ik1  (Alomone Labs)


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    Alomone Labs ik1
    Ik1, 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/ik1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ik1 - by Bioz Stars, 2022-08
    93/100 stars

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    Alomone Labs mouse anti kca3 1
    Role of TRPV4 and <t>KCa3.1</t> in alteration of membrane potential and Ca 2+ entry in astrocytes following OGD. a–f Changes in membrane potential in response to activation of KCa3.1 channels and TRPV4 channels in astrocytes exposed to OGD 1 h. a , b 1-EBIO was added to WT astrocytes and membrane potential measured with or without OGD or HC 067047. Data are presented as means ± SEM. n = 10–20. *** p
    Mouse Anti Kca3 1, 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/mouse anti kca3 1/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mouse anti kca3 1 - by Bioz Stars, 2022-08
    93/100 stars
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    Role of TRPV4 and KCa3.1 in alteration of membrane potential and Ca 2+ entry in astrocytes following OGD. a–f Changes in membrane potential in response to activation of KCa3.1 channels and TRPV4 channels in astrocytes exposed to OGD 1 h. a , b 1-EBIO was added to WT astrocytes and membrane potential measured with or without OGD or HC 067047. Data are presented as means ± SEM. n = 10–20. *** p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: Role of TRPV4 and KCa3.1 in alteration of membrane potential and Ca 2+ entry in astrocytes following OGD. a–f Changes in membrane potential in response to activation of KCa3.1 channels and TRPV4 channels in astrocytes exposed to OGD 1 h. a , b 1-EBIO was added to WT astrocytes and membrane potential measured with or without OGD or HC 067047. Data are presented as means ± SEM. n = 10–20. *** p

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Activation Assay

    KCa3.1 and TRPV4 co-localized in primary cultured astrocytes and mouse brain cortex. Double immunofluorescence images of KCa3.1 (green) and TRPV4 (red) in normal mouse brains ( a , b ), and primary cultured astrocytes ( c , d ). Note the strong co-localization indicated by merge yellow fluorescence, quantification of the co-localization observed in experiments as shown in g. ( e ) The histograms represent the ratio of the mean Pearson correlation coefficient calculated from the co-labeling in a number of samples, as indicated above the bar. Scale bar: 25 μm

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: KCa3.1 and TRPV4 co-localized in primary cultured astrocytes and mouse brain cortex. Double immunofluorescence images of KCa3.1 (green) and TRPV4 (red) in normal mouse brains ( a , b ), and primary cultured astrocytes ( c , d ). Note the strong co-localization indicated by merge yellow fluorescence, quantification of the co-localization observed in experiments as shown in g. ( e ) The histograms represent the ratio of the mean Pearson correlation coefficient calculated from the co-labeling in a number of samples, as indicated above the bar. Scale bar: 25 μm

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Cell Culture, Immunofluorescence, Fluorescence, Labeling

    Involvement of KCa3.1 in OGD-induced reactive astrogliosis. a , b Representative western blot showing GFAP expression in cultured astrocytes treated with OGD for 4 h in the presence of 1 μM TRAM-34 and 10 μM HC 067047. Quantification of western blot for GFAP expression ( n = 3). Data are presented as means ± SEM. # p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: Involvement of KCa3.1 in OGD-induced reactive astrogliosis. a , b Representative western blot showing GFAP expression in cultured astrocytes treated with OGD for 4 h in the presence of 1 μM TRAM-34 and 10 μM HC 067047. Quantification of western blot for GFAP expression ( n = 3). Data are presented as means ± SEM. # p

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Western Blot, Expressing, Cell Culture

    Upregulation of KCa3.1 channels and GFAP in mouse brains following pMCAO. a , b Western blot analysis of lysates from 10-week-old male WT mice following 1, 3, 6, or 12 h of pMCAO analyzed by antibodies to KCa3.1 ( a ) and GFAP ( b ). Data represent the means ± SEM of KCa3.1 and GFAP density normalized to β-actin values for n = 3. * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: Upregulation of KCa3.1 channels and GFAP in mouse brains following pMCAO. a , b Western blot analysis of lysates from 10-week-old male WT mice following 1, 3, 6, or 12 h of pMCAO analyzed by antibodies to KCa3.1 ( a ) and GFAP ( b ). Data represent the means ± SEM of KCa3.1 and GFAP density normalized to β-actin values for n = 3. * p

