cav1 2  (Alomone Labs)


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    Structured Review

    Alomone Labs cav1 2
    <t>Cav1.2</t> knock-down prevents astrocyte activation after scratch
    Cav1 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cav1 2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cav1 2 - by Bioz Stars, 2022-01
    93/100 stars

    Images

    1) Product Images from "L-type voltage-operated calcium channels contribute to astrocyte activation in vitro"

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    Journal: Glia

    doi: 10.1002/glia.23013

    Cav1.2 knock-down prevents astrocyte activation after scratch
    Figure Legend Snippet: Cav1.2 knock-down prevents astrocyte activation after scratch

    Techniques Used: Activation Assay

    LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes
    Figure Legend Snippet: LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes

    Techniques Used: Activity Assay, Expressing

    Cav1.2 KO astrocytes are not sensitive to LPS
    Figure Legend Snippet: Cav1.2 KO astrocytes are not sensitive to LPS

    Techniques Used:

    Cav1.2 knock-down prevents astrocyte activation by LPS
    Figure Legend Snippet: Cav1.2 knock-down prevents astrocyte activation by LPS

    Techniques Used: Activation Assay

    2) Product Images from "The effect of Sirt1 deficiency on Ca2+ and Na+ regulation in mouse ventricular myocytes, et al. The effect of Sirt1 deficiency on Ca2+ and Na+ regulation in mouse ventricular myocytes"

    Article Title: The effect of Sirt1 deficiency on Ca2+ and Na+ regulation in mouse ventricular myocytes, et al. The effect of Sirt1 deficiency on Ca2+ and Na+ regulation in mouse ventricular myocytes

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.15327

    Ca 2+ regulatory proteins in control and Sirt1 −/− ventricular myocytes. A, Representative immunoblot and mean data for Cav1.2, SERCA2a, NCX and CaMKII in control and Sirt1 −/− mice ventricular myocytes. B, Normalized densitometry for the protein levels (α‐Tubulin was used as an internal control; Control N = 6 and Sirt1 −/− N = 6; * P
    Figure Legend Snippet: Ca 2+ regulatory proteins in control and Sirt1 −/− ventricular myocytes. A, Representative immunoblot and mean data for Cav1.2, SERCA2a, NCX and CaMKII in control and Sirt1 −/− mice ventricular myocytes. B, Normalized densitometry for the protein levels (α‐Tubulin was used as an internal control; Control N = 6 and Sirt1 −/− N = 6; * P

    Techniques Used: Mouse Assay

    3) Product Images from "Colchicine modulates calcium homeostasis and electrical property of HL‐1 cells"

    Article Title: Colchicine modulates calcium homeostasis and electrical property of HL‐1 cells

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.12818

    Effect of colchicine on the protein expression of calcium (Ca 2+ ) regulatory proteins and potassium channel proteins. ( A ) Representative immunoblotting and average data of sarcoplasmic reticulum Ca 2+ ATPase (SERCA2a), Cav1.2, Ca 2+ /calmodulin‐dependent protein kinase II (CaMKII), PLB, Ser16‐ and Thr17‐phosphorylated PLB (PLB‐Ser16 and PLB‐Thr17) from control and colchicine (3 nM)‐treated HL‐1 cells. ( n = 9) ( B ) Representative immunoblotting and average data of RyR type 2, phosphorylation of RyR at S2808 and S2814 (RyR‐2808 and RyR‐2814), the Na + –Ca 2+ exchanger (NCX), Kv1.4, Kv1.5 and Kv4.2 from control and colchicine (3 nM)‐treated HL‐1 cells ( n = 7). * P
    Figure Legend Snippet: Effect of colchicine on the protein expression of calcium (Ca 2+ ) regulatory proteins and potassium channel proteins. ( A ) Representative immunoblotting and average data of sarcoplasmic reticulum Ca 2+ ATPase (SERCA2a), Cav1.2, Ca 2+ /calmodulin‐dependent protein kinase II (CaMKII), PLB, Ser16‐ and Thr17‐phosphorylated PLB (PLB‐Ser16 and PLB‐Thr17) from control and colchicine (3 nM)‐treated HL‐1 cells. ( n = 9) ( B ) Representative immunoblotting and average data of RyR type 2, phosphorylation of RyR at S2808 and S2814 (RyR‐2808 and RyR‐2814), the Na + –Ca 2+ exchanger (NCX), Kv1.4, Kv1.5 and Kv4.2 from control and colchicine (3 nM)‐treated HL‐1 cells ( n = 7). * P

    Techniques Used: Expressing

    4) Product Images from "Metformin Shortens Prolonged QT Interval in Diabetic Mice by Inhibiting L-Type Calcium Current: A Possible Therapeutic Approach"

    Article Title: Metformin Shortens Prolonged QT Interval in Diabetic Mice by Inhibiting L-Type Calcium Current: A Possible Therapeutic Approach

