rabbit α pcamkii thr286  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit α pcamkii thr286
    Rabbit α Pcamkii Thr286, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit α pcamkii thr286  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit α pcamkii thr286
    Rabbit α Pcamkii Thr286, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    phospho camk ii  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho camk ii
    (a) The expression of <t>CaMK</t> II and <t>related</t> <t>proteins</t> in the CaMK II signal transduction pathway in the left ventricular areas after treatment for 3 and 9 weeks were analyzed by western blotting. (b) The expression of CaMK II ( n = 5). (c) The expression of p-CaMK II (Thr-286) ( n = 5). (d) The expression of PLB ( n = 5). (e) The expression of p-PLB (Thr-17) ( n = 5). (f) The expression of RyR2 ( n = 5). (g) The expression of p-RyR2 (Ser-2814) ( n = 5). ∗ P < 0.05 and ∗∗ P < 0.01 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TAC group.
    Phospho Camk Ii, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Effects of Wenxin Keli on Cardiac Hypertrophy and Arrhythmia via Regulation of the Calcium/Calmodulin Dependent Kinase II Signaling Pathway"

    Article Title: Effects of Wenxin Keli on Cardiac Hypertrophy and Arrhythmia via Regulation of the Calcium/Calmodulin Dependent Kinase II Signaling Pathway

    Journal: BioMed Research International

    doi: 10.1155/2017/1569235

    (a) The expression of CaMK II and related proteins in the CaMK II signal transduction pathway in the left ventricular areas after treatment for 3 and 9 weeks were analyzed by western blotting. (b) The expression of CaMK II ( n = 5). (c) The expression of p-CaMK II (Thr-286) ( n = 5). (d) The expression of PLB ( n = 5). (e) The expression of p-PLB (Thr-17) ( n = 5). (f) The expression of RyR2 ( n = 5). (g) The expression of p-RyR2 (Ser-2814) ( n = 5). ∗ P < 0.05 and ∗∗ P < 0.01 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TAC group.
    Figure Legend Snippet: (a) The expression of CaMK II and related proteins in the CaMK II signal transduction pathway in the left ventricular areas after treatment for 3 and 9 weeks were analyzed by western blotting. (b) The expression of CaMK II ( n = 5). (c) The expression of p-CaMK II (Thr-286) ( n = 5). (d) The expression of PLB ( n = 5). (e) The expression of p-PLB (Thr-17) ( n = 5). (f) The expression of RyR2 ( n = 5). (g) The expression of p-RyR2 (Ser-2814) ( n = 5). ∗ P < 0.05 and ∗∗ P < 0.01 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TAC group.

    Techniques Used: Expressing, Transduction, Western Blot

    camkii phospho thr286  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc camkii phospho thr286
    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the <t>Thr286</t> autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
    Camkii Phospho Thr286, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Mu-Opioid Receptors Transiently Activate the Akt-nNOS Pathway to Produce Sustained Potentiation of PKC-Mediated NMDAR-CaMKII Signaling"

    Article Title: Mu-Opioid Receptors Transiently Activate the Akt-nNOS Pathway to Produce Sustained Potentiation of PKC-Mediated NMDAR-CaMKII Signaling

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0011278

    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the Thr286 autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
    Figure Legend Snippet: Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the Thr286 autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.

    Techniques Used: Activity Assay

    protein kinases ii camkii thr 286 antibodies  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc protein kinases ii camkii thr 286 antibodies
    Protein Kinases Ii Camkii Thr 286 Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit monoclonal anti jnk  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit monoclonal anti jnk
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    rabbit monoclonal antibody against phospho jnk thr183 thr185  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit monoclonal antibody against phospho jnk thr183 thr185
    Rabbit Monoclonal Antibody Against Phospho Jnk Thr183 Thr185, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbit polyclonal anti phospho-camkii thr286 (p-camkii)  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit polyclonal anti phospho-camkii thr286 (p-camkii)
    Rabbit Polyclonal Anti Phospho Camkii Thr286 (P Camkii), supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti phospho camkii p camkii thr286 rabbit polyclonal antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho camkii p camkii thr286 rabbit polyclonal antibody
    Effects of CTS on expression levels of p-NMDAR1, NMDAR1, <t>p-CaMKII,</t> CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . Typical photos indicating the expression levels of each factor in the cerebral cortex of vehicle-treated SAMR1 control (lane 1), vehicle-treated sham-SAMP8 (lane 2), CTS (750 mg/kg/day)-treated sham-SAMP8 (lane 3), vehicle-treated T2VO-SAMP8 (lane 4), and CTS-treated T2VO-SAMP8 group (lane 5). After completing the behavioral studies, the animals were decapitated and proteins were extracted from the cerebral cortices in each animal group.
    Anti Phospho Camkii P Camkii Thr286 Rabbit Polyclonal Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Chotosan ( Diaoteng San )-induced improvement of cognitive deficits in senescence-accelerated mouse (SAMP8) involves the amelioration of angiogenic/neurotrophic factors and neuroplasticity systems in the brain"