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Western Blot, Mouse Assay

    KCa3.1 deficiency reduces infarction volume and improves of neurological conditions. Focal cerebral ischemia was induced by pMCAO. a , c , and e Representative TTC staining of five corresponding coronal brain sections of a 10-week-old male WT mouse and a 10 week-old male KCa3.1 −/− mouse after 3 h ( a ), 6 h ( c ), and 24 h ( e ) of pMCAO. b , d , and f . Quantitative analysis of infarction volume in a, c, and e, respectively. Data are presented as means ± SEM. n = 6. * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: KCa3.1 deficiency reduces infarction volume and improves of neurological conditions. Focal cerebral ischemia was induced by pMCAO. a , c , and e Representative TTC staining of five corresponding coronal brain sections of a 10-week-old male WT mouse and a 10 week-old male KCa3.1 −/− mouse after 3 h ( a ), 6 h ( c ), and 24 h ( e ) of pMCAO. b , d , and f . Quantitative analysis of infarction volume in a, c, and e, respectively. Data are presented as means ± SEM. n = 6. * p

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Staining

    Upregulation of KCa3.1, GFAP, and TRPV4 channels following OGD in cultured astrocytes. Western blot analysis of ( a ) KCa3.1, ( b ) GFAP, and ( c ) TRPV4 expression after OGD-treatment for 0, 1, 3, 4, 6, 12 h. Data represent the means ± SEM of KCa3.1, GFAP, and TRPV4 density normalized to β-actin values for n = 3 cultures. * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: Upregulation of KCa3.1, GFAP, and TRPV4 channels following OGD in cultured astrocytes. Western blot analysis of ( a ) KCa3.1, ( b ) GFAP, and ( c ) TRPV4 expression after OGD-treatment for 0, 1, 3, 4, 6, 12 h. Data represent the means ± SEM of KCa3.1, GFAP, and TRPV4 density normalized to β-actin values for n = 3 cultures. * p

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Cell Culture, Western Blot, Expressing

    Decreased glial activation and neuronal loss in brains of KCa3.1 deletion mice following pMCAO. Reactive astrocytes ( a ), activated microglia ( b ), and neurons ( c ) from the hippocampal CA1 regions of WT or KCa3.1 −/− mice at 6 h after pMCAO were visualized by GFAP, Iba1, and NeuN immunostaining, respectively. At least four coronal slices from each mouse brain and at least three brains of each genotype were used for immunostaining and counting. n = 4 per group. Scale bar: 75 μm. Data represent means ± SEM. * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 constitutes a pharmacological target for astrogliosis associated with ischemia stroke

    doi: 10.1186/s12974-017-0973-8

    Figure Lengend Snippet: Decreased glial activation and neuronal loss in brains of KCa3.1 deletion mice following pMCAO. Reactive astrocytes ( a ), activated microglia ( b ), and neurons ( c ) from the hippocampal CA1 regions of WT or KCa3.1 −/− mice at 6 h after pMCAO were visualized by GFAP, Iba1, and NeuN immunostaining, respectively. At least four coronal slices from each mouse brain and at least three brains of each genotype were used for immunostaining and counting. n = 4 per group. Scale bar: 75 μm. Data represent means ± SEM. * p

    Article Snippet: Sections and cells were incubated at 4 °C overnight with primary antibodies: mouse anti-KCa3.1 (1:100; Alomone Labs), rabbit anti-GFAP (1:500; Dako); rabbit anti-Iba1 (1:500; Abcam); rabbit anti-NeuN antibody (1:500; Millipore), rabbit anti-TRPV4 (1:200; Alomone Labs).