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.00614

    Treatment effects of metformin on the mRNA and protein levels of Cav1.2 in diabetic mice. (A) Relative levels of CACNA1C with metformin in diabetic mice detected by real-time PCR, n=6. (B) Relative levels of Cav1.2 in the Ctrl group, DM group, and the metformin-treatment group detected by western blot, n=6. (C) Representative confocal images of α-Actinin (left) or CaV1.2 (middle) in the Ctrl group, DM group, and the metformin-treatment group. (D) Relative levels of Cav1.2 in the Ctrl group, DM group, and the metformin-treatment group by immunofluorescences, n=9. Values represent mean ± SEM, *P
    Figure Legend Snippet: Treatment effects of metformin on the mRNA and protein levels of Cav1.2 in diabetic mice. (A) Relative levels of CACNA1C with metformin in diabetic mice detected by real-time PCR, n=6. (B) Relative levels of Cav1.2 in the Ctrl group, DM group, and the metformin-treatment group detected by western blot, n=6. (C) Representative confocal images of α-Actinin (left) or CaV1.2 (middle) in the Ctrl group, DM group, and the metformin-treatment group. (D) Relative levels of Cav1.2 in the Ctrl group, DM group, and the metformin-treatment group by immunofluorescences, n=9. Values represent mean ± SEM, *P

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

    Treatment effects of metformin on the mRNA and protein levels of Cav1.2 in primary cultured neonatal mice cardiomyocytes. (A) Relative levels of CACNA1C with metformin of primary cardiomyocytes in NC group, HG group and metformin-treatment group detected by real-time PCR, n=6. (B) Relative levels of Cav1.2 of primary cardiomyocytes in NC group, HG group and metformin-treatment group detected by western blot, n=6. (C) Representative confocal images of α-Actinin (left) or CaV1.2 (middle) of primary cardiomyocytes in NC group, HG group and metformin-treatment group. (D) Relative levels of Cav1.2 of primary cardiomyocytes in NC group, HG group and metformin-treatment group detected by immunofluorescences, n=9. Values represent mean ± SEM, *P
    Figure Legend Snippet: Treatment effects of metformin on the mRNA and protein levels of Cav1.2 in primary cultured neonatal mice cardiomyocytes. (A) Relative levels of CACNA1C with metformin of primary cardiomyocytes in NC group, HG group and metformin-treatment group detected by real-time PCR, n=6. (B) Relative levels of Cav1.2 of primary cardiomyocytes in NC group, HG group and metformin-treatment group detected by western blot, n=6. (C) Representative confocal images of α-Actinin (left) or CaV1.2 (middle) of primary cardiomyocytes in NC group, HG group and metformin-treatment group. (D) Relative levels of Cav1.2 of primary cardiomyocytes in NC group, HG group and metformin-treatment group detected by immunofluorescences, n=9. Values represent mean ± SEM, *P

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

    5) Product Images from "Relaxin-2 therapy reverses radiation-induced fibrosis and restores bladder function in mice"

    Article Title: Relaxin-2 therapy reverses radiation-induced fibrosis and restores bladder function in mice

    Journal: Neurourology and urodynamics

    doi: 10.1002/nau.23721

    Structure of hRLX2, hypothetical pathway intermediates of RXFP1/2 and the benefits of hRLX2 therapy in radiation cystitis. A and B, The α-chain of hRLX2 can bind to RXFP1/2 receptors located on detrusor smooth muscle to increase cAMP levels and the expression of Cav1.2 (potentially via inhibition of RhoA activity) resulting in enhancement of force generation. hRLX2-mediated cAMP generation in the bladder vasculature may also increase Akt phosphorylation, platelet derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) expression to promote angiogenesis. The β-chain of hRLX2 can interact with RXFP1 to selectively stimulate pERK1/2 pathways upregulating nNOS and cGMP levels. This leads to decreased collagen synthesis and tissue inhibitors of matrix metalloproteases (TIMP), and increased matrix metalloprotease (MMP) expression to reverse fibrosis in the ECM. C, One of the initial responses following radiation exposure is inflammation due to urothelial apoptosis and urine infiltration. Concurrently, there is damage to the vascular endothelium leading to ischemia. These processes cause increased collagen deposition, and decreased bladder compliance and force generation. Treatment with hRLX2 reverses fibrosis through inhibition of collagen synthesis and enhancement of its degradation by MMPs. It also enhances contractile function through increased Cav1.2 (ie, L-type Ca 2+ channel) expression and improved tissue perfusion via NO• induced vasodilation. hRLX2 is also anti-inflammatory, inhibiting recurrent damage to the bladder wall
    Figure Legend Snippet: Structure of hRLX2, hypothetical pathway intermediates of RXFP1/2 and the benefits of hRLX2 therapy in radiation cystitis. A and B, The α-chain of hRLX2 can bind to RXFP1/2 receptors located on detrusor smooth muscle to increase cAMP levels and the expression of Cav1.2 (potentially via inhibition of RhoA activity) resulting in enhancement of force generation. hRLX2-mediated cAMP generation in the bladder vasculature may also increase Akt phosphorylation, platelet derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) expression to promote angiogenesis. The β-chain of hRLX2 can interact with RXFP1 to selectively stimulate pERK1/2 pathways upregulating nNOS and cGMP levels. This leads to decreased collagen synthesis and tissue inhibitors of matrix metalloproteases (TIMP), and increased matrix metalloprotease (MMP) expression to reverse fibrosis in the ECM. C, One of the initial responses following radiation exposure is inflammation due to urothelial apoptosis and urine infiltration. Concurrently, there is damage to the vascular endothelium leading to ischemia. These processes cause increased collagen deposition, and decreased bladder compliance and force generation. Treatment with hRLX2 reverses fibrosis through inhibition of collagen synthesis and enhancement of its degradation by MMPs. It also enhances contractile function through increased Cav1.2 (ie, L-type Ca 2+ channel) expression and improved tissue perfusion via NO• induced vasodilation. hRLX2 is also anti-inflammatory, inhibiting recurrent damage to the bladder wall