    Article Title: Chotosan ( Diaoteng San )-induced improvement of cognitive deficits in senescence-accelerated mouse (SAMP8) involves the amelioration of angiogenic/neurotrophic factors and neuroplasticity systems in the brain

    Journal: Chinese Medicine

    doi: 10.1186/1749-8546-6-33

    Effects of CTS on expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . Typical photos indicating the expression levels of each factor in the cerebral cortex of vehicle-treated SAMR1 control (lane 1), vehicle-treated sham-SAMP8 (lane 2), CTS (750 mg/kg/day)-treated sham-SAMP8 (lane 3), vehicle-treated T2VO-SAMP8 (lane 4), and CTS-treated T2VO-SAMP8 group (lane 5). After completing the behavioral studies, the animals were decapitated and proteins were extracted from the cerebral cortices in each animal group.
    Figure Legend Snippet: Effects of CTS on expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . Typical photos indicating the expression levels of each factor in the cerebral cortex of vehicle-treated SAMR1 control (lane 1), vehicle-treated sham-SAMP8 (lane 2), CTS (750 mg/kg/day)-treated sham-SAMP8 (lane 3), vehicle-treated T2VO-SAMP8 (lane 4), and CTS-treated T2VO-SAMP8 group (lane 5). After completing the behavioral studies, the animals were decapitated and proteins were extracted from the cerebral cortices in each animal group.

    Techniques Used: Expressing

    Quantitative comparisons of CTS-induced changes in expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . The data are expressed as the percentage of the value obtained from naïve control SAMR1 mice. Each data column represents the mean ± SD obtained from 4-5 brain samples. # P < 0.05 or ## P < 0.01 vs. compared with vehicle-treated SAMR1 group (t-test). *** P < 0.001, ** P < 0.01 vs. respective vehicle-treated sham- or T2VO-SAMP8 group (two-way ANOVA).
    Figure Legend Snippet: Quantitative comparisons of CTS-induced changes in expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . The data are expressed as the percentage of the value obtained from naïve control SAMR1 mice. Each data column represents the mean ± SD obtained from 4-5 brain samples. # P < 0.05 or ## P < 0.01 vs. compared with vehicle-treated SAMR1 group (t-test). *** P < 0.001, ** P < 0.01 vs. respective vehicle-treated sham- or T2VO-SAMP8 group (two-way ANOVA).

    Techniques Used: Expressing

    phospho camkii  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho camkii
    ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) <t>phosphorylated-CaMKII,</t> and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. <t>p-CaMKII,</t> Phosphorylated calcium/calmodulin-dependent protein kinase type II.
    Phospho Camkii, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "ANKRD22 Drives Rapid Proliferation of Lgr5 + Cells and Acts as a Promising Therapeutic Target in Gastric Mucosal Injury"

    Article Title: ANKRD22 Drives Rapid Proliferation of Lgr5 + Cells and Acts as a Promising Therapeutic Target in Gastric Mucosal Injury

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2021.06.020

    ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) phosphorylated-CaMKII, and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. p-CaMKII, Phosphorylated calcium/calmodulin-dependent protein kinase type II.
    Figure Legend Snippet: ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) phosphorylated-CaMKII, and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. p-CaMKII, Phosphorylated calcium/calmodulin-dependent protein kinase type II.

    Techniques Used: Knock-Out, Western Blot, Cell Culture, Expressing, Confocal Microscopy, Fluorescence, Inhibition, Activity Assay, Immunohistochemistry, Negative Control