    Techniques: Activation Assay, Mouse Assay, Immunostaining

    AKT modulation is crucial for KCa3.1-mediated ER stress in microglia. a , b Representative blots of p-AKT and total AKT in SNpc from a WT, WT+MPTP, KCa3.1 −/− , KCa3.1 −/− +MPTP group mice and from b control, MPTP, MPTP+Se, Se group mice. Data are presented as the mean ± SEM ( n = 3–5). Western blot was repeated three times and showed similar results. The OD value of p-AKT was normalized to that of AKT. * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson’s disease

    doi: 10.1186/s12974-019-1682-2

    Figure Lengend Snippet: AKT modulation is crucial for KCa3.1-mediated ER stress in microglia. a , b Representative blots of p-AKT and total AKT in SNpc from a WT, WT+MPTP, KCa3.1 −/− , KCa3.1 −/− +MPTP group mice and from b control, MPTP, MPTP+Se, Se group mice. Data are presented as the mean ± SEM ( n = 3–5). Western blot was repeated three times and showed similar results. The OD value of p-AKT was normalized to that of AKT. * p

    Article Snippet: The blots were then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:3000; Sigma-Aldrich), rabbit anti-mTOR, rabbit anti-phospho-mTOR (Ser2448), rabbit anti-GRP78, mouse anti-CHOP, rabbit anti-phospho-Akt (Ser473), rabbit anti-phospho-Akt (Thr308), rabbit anti-Akt, rabbit anti-phospho-4E-BP1, rabbit anti-phospho-p70 S6 (1:1000; Cell Signaling Technology, Danvers, MA, USA), and mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel).

    Techniques: Mouse Assay, Western Blot

    KCa3.1 involved in microglia SOCE and ER stress. a , b Representative images of GRP78, p-PERK, and p-eIF2α in KCa3.1 −/− microglia, responses to 500 μM MPP + ( a ) or 1 μM Tg ( b ) vs. WT cells. Mean values of GRP78, p-PERK, and p-eIF2α relative to β-actin. Data are presented as the mean ± SEM ( n = 3). Western blot was repeated three times and showed similar results. * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson’s disease

    doi: 10.1186/s12974-019-1682-2

    Figure Lengend Snippet: KCa3.1 involved in microglia SOCE and ER stress. a , b Representative images of GRP78, p-PERK, and p-eIF2α in KCa3.1 −/− microglia, responses to 500 μM MPP + ( a ) or 1 μM Tg ( b ) vs. WT cells. Mean values of GRP78, p-PERK, and p-eIF2α relative to β-actin. Data are presented as the mean ± SEM ( n = 3). Western blot was repeated three times and showed similar results. * p

    Article Snippet: The blots were then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:3000; Sigma-Aldrich), rabbit anti-mTOR, rabbit anti-phospho-mTOR (Ser2448), rabbit anti-GRP78, mouse anti-CHOP, rabbit anti-phospho-Akt (Ser473), rabbit anti-phospho-Akt (Thr308), rabbit anti-Akt, rabbit anti-phospho-4E-BP1, rabbit anti-phospho-p70 S6 (1:1000; Cell Signaling Technology, Danvers, MA, USA), and mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel).

    Techniques: Western Blot

    Upregulation of KCa3.1 channels and Iba1 in the brains of PD mouse model. a Western blot analysis of SNpc lysates from control and MPTP-induced PD mouse model analyzed by antibodies to TH, GFAP, Iba1, and KCa3.1. Data represent the mean ± SEM ( n = 3). Western blot was repeated three times and showed similar results; * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson’s disease

    doi: 10.1186/s12974-019-1682-2

    Figure Lengend Snippet: Upregulation of KCa3.1 channels and Iba1 in the brains of PD mouse model. a Western blot analysis of SNpc lysates from control and MPTP-induced PD mouse model analyzed by antibodies to TH, GFAP, Iba1, and KCa3.1. Data represent the mean ± SEM ( n = 3). Western blot was repeated three times and showed similar results; * p

    Article Snippet: The blots were then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:3000; Sigma-Aldrich), rabbit anti-mTOR, rabbit anti-phospho-mTOR (Ser2448), rabbit anti-GRP78, mouse anti-CHOP, rabbit anti-phospho-Akt (Ser473), rabbit anti-phospho-Akt (Thr308), rabbit anti-Akt, rabbit anti-phospho-4E-BP1, rabbit anti-phospho-p70 S6 (1:1000; Cell Signaling Technology, Danvers, MA, USA), and mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel).