    Techniques Used: Expressing, Inhibition, Activity Assay, Derivative Assay

    6) Product Images from "L-type voltage-operated calcium channels contribute to astrocyte activation in vitro"

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    Journal: Glia

    doi: 10.1002/glia.23013

    Cav1.2 knock-down prevents astrocyte activation after scratch
    Figure Legend Snippet: Cav1.2 knock-down prevents astrocyte activation after scratch

    Techniques Used: Activation Assay

    LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes
    Figure Legend Snippet: LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes

    Techniques Used: Activity Assay, Expressing

    Cav1.2 KO astrocytes are not sensitive to LPS
    Figure Legend Snippet: Cav1.2 KO astrocytes are not sensitive to LPS

    Techniques Used:

    Cav1.2 knock-down prevents astrocyte activation by LPS
    Figure Legend Snippet: Cav1.2 knock-down prevents astrocyte activation by LPS

    Techniques Used: Activation Assay

    7) Product Images from "Partial Mechanical Unloading of the Heart Disrupts L-Type Calcium Channel and Beta-Adrenoceptor Signaling Microdomains"

    Article Title: Partial Mechanical Unloading of the Heart Disrupts L-Type Calcium Channel and Beta-Adrenoceptor Signaling Microdomains

    Journal: Frontiers in Physiology

    doi: 10.3389/fphys.2018.01302

    (A) PLA image demonstrating the association of Cav1.2 and Cav-3 in loaded and unloaded cells. (B) Graph comparing the size of loaded and unloaded cells (loaded 3271 ± 212.4 μm 2 vs. unloaded 1444 ± 92.03 μm 2 N,n 3/17-25 mean ± SEM ∗∗∗ p
    Figure Legend Snippet: (A) PLA image demonstrating the association of Cav1.2 and Cav-3 in loaded and unloaded cells. (B) Graph comparing the size of loaded and unloaded cells (loaded 3271 ± 212.4 μm 2 vs. unloaded 1444 ± 92.03 μm 2 N,n 3/17-25 mean ± SEM ∗∗∗ p

    Techniques Used: Proximity Ligation Assay

    Schematic demonstrating the speculated state of a t-tubular microdomain in loaded or unloaded scenarios with or without isoprenaline stimulation. (1) Loaded cell. LTCC are generally active within the tubule owning to some constitutive cAMP production and consequent PKA activity, scaffolded by Cav-3 and JPH-2. Calcium spark activity at the sarcoplasmic reticulum is nominal. (2) Unloaded cell. LTCC are generally inactive as there is a loss of coherent confinement of cAMP and PKA activity to the t-tubular microdomain. This is due to the mechanosensitivity of the association between Cav1.2, Cav-3, and JPH-2 and the loss of t-tubules. Even though there is a smaller amount of LTCC activity spark activity increases as orphaned RyR no longer receive effective control and thus experience a gain of function. (3) Loaded cell stimulated with ISO. After stimulation β2AR increase cAMP levels in the cytoplasm of the sarcomeric dyad and this activates a sub-population of PKA which activates almost all LTCC. Spark activity remains nominal as effective measures to control LTCC and RYR phosphorylation and the degradation of cAMP remain effective due to scaffolding by the cellular microdomain. (4) Unloaded cell stimulated with ISO. Despite a reduction in the amount of cAMP response initiated by β 2 AR in the cytosol, signals still reach RII_PKA domains, due to the loss of efficient cAMP compartmentation. This stimulates further aberrant spark activity due to the relatively uncontrolled calcium influx in the cell and EC mediator hyperphosphorylation following the loss of normal structure within the sarcomeric dyad following unloading.
    Figure Legend Snippet: Schematic demonstrating the speculated state of a t-tubular microdomain in loaded or unloaded scenarios with or without isoprenaline stimulation. (1) Loaded cell. LTCC are generally active within the tubule owning to some constitutive cAMP production and consequent PKA activity, scaffolded by Cav-3 and JPH-2. Calcium spark activity at the sarcoplasmic reticulum is nominal. (2) Unloaded cell. LTCC are generally inactive as there is a loss of coherent confinement of cAMP and PKA activity to the t-tubular microdomain. This is due to the mechanosensitivity of the association between Cav1.2, Cav-3, and JPH-2 and the loss of t-tubules. Even though there is a smaller amount of LTCC activity spark activity increases as orphaned RyR no longer receive effective control and thus experience a gain of function. (3) Loaded cell stimulated with ISO. After stimulation β2AR increase cAMP levels in the cytoplasm of the sarcomeric dyad and this activates a sub-population of PKA which activates almost all LTCC. Spark activity remains nominal as effective measures to control LTCC and RYR phosphorylation and the degradation of cAMP remain effective due to scaffolding by the cellular microdomain. (4) Unloaded cell stimulated with ISO. Despite a reduction in the amount of cAMP response initiated by β 2 AR in the cytosol, signals still reach RII_PKA domains, due to the loss of efficient cAMP compartmentation. This stimulates further aberrant spark activity due to the relatively uncontrolled calcium influx in the cell and EC mediator hyperphosphorylation following the loss of normal structure within the sarcomeric dyad following unloading.