    rabbit anti phospho camkii thr286 antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti phospho camkii thr286 antibody
    Rabbit Anti Phospho Camkii Thr286 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc rabbit α pcamkii thr286
    Rabbit α Pcamkii Thr286, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc phospho camk ii
    (a) The expression of <t>CaMK</t> II and <t>related</t> <t>proteins</t> in the CaMK II signal transduction pathway in the left ventricular areas after treatment for 3 and 9 weeks were analyzed by western blotting. (b) The expression of CaMK II ( n = 5). (c) The expression of p-CaMK II (Thr-286) ( n = 5). (d) The expression of PLB ( n = 5). (e) The expression of p-PLB (Thr-17) ( n = 5). (f) The expression of RyR2 ( n = 5). (g) The expression of p-RyR2 (Ser-2814) ( n = 5). ∗ P < 0.05 and ∗∗ P < 0.01 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TAC group.
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    Cell Signaling Technology Inc camkii phospho thr286
    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the <t>Thr286</t> autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
    Camkii Phospho Thr286, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the <t>Thr286</t> autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
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    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the <t>Thr286</t> autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
    Rabbit Monoclonal Anti Jnk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the <t>Thr286</t> autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
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    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the <t>Thr286</t> autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.
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    Effects of CTS on expression levels of p-NMDAR1, NMDAR1, <t>p-CaMKII,</t> CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . Typical photos indicating the expression levels of each factor in the cerebral cortex of vehicle-treated SAMR1 control (lane 1), vehicle-treated sham-SAMP8 (lane 2), CTS (750 mg/kg/day)-treated sham-SAMP8 (lane 3), vehicle-treated T2VO-SAMP8 (lane 4), and CTS-treated T2VO-SAMP8 group (lane 5). After completing the behavioral studies, the animals were decapitated and proteins were extracted from the cerebral cortices in each animal group.
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    ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) <t>phosphorylated-CaMKII,</t> and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. <t>p-CaMKII,</t> Phosphorylated calcium/calmodulin-dependent protein kinase type II.
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    ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) <t>phosphorylated-CaMKII,</t> and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. <t>p-CaMKII,</t> Phosphorylated calcium/calmodulin-dependent protein kinase type II.
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    Image Search Results


    (a) The expression of CaMK II and related proteins in the CaMK II signal transduction pathway in the left ventricular areas after treatment for 3 and 9 weeks were analyzed by western blotting. (b) The expression of CaMK II ( n = 5). (c) The expression of p-CaMK II (Thr-286) ( n = 5). (d) The expression of PLB ( n = 5). (e) The expression of p-PLB (Thr-17) ( n = 5). (f) The expression of RyR2 ( n = 5). (g) The expression of p-RyR2 (Ser-2814) ( n = 5). ∗ P < 0.05 and ∗∗ P < 0.01 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TAC group.

    Journal: BioMed Research International

    Article Title: Effects of Wenxin Keli on Cardiac Hypertrophy and Arrhythmia via Regulation of the Calcium/Calmodulin Dependent Kinase II Signaling Pathway

    doi: 10.1155/2017/1569235

    Figure Lengend Snippet: (a) The expression of CaMK II and related proteins in the CaMK II signal transduction pathway in the left ventricular areas after treatment for 3 and 9 weeks were analyzed by western blotting. (b) The expression of CaMK II ( n = 5). (c) The expression of p-CaMK II (Thr-286) ( n = 5). (d) The expression of PLB ( n = 5). (e) The expression of p-PLB (Thr-17) ( n = 5). (f) The expression of RyR2 ( n = 5). (g) The expression of p-RyR2 (Ser-2814) ( n = 5). ∗ P < 0.05 and ∗∗ P < 0.01 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TAC group.

    Article Snippet: The antibodies to the following proteins were used: CaMK II delta (1 : 1000, Abcam Corporation.), phospho-CaMK II (1 : 1000, Cell Signaling Technology Inc.), PLB (G-18) (1 : 200, Santa Cruz Biotechnology Inc.), p-phospholamban-R (1 : 200, Santa Cruz Biotechnology Inc.), and ryanodine receptor 2 (1 : 1000, Millipore Corporation.).

    Techniques: Expressing, Transduction, Western Blot

    Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the Thr286 autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.

    Journal: PLoS ONE

    Article Title: Mu-Opioid Receptors Transiently Activate the Akt-nNOS Pathway to Produce Sustained Potentiation of PKC-Mediated NMDAR-CaMKII Signaling

    doi: 10.1371/journal.pone.0011278

    Figure Lengend Snippet: Upper panel : The influence of 10 nmol icv morphine on NMDAR activity was evaluated. The levels of NMDAR1 and of NMDAR2A subunits and activating phosphorylations at NR1 Ser890 (PKC site) and NR2A Tyr1325 (Src site) were monitored in the CD1 PAG synaptosomal membranes during the post-morphine intervals indicated. The presence of the Thr286 autophosphorylation of NMDAR-activated CaMKII was also determined. Administration of LNNA or naltrindole before morphine greatly reduced NR1, NR2A and CaMKII phosphorylation. Lower panel : Naltrindole decreased Akt/PKB activating phosphorylation. Please see for further details.

    Article Snippet: Western blots were probed with affinity-purified IgG antibodies directed against: murine MOR (1∶1000 dilution) ; Gαi2, Gαz (1∶2000) ; RGS17(Z2) , ; NMDAR1 (1∶1000, Abcam ab1880); NMDAR1 phospho-Ser890 (Cell Signaling #3381); NMDAR2A (1∶1000, ab14596); NMDAR2A phospho-Y1325 (1∶300, ab16646); CaMKII (1∶3000; BD Transduction labs 611292); CaMKII phospho-Thr286 (1∶2000; Cell Signaling 3361); PKCγ (1∶1000; Abcam ab4145).