    Techniques: Western Blot

    Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuate MPTP-induced loss of DA neurons. a – g WT or KCa3.1 −/− mice received sequential intraperitoneal injections of MPTP (20 mg/kg) with or without senicapoc (100 mg/kg, once daily, p.o.) treatment for 5 days as described in the “ Material and methods ” section. Open field test ( b – e ) and the rotarod test ( f , g ) for bradykinesia were performed. Behavioral tests for MPTP-induced bradykinesia were conducted on the indicated days. Data are presented as mean ± SEM ( n = 10–15). b – e ** p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson’s disease

    doi: 10.1186/s12974-019-1682-2

    Figure Lengend Snippet: Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuate MPTP-induced loss of DA neurons. a – g WT or KCa3.1 −/− mice received sequential intraperitoneal injections of MPTP (20 mg/kg) with or without senicapoc (100 mg/kg, once daily, p.o.) treatment for 5 days as described in the “ Material and methods ” section. Open field test ( b – e ) and the rotarod test ( f , g ) for bradykinesia were performed. Behavioral tests for MPTP-induced bradykinesia were conducted on the indicated days. Data are presented as mean ± SEM ( n = 10–15). b – e ** p

    Article Snippet: The blots were then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:3000; Sigma-Aldrich), rabbit anti-mTOR, rabbit anti-phospho-mTOR (Ser2448), rabbit anti-GRP78, mouse anti-CHOP, rabbit anti-phospho-Akt (Ser473), rabbit anti-phospho-Akt (Thr308), rabbit anti-Akt, rabbit anti-phospho-4E-BP1, rabbit anti-phospho-p70 S6 (1:1000; Cell Signaling Technology, Danvers, MA, USA), and mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel).

    Techniques: Mouse Assay

    Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuated MPTP-induced ER stress. a , d Western blot analysis of GRP78 and CHOP protein levels in SNpc. b , c , e , f Data are presented as the mean ± SEM ( n = 5–6). Western blot was repeated three times and showed similar results. # p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson’s disease

    doi: 10.1186/s12974-019-1682-2

    Figure Lengend Snippet: Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuated MPTP-induced ER stress. a , d Western blot analysis of GRP78 and CHOP protein levels in SNpc. b , c , e , f Data are presented as the mean ± SEM ( n = 5–6). Western blot was repeated three times and showed similar results. # p

    Article Snippet: The blots were then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:3000; Sigma-Aldrich), rabbit anti-mTOR, rabbit anti-phospho-mTOR (Ser2448), rabbit anti-GRP78, mouse anti-CHOP, rabbit anti-phospho-Akt (Ser473), rabbit anti-phospho-Akt (Thr308), rabbit anti-Akt, rabbit anti-phospho-4E-BP1, rabbit anti-phospho-p70 S6 (1:1000; Cell Signaling Technology, Danvers, MA, USA), and mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel).

    Techniques: Western Blot

    Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuate MPTP-induced microgliosis. a , c Immunostaining for Iba1 in SNpc. Bar 50 μM. Quantitative analysis of Iba1 + cells in SNpc. Data are presented as mean ± SEM ( n = 5–8). * p

    Journal: Journal of Neuroinflammation

    Article Title: The potassium channel KCa3.1 represents a valid pharmacological target for microgliosis-induced neuronal impairment in a mouse model of Parkinson’s disease

    doi: 10.1186/s12974-019-1682-2

    Figure Lengend Snippet: Genetic KCa3.1 deletion and pharmacological blockade with senicapoc attenuate MPTP-induced microgliosis. a , c Immunostaining for Iba1 in SNpc. Bar 50 μM. Quantitative analysis of Iba1 + cells in SNpc. Data are presented as mean ± SEM ( n = 5–8). * p

    Article Snippet: The blots were then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:3000; Sigma-Aldrich), rabbit anti-mTOR, rabbit anti-phospho-mTOR (Ser2448), rabbit anti-GRP78, mouse anti-CHOP, rabbit anti-phospho-Akt (Ser473), rabbit anti-phospho-Akt (Thr308), rabbit anti-Akt, rabbit anti-phospho-4E-BP1, rabbit anti-phospho-p70 S6 (1:1000; Cell Signaling Technology, Danvers, MA, USA), and mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel).