    Techniques Used: Activity Assay, Scaffolding

    8) Product Images from "Deletion of Voltage-Gated Calcium Channels in Astrocytes during Demyelination Reduces Brain Inflammation and Promotes Myelin Regeneration in Mice"

    Article Title: Deletion of Voltage-Gated Calcium Channels in Astrocytes during Demyelination Reduces Brain Inflammation and Promotes Myelin Regeneration in Mice

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.1644-19.2020

    Attenuated microglia reactivity and reduced production of pro-inflammatory factors in the Cav1.2 KO brain. A , Representative coronal sections of the corpus callosum and cortex immunostained for CD68 and Iba1. Brain tissue was collected from untreated and CPZ-treated (CPZ) control and Cav1.2 KO mice injected with tamoxifen following Protocol b. Scale bar, 180 µm. B , The integrated fluorescent intensity of CD68 and Iba1 was measured in the lateral portion of the corpus callosum (CC) and in the cortex (CX) of untreated and CPZ-treated (CPZ) control and Cav1.2 KO mice injected with tamoxifen according to Protocol a or b. Exact p values from left to right: CD68 CC:
    Figure Legend Snippet: Attenuated microglia reactivity and reduced production of pro-inflammatory factors in the Cav1.2 KO brain. A , Representative coronal sections of the corpus callosum and cortex immunostained for CD68 and Iba1. Brain tissue was collected from untreated and CPZ-treated (CPZ) control and Cav1.2 KO mice injected with tamoxifen following Protocol b. Scale bar, 180 µm. B , The integrated fluorescent intensity of CD68 and Iba1 was measured in the lateral portion of the corpus callosum (CC) and in the cortex (CX) of untreated and CPZ-treated (CPZ) control and Cav1.2 KO mice injected with tamoxifen according to Protocol a or b. Exact p values from left to right: CD68 CC:

    Techniques Used: Mouse Assay, Injection

    Gliotic response throughout the recovery period of the CPZ treatment. A , Representative coronal sections of the corpus callosum (CC) and cortex (CX) immunostained for GFAP. Tissue was collected from untreated and CPZ-treated control and Cav1.2 KO mice at 2 and 4 weeks of recovery (2 or 4W Rec). Scale bar, 180 µm. B , C , Bar graphs display number of GFAP and GFAP/Ki67 double-positive cells in the lateral CC and in the CX of untreated, control and Cav1.2 KO mice at the end of CPZ treatment (CPZ) and after 2 and 4 weeks of recovery (2 or 4W Rec). Exact p values from left to right: GFAP CC:
    Figure Legend Snippet: Gliotic response throughout the recovery period of the CPZ treatment. A , Representative coronal sections of the corpus callosum (CC) and cortex (CX) immunostained for GFAP. Tissue was collected from untreated and CPZ-treated control and Cav1.2 KO mice at 2 and 4 weeks of recovery (2 or 4W Rec). Scale bar, 180 µm. B , C , Bar graphs display number of GFAP and GFAP/Ki67 double-positive cells in the lateral CC and in the CX of untreated, control and Cav1.2 KO mice at the end of CPZ treatment (CPZ) and after 2 and 4 weeks of recovery (2 or 4W Rec). Exact p values from left to right: GFAP CC:

    Techniques Used: Mouse Assay

    Reduced astrocyte activation in the Cav1.2 KO brain following CPZ treatment. A , Control and Cav1.2 KO mice were treated with CPZ for 6 weeks and injected with tamoxifen according to Protocols a or b. B , Representative coronal sections of the lateral portion of the corpus callosum immunostained for GFAP and Cre . Scale bar, 90 µm. C , Quantitative RT-PCR analysis of Cav1.2 expression performed with mRNA from acute isolated cortical astrocytes. D , F , Representative coronal sections of the corpus callosum (CC) and cortex (CX) immunostained for GFAP and GFAP/Ki67. Brain tissue was collected from untreated and CPZ-treated (CPZ) control and Cav1.2 KO mice injected with tamoxifen following Protocol b. Scale bars: D , top, 180 µm, bottom, 90 µm; F , top, 90 µm; bottom, 45 µm. E , The total number of GFAP, s100β and GFAP/Ki67 double-positive cells was quantified in the cortex and in the corpus callosum of untreated and CPZ-treated control and Cav1.2 KO mice injected according to Protocols a or b. Exact p values from left to right: GFAP CX:
    Figure Legend Snippet: Reduced astrocyte activation in the Cav1.2 KO brain following CPZ treatment. A , Control and Cav1.2 KO mice were treated with CPZ for 6 weeks and injected with tamoxifen according to Protocols a or b. B , Representative coronal sections of the lateral portion of the corpus callosum immunostained for GFAP and Cre . Scale bar, 90 µm. C , Quantitative RT-PCR analysis of Cav1.2 expression performed with mRNA from acute isolated cortical astrocytes. D , F , Representative coronal sections of the corpus callosum (CC) and cortex (CX) immunostained for GFAP and GFAP/Ki67. Brain tissue was collected from untreated and CPZ-treated (CPZ) control and Cav1.2 KO mice injected with tamoxifen following Protocol b. Scale bars: D , top, 180 µm, bottom, 90 µm; F , top, 90 µm; bottom, 45 µm. E , The total number of GFAP, s100β and GFAP/Ki67 double-positive cells was quantified in the cortex and in the corpus callosum of untreated and CPZ-treated control and Cav1.2 KO mice injected according to Protocols a or b. Exact p values from left to right: GFAP CX:

    Techniques Used: Activation Assay, Mouse Assay, Injection, Quantitative RT-PCR, Expressing, Isolation

    Electron microscopy of the Cav1.2 KO corpus callosum. A , Electron micrographs of axons in the body of the corpus callosum of untreated, control and Cav1.2 KO mice at the end of CPZ treatment (CPZ) and after 2 weeks of recovery (2W Rec). Scale bars: top, 8 µm; bottom, 2 µm. B , Scatter plot of g-ratio values of untreated, control and Cav1.2 KO mice at the end of the CPZ treatment and after 2 and 4 weeks of recovery (2 or 4W Rec). Four animals per experimental group and ∼150 fibers per mice were analyzed. The lines represent the regression equation with 95% confidence intervals. CPZ untreated: r 2 : 0.2744; slope: 0.2884; 1/slope: 3.467; F: 134.6; CPZ control: r 2 : 0.4809; slope: 0.2105; 1/slope: 3.442; F: 113.0; CPZ Cav1.2 KO : r 2 : 0.4031; slope: 0.2281; 1/slope: 4.385; F: 158.7; 2W Rec control: r 2 : 0.2122; slope: 0.2365; 1/slope: 4.228; F: 120.4; 2W Rec Cav1.2 KO : r 2 : 0.5209; slope: 0.2887; 1/slope: 3.463; F: 572.0; 4W Rec control: r 2 : 0.1861; slope: 0.1363; 1/slope: 7.334; F: 115.2; 4W Rec Cav1.2 KO : r 2 : 0.2471; slope: 0.1840; 1/slope: 5.436; F: 197.2. C , Mean axonal diameter of myelinated axons for the same experimental conditions. D , Mean g-ratio values. E , Percentage of myelinated axons. Four animals per experimental group and ∼150 fibers per mice were analyzed. Exact p values from left to right: g- ratios:
    Figure Legend Snippet: Electron microscopy of the Cav1.2 KO corpus callosum. A , Electron micrographs of axons in the body of the corpus callosum of untreated, control and Cav1.2 KO mice at the end of CPZ treatment (CPZ) and after 2 weeks of recovery (2W Rec). Scale bars: top, 8 µm; bottom, 2 µm. B , Scatter plot of g-ratio values of untreated, control and Cav1.2 KO mice at the end of the CPZ treatment and after 2 and 4 weeks of recovery (2 or 4W Rec). Four animals per experimental group and ∼150 fibers per mice were analyzed. The lines represent the regression equation with 95% confidence intervals. CPZ untreated: r 2 : 0.2744; slope: 0.2884; 1/slope: 3.467; F: 134.6; CPZ control: r 2 : 0.4809; slope: 0.2105; 1/slope: 3.442; F: 113.0; CPZ Cav1.2 KO : r 2 : 0.4031; slope: 0.2281; 1/slope: 4.385; F: 158.7; 2W Rec control: r 2 : 0.2122; slope: 0.2365; 1/slope: 4.228; F: 120.4; 2W Rec Cav1.2 KO : r 2 : 0.5209; slope: 0.2887; 1/slope: 3.463; F: 572.0; 4W Rec control: r 2 : 0.1861; slope: 0.1363; 1/slope: 7.334; F: 115.2; 4W Rec Cav1.2 KO : r 2 : 0.2471; slope: 0.1840; 1/slope: 5.436; F: 197.2. C , Mean axonal diameter of myelinated axons for the same experimental conditions. D , Mean g-ratio values. E , Percentage of myelinated axons. Four animals per experimental group and ∼150 fibers per mice were analyzed. Exact p values from left to right: g- ratios:

    Techniques Used: Electron Microscopy, Mouse Assay

    Increased number of mature oligodendrocytes in the Cav1.2 KO mouse. A , D , Representative coronal sections of the corpus callosum (CC) and cortex (CX) immunostained for CC1, Olig2/Ki67 and Olig2/Sox2. Tissue was collected from untreated, control and Cav1.2 KO mice after 2 weeks of recovery (2W Rec). Scale bar, 90 µm. B , C , The total number of Olig2 and CC1-positive cells was quantified in the lateral portion of the CC and in the CX. Exact p values from left to right: Olig2 CC:
    Figure Legend Snippet: Increased number of mature oligodendrocytes in the Cav1.2 KO mouse. A , D , Representative coronal sections of the corpus callosum (CC) and cortex (CX) immunostained for CC1, Olig2/Ki67 and Olig2/Sox2. Tissue was collected from untreated, control and Cav1.2 KO mice after 2 weeks of recovery (2W Rec). Scale bar, 90 µm. B , C , The total number of Olig2 and CC1-positive cells was quantified in the lateral portion of the CC and in the CX. Exact p values from left to right: Olig2 CC:

    Techniques Used: Mouse Assay

    Enhanced myelin proteins synthesis through the remyelination phase of the Cav1.2 KO brain. A , Representative coronal sections of the corpus callosum and cortex immunostained for PLP and MBP. Tissue was collected from untreated, control and Cav1.2 KO mice at the end of the CPZ treatment (CPZ) and after 4 weeks of recovery (4W Rec). Scale bar, 180 µm. B , PLP and MBP fluorescent intensity was quantified in the lateral corpus callosum (CC) and in the cortex (CX). Fluorescent intensity data are presented as percentage of untreated mice. Exact p values from left to right: PLP CC:
    Figure Legend Snippet: Enhanced myelin proteins synthesis through the remyelination phase of the Cav1.2 KO brain. A , Representative coronal sections of the corpus callosum and cortex immunostained for PLP and MBP. Tissue was collected from untreated, control and Cav1.2 KO mice at the end of the CPZ treatment (CPZ) and after 4 weeks of recovery (4W Rec). Scale bar, 180 µm. B , PLP and MBP fluorescent intensity was quantified in the lateral corpus callosum (CC) and in the cortex (CX). Fluorescent intensity data are presented as percentage of untreated mice. Exact p values from left to right: PLP CC:

    Techniques Used: Plasmid Purification, Mouse Assay

    9) Product Images from "L-type voltage-operated calcium channels contribute to astrocyte activation in vitro"

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    Journal: Glia

    doi: 10.1002/glia.23013

    Cav1.2 knock-down prevents astrocyte activation after scratch
    Figure Legend Snippet: Cav1.2 knock-down prevents astrocyte activation after scratch

    Techniques Used: Activation Assay

    LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes
    Figure Legend Snippet: LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes

    Techniques Used: Activity Assay, Expressing

    Cav1.2 KO astrocytes are not sensitive to LPS
    Figure Legend Snippet: Cav1.2 KO astrocytes are not sensitive to LPS

    Techniques Used:

    Cav1.2 knock-down prevents astrocyte activation by LPS
    Figure Legend Snippet: Cav1.2 knock-down prevents astrocyte activation by LPS

    Techniques Used: Activation Assay

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    Alomone Labs cav1 2
    <t>Cav1.2</t> knock-down prevents astrocyte activation after scratch
    Cav1 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cav1 2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cav1 2 - by Bioz Stars, 2022-01
    93/100 stars
      Buy from Supplier

    86
    Alomone Labs anti cav1 2
    Expressions of calcium handling proteins. The confocal image showed fluorescein isothiocyanate (green)-labeled <t>Cav1.2,</t> SERCA2a, and NCX1 expressed in isolated rat cardiac ventricular myocytes in SO (left panel), HF (middle panel), and NRG group (right panel). Nuclei were stained with DAPI (blue). The scale bar represents 20 μm (n = 5 for each set of staining).
    Anti Cav1 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti cav1 2/product/Alomone Labs
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti cav1 2 - by Bioz Stars, 2022-01
    86/100 stars
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    95
    Alomone Labs acc 003 antibody
    Location of antibody epitopes. Shown is a schematic of the Ca v 1.2 α 1 1.2 subunit, in which regions used as immunogens for the depicted antibodies are identified by arrows. Exact residues are listed in the table and numbered according to α 1 1.2 given in Gene Bank Accession number CAA33546. FP1, CNC1, and <t>ACC-003</t> are directed against the loop between domains II and III, pS1700 against phosphorylated S1700, pS1928 against phosphorylated S1928, and CNC2 against residues 2122-2138 of α 1 1.2, which are ~40 residues upstream of the very C terminus of α 1 1.2.
    Acc 003 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
    https://www.bioz.com/result/acc 003 antibody/product/Alomone Labs
    Average 95 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    acc 003 antibody - by Bioz Stars, 2022-01
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    Cav1.2 knock-down prevents astrocyte activation after scratch

    Journal: Glia

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    doi: 10.1002/glia.23013

    Figure Lengend Snippet: Cav1.2 knock-down prevents astrocyte activation after scratch

    Article Snippet: In contrast, RT-PCR, western blot and immunocytochemistry experiments show that Cav1.2 and Cav1.3 are highly expressed in cortical astrocytes ( ). shows representative images of labeled cultured astrocytes at 6 days in vitro ( DIV ); while GFAP abundantly labeled cell processes and cell bodies, labeling with Cav1.2 and Cav1.3 antibodies displayed a punctate staining on the cells surface ( ).

    Techniques: Activation Assay

    LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes

    Journal: Glia

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    doi: 10.1002/glia.23013

    Figure Lengend Snippet: LPS enhance the activity and the expression of Cav1.2 Ca ++ channels in astrocytes

    Article Snippet: In contrast, RT-PCR, western blot and immunocytochemistry experiments show that Cav1.2 and Cav1.3 are highly expressed in cortical astrocytes ( ). shows representative images of labeled cultured astrocytes at 6 days in vitro ( DIV ); while GFAP abundantly labeled cell processes and cell bodies, labeling with Cav1.2 and Cav1.3 antibodies displayed a punctate staining on the cells surface ( ).

