cruz, SC-7294), and mouse anti-β-catenin (1:500, Santa Cruz, SC-7963).

    Techniques: Activity Assay

    Protein expression patterns of Cav1.2 in patient tissue samples without and with epipharyngeal abrasive therapy (EAT). (A) Cav1.2 expression in the epipharynx of the EAT-treated and non-treated groups. (B) Immunohistochemical (IHC) scores for Cav1.2 expression on the epipharyngeal mucosa of the EAT-treated (n = 11) and non-treated groups (n = 7). **Significantly different at p

    Journal: In Vivo

    Article Title: Epipharyngeal Abrasive Therapy Down-regulates the Expression of Cav1.2: A Key Molecule in Influenza Virus Entry

    doi: 10.21873/invivo.12967

    Figure Lengend Snippet: Protein expression patterns of Cav1.2 in patient tissue samples without and with epipharyngeal abrasive therapy (EAT). (A) Cav1.2 expression in the epipharynx of the EAT-treated and non-treated groups. (B) Immunohistochemical (IHC) scores for Cav1.2 expression on the epipharyngeal mucosa of the EAT-treated (n = 11) and non-treated groups (n = 7). **Significantly different at p

    Article Snippet: Rabbit antibody to CaV1.2 (#ACC-003) was purchased from Alomone Labs (Jerusalem, Israel).

    Techniques: Expressing, Immunohistochemistry