    Techniques: Immunostaining

    Involvement of KCa3.1 in OGD-induced phenotypic modulation of astrocytes through the ERK1/2 and JNK signaling pathways. (A,C,E) Representative images of total JNK, ERK1/2, P38 and phosphorylated JNK (p-JNK), ERK1/2 (p-ERK1/2), P38 (p-P38) in WT and KO astrocytes with or without OGD (1 h). (B,D,F) Mean values of p-JNK, p-ERK1/2 and p-P38 relative to total JNK, ERK1/2 and P38 protein ( n = 3). Data are presented as means ± SEM. * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: Involvement of KCa3.1 in OGD-induced phenotypic modulation of astrocytes through the ERK1/2 and JNK signaling pathways. (A,C,E) Representative images of total JNK, ERK1/2, P38 and phosphorylated JNK (p-JNK), ERK1/2 (p-ERK1/2), P38 (p-P38) in WT and KO astrocytes with or without OGD (1 h). (B,D,F) Mean values of p-JNK, p-ERK1/2 and p-P38 relative to total JNK, ERK1/2 and P38 protein ( n = 3). Data are presented as means ± SEM. * p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques:

    Involvement of KCa3.1 in pMCAO mouse model through ERK1/2 and JNK signaling pathways. Focal cerebral ischemia was induced by pMCAO in WT and KO mice. (A–D) Western blot analysis of lysates from 10-week-old male WT and KO mice 1, 3, 6 and 24 h after pMCAO, analyzed by antibodies to phosphorylated ERK1/2 (p-ERK1/2), JNK (p-JNK), P38 (p-P38). Data represent means ± SEM of p-ERK1/2, p-JNK, p-P38 density, normalized to β-actin values ( n = 3). * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: Involvement of KCa3.1 in pMCAO mouse model through ERK1/2 and JNK signaling pathways. Focal cerebral ischemia was induced by pMCAO in WT and KO mice. (A–D) Western blot analysis of lysates from 10-week-old male WT and KO mice 1, 3, 6 and 24 h after pMCAO, analyzed by antibodies to phosphorylated ERK1/2 (p-ERK1/2), JNK (p-JNK), P38 (p-P38). Data represent means ± SEM of p-ERK1/2, p-JNK, p-P38 density, normalized to β-actin values ( n = 3). * p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: Mouse Assay, Western Blot

    KCa3.1 is involved in ER stress in vivo . Focal cerebral ischemia was induced by pMCAO in WT and KO mice. (A–C) Western blot analysis of lysates from 10-week-old male WT and KO mice 1, 3, 6 and 24 h after pMCAO, analyzed by antibodies to GFAP and GRP78. Data represent means ± SEM of GFAP and GRP78 density, normalized to β-actin values ( n = 3). * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: KCa3.1 is involved in ER stress in vivo . Focal cerebral ischemia was induced by pMCAO in WT and KO mice. (A–C) Western blot analysis of lysates from 10-week-old male WT and KO mice 1, 3, 6 and 24 h after pMCAO, analyzed by antibodies to GFAP and GRP78. Data represent means ± SEM of GFAP and GRP78 density, normalized to β-actin values ( n = 3). * p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: In Vivo, Mouse Assay, Western Blot

    Blockade of KCa3.1 attenuated OGD-induced astrogliosis and endoplasmic reticulum (ER) stress in primary astrocytes. (A) Whole-cell lysates were collected to evaluate the expression of GFAP and 78 kDa glucose-regulated protein (GRP78) in primary astrocytes by western blotting after 4 h OGD. β-Actin was used as a loading control. (B) The bar graphs represent the ratio of GFAP/β-actin and GRP78/β-actin, normalized to the control ( n = 3–4). β-Actin was used as a loading control. The data are expressed as means ± SEM. # p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: Blockade of KCa3.1 attenuated OGD-induced astrogliosis and endoplasmic reticulum (ER) stress in primary astrocytes. (A) Whole-cell lysates were collected to evaluate the expression of GFAP and 78 kDa glucose-regulated protein (GRP78) in primary astrocytes by western blotting after 4 h OGD. β-Actin was used as a loading control. (B) The bar graphs represent the ratio of GFAP/β-actin and GRP78/β-actin, normalized to the control ( n = 3–4). β-Actin was used as a loading control. The data are expressed as means ± SEM. # p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: Expressing, Western Blot