    Techniques: Activity Assay, Expressing

    Cav1.2 KO astrocytes are not sensitive to LPS

    Journal: Glia

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    doi: 10.1002/glia.23013

    Figure Lengend Snippet: Cav1.2 KO astrocytes are not sensitive to LPS

    Article Snippet: In contrast, RT-PCR, western blot and immunocytochemistry experiments show that Cav1.2 and Cav1.3 are highly expressed in cortical astrocytes ( ). shows representative images of labeled cultured astrocytes at 6 days in vitro ( DIV ); while GFAP abundantly labeled cell processes and cell bodies, labeling with Cav1.2 and Cav1.3 antibodies displayed a punctate staining on the cells surface ( ).

    Techniques:

    Cav1.2 knock-down prevents astrocyte activation by LPS

    Journal: Glia

    Article Title: L-type voltage-operated calcium channels contribute to astrocyte activation in vitro

    doi: 10.1002/glia.23013

    Figure Lengend Snippet: Cav1.2 knock-down prevents astrocyte activation by LPS

    Article Snippet: In contrast, RT-PCR, western blot and immunocytochemistry experiments show that Cav1.2 and Cav1.3 are highly expressed in cortical astrocytes ( ). shows representative images of labeled cultured astrocytes at 6 days in vitro ( DIV ); while GFAP abundantly labeled cell processes and cell bodies, labeling with Cav1.2 and Cav1.3 antibodies displayed a punctate staining on the cells surface ( ).

    Techniques: Activation Assay

    Expressions of calcium handling proteins. The confocal image showed fluorescein isothiocyanate (green)-labeled Cav1.2, SERCA2a, and NCX1 expressed in isolated rat cardiac ventricular myocytes in SO (left panel), HF (middle panel), and NRG group (right panel). Nuclei were stained with DAPI (blue). The scale bar represents 20 μm (n = 5 for each set of staining).

    Journal: Frontiers in Pharmacology

    Article Title: Neuregulin-1β Partially Improves Cardiac Function in Volume-Overload Heart Failure Through Regulation of Abnormal Calcium Handling

    doi: 10.3389/fphar.2019.00616

    Figure Lengend Snippet: Expressions of calcium handling proteins. The confocal image showed fluorescein isothiocyanate (green)-labeled Cav1.2, SERCA2a, and NCX1 expressed in isolated rat cardiac ventricular myocytes in SO (left panel), HF (middle panel), and NRG group (right panel). Nuclei were stained with DAPI (blue). The scale bar represents 20 μm (n = 5 for each set of staining).

    Article Snippet: Anti-Cav1.2, anti-SERCA2a, and anti-NCX1 antibody were purchased from Alomone (Jerusalem, ACC-003, Israel), Millipore (MA, AB3516P, USA), and Santa Cruz Biotechnology (CA, SC-8094, USA), and secondary antibodies, anti-rabbit488 conjugated antibody was purchased from Santa Cruz Biotechnology (CA, sc-362262, USA).

    Techniques: Labeling, Isolation, Staining

    Quantitative analysis of calcium handling proteins expressions. (A) Representative expression of Cav1.2, SERCA2a, and NCX1, β-actin as loading controls. (B) Comparison of Cav1.2 protein expression (n = 3 rats). (C) Comparison of SERCA2a protein expression (n = 4 rats). (D) Comparison of NCX1 protein expression (n = 4 rats). * P

    Journal: Frontiers in Pharmacology

    Article Title: Neuregulin-1β Partially Improves Cardiac Function in Volume-Overload Heart Failure Through Regulation of Abnormal Calcium Handling

    doi: 10.3389/fphar.2019.00616

    Figure Lengend Snippet: Quantitative analysis of calcium handling proteins expressions. (A) Representative expression of Cav1.2, SERCA2a, and NCX1, β-actin as loading controls. (B) Comparison of Cav1.2 protein expression (n = 3 rats). (C) Comparison of SERCA2a protein expression (n = 4 rats). (D) Comparison of NCX1 protein expression (n = 4 rats). * P

    Article Snippet: Anti-Cav1.2, anti-SERCA2a, and anti-NCX1 antibody were purchased from Alomone (Jerusalem, ACC-003, Israel), Millipore (MA, AB3516P, USA), and Santa Cruz Biotechnology (CA, SC-8094, USA), and secondary antibodies, anti-rabbit488 conjugated antibody was purchased from Santa Cruz Biotechnology (CA, sc-362262, USA).

    Techniques: Expressing

    Location of antibody epitopes. Shown is a schematic of the Ca v 1.2 α 1 1.2 subunit, in which regions used as immunogens for the depicted antibodies are identified by arrows. Exact residues are listed in the table and numbered according to α 1 1.2 given in Gene Bank Accession number CAA33546. FP1, CNC1, and ACC-003 are directed against the loop between domains II and III, pS1700 against phosphorylated S1700, pS1928 against phosphorylated S1928, and CNC2 against residues 2122-2138 of α 1 1.2, which are ~40 residues upstream of the very C terminus of α 1 1.2.