    Genetic deletion of KCa3.1 attenuated OGD-induced ER stress in primary astrocytes. (A,B) Whole-cell lysates were collected to evaluate the expression of GFAP in wildtype (WT) and KCa3.1 KO astrocytes by western blotting after 4 h OGD. β-Actin was used as a loading control. The bar graphs represent the ratio of GFAP/β-actin, normalized to the control ( n = 3–4). (C,D) Whole-cell lysates were collected to evaluate the expression of GRP78 in WT and KCa3.1 KO astrocytes by western blotting after 1 h OGD. β-Actin was used as a loading control. The bar graphs represent the ratio of GRP78/β-actin, normalized to the control ( n = 3–4). (E,F) Whole-cell lysates were collected to evaluate the expression of p-eIF-2α in WT and KCa3.1 KO astrocytes by western blotting after 4 h OGD. β-Actin was used as a loading control. The bar graphs represent the ratio of p-eIF-2α/β-actin, normalized to the control ( n = 3–4). The data are expressed as means ± SEM. ** p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: Genetic deletion of KCa3.1 attenuated OGD-induced ER stress in primary astrocytes. (A,B) Whole-cell lysates were collected to evaluate the expression of GFAP in wildtype (WT) and KCa3.1 KO astrocytes by western blotting after 4 h OGD. β-Actin was used as a loading control. The bar graphs represent the ratio of GFAP/β-actin, normalized to the control ( n = 3–4). (C,D) Whole-cell lysates were collected to evaluate the expression of GRP78 in WT and KCa3.1 KO astrocytes by western blotting after 1 h OGD. β-Actin was used as a loading control. The bar graphs represent the ratio of GRP78/β-actin, normalized to the control ( n = 3–4). (E,F) Whole-cell lysates were collected to evaluate the expression of p-eIF-2α in WT and KCa3.1 KO astrocytes by western blotting after 4 h OGD. β-Actin was used as a loading control. The bar graphs represent the ratio of p-eIF-2α/β-actin, normalized to the control ( n = 3–4). The data are expressed as means ± SEM. ** p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: Expressing, Western Blot

    KCa3.1 channel is involved in OGD-induced reduction in viability of astrocytes. Cell viability was determined using the CCK-8 assay. The values represent the fold changes of cell viability induced by OGD. Genetic deletion of the KCa3.1 channel attenuated the decrease in viability of astrocytes after 4 h OGD, compared with WT cells ( n = 5). The data are expressed as means ± SEM. ** p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: KCa3.1 channel is involved in OGD-induced reduction in viability of astrocytes. Cell viability was determined using the CCK-8 assay. The values represent the fold changes of cell viability induced by OGD. Genetic deletion of the KCa3.1 channel attenuated the decrease in viability of astrocytes after 4 h OGD, compared with WT cells ( n = 5). The data are expressed as means ± SEM. ** p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: CCK-8 Assay

    KCa3.1 deficiency reduces infarction volume. Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion (pMCAO). (A–C) Representative TTC staining of five corresponding coronal brain sections of WT and KO mouse after 3 h (A) , 6 h (B) and 24 h (C) of pMCAO. (D) Quantitative analysis of infarction volume in 3, 6 and 24 h, respectively. Data are presented as means ± SEM. n = 5. * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: KCa3.1 deficiency reduces infarction volume. Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion (pMCAO). (A–C) Representative TTC staining of five corresponding coronal brain sections of WT and KO mouse after 3 h (A) , 6 h (B) and 24 h (C) of pMCAO. (D) Quantitative analysis of infarction volume in 3, 6 and 24 h, respectively. Data are presented as means ± SEM. n = 5. * p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: Staining

    Up-regulation of KCa3.1 in OGD-induced reactive astrogliosis. Primary cultured astrocytes were subjected to OGD in vitro for different time periods, as shown. (A) Western blot analysis of astrocytic lysates following 1, 3, 4, 6 or 12 h of OGD, analyzed by antibodies to KCa3.1 and glial fibrillary acidic protein (GFAP). β-Actin was used as a loading control. (B) The bar graphs represent the fold changes of KCa3.1 and GFAP, normalized to control cells ( n = 3). The data are expressed as means ± SEM. * p

    Journal: Frontiers in Cellular Neuroscience

    Article Title: KCa3.1 Inhibition Switches the Astrocyte Phenotype during Astrogliosis Associated with Ischemic Stroke Via Endoplasmic Reticulum Stress and MAPK Signaling Pathways

    doi: 10.3389/fncel.2017.00319

    Figure Lengend Snippet: Up-regulation of KCa3.1 in OGD-induced reactive astrogliosis. Primary cultured astrocytes were subjected to OGD in vitro for different time periods, as shown. (A) Western blot analysis of astrocytic lysates following 1, 3, 4, 6 or 12 h of OGD, analyzed by antibodies to KCa3.1 and glial fibrillary acidic protein (GFAP). β-Actin was used as a loading control. (B) The bar graphs represent the fold changes of KCa3.1 and GFAP, normalized to control cells ( n = 3). The data are expressed as means ± SEM. * p

    Article Snippet: The membranes were first incubated (overnight, 4°C) with the following primary antibodies: anti-total p38/JNK/ERK/c-Jun/eIF-2α, anti-phospho-p38/JNK/ERK/c-Jun/eIF-2α antibodies (1:1000, Cell Signaling Technology, Danvers, MA, USA), anti-GRP78 antibody (1:1000, Abcam), anti-GFAP antibody (1:5000, Dako, Glostrup, Denmark), anti-KCa3.1 antibody (1:500, Alomone Labs, Jerusalem, Israel) and anti-β-actin (1:1000, Sigma).

    Techniques: Cell Culture, In Vitro, Western Blot

    AKT modulation is crucial for KCa3.1-mediated ER stress in astrocytes. a Representative blots of p-AKT and total AKT from the hippocampi of postmortem human AD patients and age-matched controls. b Data are presented as the mean ± SEM ( n = 3–5). The OD value of p-AKT was normalized to that of AKT. ** p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: AKT modulation is crucial for KCa3.1-mediated ER stress in astrocytes. a Representative blots of p-AKT and total AKT from the hippocampi of postmortem human AD patients and age-matched controls. b Data are presented as the mean ± SEM ( n = 3–5). The OD value of p-AKT was normalized to that of AKT. ** p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques:

    Elimination of KCa3.1 in APP/PS1 mice rescues spatial memory deficits in the MWM test. MWM testing of 15-month-old WT, KCa3.1 −/− , APP/PS1, and KCa3.1 −/− /APP/PS1 mice was performed as described in the “ Materials and methods ” section. a Escape latency. b Number of crossing the target quadrant by each group during the probe trials (no platform). c Percentage of swimming time spent in the target quadrant by each group during the probe trials (no platform). d Percentage of swimming distance spent in the target quadrant by each group during the probe trials (no platform). Data are presented as the mean ± SEM ( n = 10–12). # p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: Elimination of KCa3.1 in APP/PS1 mice rescues spatial memory deficits in the MWM test. MWM testing of 15-month-old WT, KCa3.1 −/− , APP/PS1, and KCa3.1 −/− /APP/PS1 mice was performed as described in the “ Materials and methods ” section. a Escape latency. b Number of crossing the target quadrant by each group during the probe trials (no platform). c Percentage of swimming time spent in the target quadrant by each group during the probe trials (no platform). d Percentage of swimming distance spent in the target quadrant by each group during the probe trials (no platform). Data are presented as the mean ± SEM ( n = 10–12). # p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques: Mouse Assay

    Neuronal loss is rescued in brains of KCa3.1 −/− /APP/PS1 mice. a Immunofluorescence analysis of NeuN levels in the hippocampi of 15-month-old WT, KCa3.1 −/− , APP/PS1, and KCa3.1 −/− /APP/PS1 mice. b Quantification of neuron number/0.01 mm 2 in the hippocampus ( n = 6). Data are presented as the mean ± SEM. * p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: Neuronal loss is rescued in brains of KCa3.1 −/− /APP/PS1 mice. a Immunofluorescence analysis of NeuN levels in the hippocampi of 15-month-old WT, KCa3.1 −/− , APP/PS1, and KCa3.1 −/− /APP/PS1 mice. b Quantification of neuron number/0.01 mm 2 in the hippocampus ( n = 6). Data are presented as the mean ± SEM. * p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques: Mouse Assay, Immunofluorescence