    Journal: F1000Research

    Article Title: Proteolytic processing of the L-type Ca2+ channel alpha11.2 subunit in neurons

    doi: 10.12688/f1000research.11808.1

    Figure Lengend Snippet: Location of antibody epitopes. Shown is a schematic of the Ca v 1.2 α 1 1.2 subunit, in which regions used as immunogens for the depicted antibodies are identified by arrows. Exact residues are listed in the table and numbered according to α 1 1.2 given in Gene Bank Accession number CAA33546. FP1, CNC1, and ACC-003 are directed against the loop between domains II and III, pS1700 against phosphorylated S1700, pS1928 against phosphorylated S1928, and CNC2 against residues 2122-2138 of α 1 1.2, which are ~40 residues upstream of the very C terminus of α 1 1.2.

    Article Snippet: Concordant with this idea, neither the ACC-003 antibody that we received from Alomone Labs that recognized a 130 kDa band in WT and cKO brains nor our CNC1 antibody recognized the strong 150 kDa band seen with FP1 in brain lysate.

    Techniques:

    Differential recognition of the strong 150 kDa FP1 band in lysate and weak 150 kDa band by FP1, CNC1, and ACC-003 after IP of α 1 1.2 with FP1. Immunoblots with CNC1 ( A , B ), FP1 ( C ), and ACC-003 ( D , E ) of Triton X-100 extracts from WT mice (lysate) and after immunoprecipitation with FP1 from cKO and WT mice. Gels were polymerized from 8% acrylamide. Note that a weak 150 kDa band is detected by CNC1, FP1, and ACC-003 after enrichment of α 1 1.2 by immunoprecipitation with FP1 but the strongly immunoreactive 150 kDa band detected by FP1 in lysate is not detectable by either CNC1 or ACC-003.

    Journal: F1000Research

    Article Title: Proteolytic processing of the L-type Ca2+ channel alpha11.2 subunit in neurons

    doi: 10.12688/f1000research.11808.1

    Figure Lengend Snippet: Differential recognition of the strong 150 kDa FP1 band in lysate and weak 150 kDa band by FP1, CNC1, and ACC-003 after IP of α 1 1.2 with FP1. Immunoblots with CNC1 ( A , B ), FP1 ( C ), and ACC-003 ( D , E ) of Triton X-100 extracts from WT mice (lysate) and after immunoprecipitation with FP1 from cKO and WT mice. Gels were polymerized from 8% acrylamide. Note that a weak 150 kDa band is detected by CNC1, FP1, and ACC-003 after enrichment of α 1 1.2 by immunoprecipitation with FP1 but the strongly immunoreactive 150 kDa band detected by FP1 in lysate is not detectable by either CNC1 or ACC-003.

    Article Snippet: Concordant with this idea, neither the ACC-003 antibody that we received from Alomone Labs that recognized a 130 kDa band in WT and cKO brains nor our CNC1 antibody recognized the strong 150 kDa band seen with FP1 in brain lysate.

    Techniques: Western Blot, Mouse Assay, Immunoprecipitation

    Effect of CAL on I Ca , LTCC expression and the systolic Ca transient. A: Representative L-type Ca currents (I Ca ) recorded at 0 mV from Sham (left) and CAL (right) myocytes. B: Mean (± SEM) I Ca density-voltage relations from Sham (circles, n = 50/15) and CAL (squares, n = 41/15) myocytes. C: Representative Western blots of Sham (S) and CAL lysates probed with antibodies against LTCC (top) or GAPDH (bottom). D: Representative whole-cell Ca transients from Sham (grey line) and CAL (black line) myocytes during field stimulation (left); the right panel shows the early rise on an expanded time scale. E: Mean (± SEM) peak ΔF/F 0 , time to peak (TTP), and rate of rise (ΔF/F 0 .ms − 1 ) of the Ca transient in Sham (open bars, n = 10) and CAL (filled bars, n = 16) myocytes. ⁎⁎⁎ p

    Journal: Journal of Molecular and Cellular Cardiology

    Article Title: Altered distribution of ICa impairs Ca release at the t-tubules of ventricular myocytes from failing hearts

    doi: 10.1016/j.yjmcc.2015.06.012

    Figure Lengend Snippet: Effect of CAL on I Ca , LTCC expression and the systolic Ca transient. A: Representative L-type Ca currents (I Ca ) recorded at 0 mV from Sham (left) and CAL (right) myocytes. B: Mean (± SEM) I Ca density-voltage relations from Sham (circles, n = 50/15) and CAL (squares, n = 41/15) myocytes. C: Representative Western blots of Sham (S) and CAL lysates probed with antibodies against LTCC (top) or GAPDH (bottom). D: Representative whole-cell Ca transients from Sham (grey line) and CAL (black line) myocytes during field stimulation (left); the right panel shows the early rise on an expanded time scale. E: Mean (± SEM) peak ΔF/F 0 , time to peak (TTP), and rate of rise (ΔF/F 0 .ms − 1 ) of the Ca transient in Sham (open bars, n = 10) and CAL (filled bars, n = 16) myocytes. ⁎⁎⁎ p

    Article Snippet: The blot was probed with anti-LTCC antibody (ACC-003; Alomone, Israel) or anti-GAPDH (G9545; Sigma) and protein bands visualized using relevant peroxidase-conjugated secondary antibodies, chemiluminescence, and autoradiography.

    Techniques: Expressing, Western Blot