    Decreased neuroinflammation in brains of KCa3.1 −/− /APP/PS1 mice. a Levels of activated microglia in CA1 areas of the mouse hippocampus were analyzed by immunostaining of the microglia marker Iba1. b Quantification of activated microglia number/0.01 mm 2 in the hippocampus ( n = 3). Data are presented as the mean ± SEM. * p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: Decreased neuroinflammation in brains of KCa3.1 −/− /APP/PS1 mice. a Levels of activated microglia in CA1 areas of the mouse hippocampus were analyzed by immunostaining of the microglia marker Iba1. b Quantification of activated microglia number/0.01 mm 2 in the hippocampus ( n = 3). Data are presented as the mean ± SEM. * p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques: Mouse Assay, Immunostaining, Marker

    KCa3.1 upregulation in Aβ-induced RA and the brains of AD patients. a Primary astrocytes were stimulated with 5 μM Aβ and lysates were subjected to Western blot analysis with antibodies against KCa3.1, Orai1, and STIM1. β-actin was used to confirm equal loading. b Data are presented as the mean ± SEM ( n = 5). The OD values of KCa3.1, Orai1, and STIM1 were normalized to that of β-actin. * p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: KCa3.1 upregulation in Aβ-induced RA and the brains of AD patients. a Primary astrocytes were stimulated with 5 μM Aβ and lysates were subjected to Western blot analysis with antibodies against KCa3.1, Orai1, and STIM1. β-actin was used to confirm equal loading. b Data are presented as the mean ± SEM ( n = 5). The OD values of KCa3.1, Orai1, and STIM1 were normalized to that of β-actin. * p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques: Western Blot

    KCa3.1 contributes to increased ER stress in APP/PS1 mice. a Western blot analysis of GRP78 and CHOP protein levels in hippocampal extracts of 15-month-old WT, KCa3.1 −/− , APP/PS1, and KCa3.1 −/− /APP/PS1 mice. b , c Data are presented as the mean ± SEM ( n = 3–5). The OD values of GRP78 ( b ) and CHOP ( c ) were normalized to that of β-actin. # p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: KCa3.1 contributes to increased ER stress in APP/PS1 mice. a Western blot analysis of GRP78 and CHOP protein levels in hippocampal extracts of 15-month-old WT, KCa3.1 −/− , APP/PS1, and KCa3.1 −/− /APP/PS1 mice. b , c Data are presented as the mean ± SEM ( n = 3–5). The OD values of GRP78 ( b ) and CHOP ( c ) were normalized to that of β-actin. # p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques: Mouse Assay, Western Blot

    KCa3.1 involved in astrocytes SOCE and ER stress. a Primary cultured astrocytes were treated with 5 μM Aβ for 12 h with or without pretreatment of the KCa3.1 blocker TRAM-34 (1 μM). Fluorescence intensities of [Ca 2+ ] i are shown. Fluorescence intensity was measured in the presence of 1 μM Tg with or without 2 mM Ca 2+ . b Data are presented as the mean ± SEM ( n = 10). # p

    Journal: Journal of Neuroinflammation

    Article Title: Ca2+-dependent endoplasmic reticulum stress correlation with astrogliosis involves upregulation of KCa3.1 and inhibition of AKT/mTOR signaling

    doi: 10.1186/s12974-018-1351-x

    Figure Lengend Snippet: KCa3.1 involved in astrocytes SOCE and ER stress. a Primary cultured astrocytes were treated with 5 μM Aβ for 12 h with or without pretreatment of the KCa3.1 blocker TRAM-34 (1 μM). Fluorescence intensities of [Ca 2+ ] i are shown. Fluorescence intensity was measured in the presence of 1 μM Tg with or without 2 mM Ca 2+ . b Data are presented as the mean ± SEM ( n = 10). # p

    Article Snippet: The brain sections were then incubated with the following primary antibodies: rabbit anti-GFAP (1:1000; Dako, Glostrup, Denmark), mouse anti-GFAP (1:200; Merck Millipore, Burlington, MA, USA), rabbit anti-NeuN (1:100; Merck Millipore, Burlington, MA, USA), rabbit anti-Iba1 (1:500; Wako Pure Chemical Industries, Ltd., Osaka, Japan), mouse anti-KCa3.1 (1:100; Alomone Labs, Ltd., Jerusalem, Israel), rabbit anti-GRP78 (1:100; Cell Signaling Technology, Inc., Beverly, MA, USA), mouse anti-NG2 (Sigma-Aldrich Corporation, St. Louis, MO, USA), and rabbit anti-Orai1 (1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA).

    Techniques: Cell Culture, Fluorescence