    Techniques: Activity Assay

    Effects of CTS on expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . Typical photos indicating the expression levels of each factor in the cerebral cortex of vehicle-treated SAMR1 control (lane 1), vehicle-treated sham-SAMP8 (lane 2), CTS (750 mg/kg/day)-treated sham-SAMP8 (lane 3), vehicle-treated T2VO-SAMP8 (lane 4), and CTS-treated T2VO-SAMP8 group (lane 5). After completing the behavioral studies, the animals were decapitated and proteins were extracted from the cerebral cortices in each animal group.

    Journal: Chinese Medicine

    Article Title: Chotosan ( Diaoteng San )-induced improvement of cognitive deficits in senescence-accelerated mouse (SAMP8) involves the amelioration of angiogenic/neurotrophic factors and neuroplasticity systems in the brain

    doi: 10.1186/1749-8546-6-33

    Figure Lengend Snippet: Effects of CTS on expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . Typical photos indicating the expression levels of each factor in the cerebral cortex of vehicle-treated SAMR1 control (lane 1), vehicle-treated sham-SAMP8 (lane 2), CTS (750 mg/kg/day)-treated sham-SAMP8 (lane 3), vehicle-treated T2VO-SAMP8 (lane 4), and CTS-treated T2VO-SAMP8 group (lane 5). After completing the behavioral studies, the animals were decapitated and proteins were extracted from the cerebral cortices in each animal group.

    Article Snippet: They were then probed with anti-NMDAR1 rabbit polyclonal antibody (1:1000 dilution) and anti-phospho-NMDAR1 (p-NMDAR1) (Ser896) rabbit polyclonal antibody (1:1000 dilution), anti-CaMKIIα (A-1: sc-13141) mouse monoclonal antibody (1:1000 dilution), anti-phospho-CaMKII (p-CaMKII) (Thr286) rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling Technology, USA), anti-CREB (48H2) rabbit monoclonal antibody (1:1000 dilution), anti-phospho-CREB (p-CREB) (Ser133) rabbit monoclonal antibody (1:1000 dilution), anti-BDNF (Tyr951) rabbit polyclonal antibody (1:500 dilution), anti-VEGF (A-20: sc-152) rabbit polyclonal antibody (1:1000 dilution) (Santa Cruz Biotechnology, USA), and anti-VEGFR2 (Ab-951) rabbit polyclonal antibody (1:1000 dilution) (Signalway Antibody, USA) and anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mouse monoclonal antibody (1:2000 dilution) (Chemicon, USA) at 4°C for 24 hours.

    Techniques: Expressing

    Quantitative comparisons of CTS-induced changes in expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . The data are expressed as the percentage of the value obtained from naïve control SAMR1 mice. Each data column represents the mean ± SD obtained from 4-5 brain samples. # P < 0.05 or ## P < 0.01 vs. compared with vehicle-treated SAMR1 group (t-test). *** P < 0.001, ** P < 0.01 vs. respective vehicle-treated sham- or T2VO-SAMP8 group (two-way ANOVA).

    Journal: Chinese Medicine

    Article Title: Chotosan ( Diaoteng San )-induced improvement of cognitive deficits in senescence-accelerated mouse (SAMP8) involves the amelioration of angiogenic/neurotrophic factors and neuroplasticity systems in the brain

    doi: 10.1186/1749-8546-6-33

    Figure Lengend Snippet: Quantitative comparisons of CTS-induced changes in expression levels of p-NMDAR1, NMDAR1, p-CaMKII, CaMKIIα, p-CREB, CREB, and GAPDH in the cerebral cortex of SAMP8 with and without ischemic insult . The data are expressed as the percentage of the value obtained from naïve control SAMR1 mice. Each data column represents the mean ± SD obtained from 4-5 brain samples. # P < 0.05 or ## P < 0.01 vs. compared with vehicle-treated SAMR1 group (t-test). *** P < 0.001, ** P < 0.01 vs. respective vehicle-treated sham- or T2VO-SAMP8 group (two-way ANOVA).

    Article Snippet: They were then probed with anti-NMDAR1 rabbit polyclonal antibody (1:1000 dilution) and anti-phospho-NMDAR1 (p-NMDAR1) (Ser896) rabbit polyclonal antibody (1:1000 dilution), anti-CaMKIIα (A-1: sc-13141) mouse monoclonal antibody (1:1000 dilution), anti-phospho-CaMKII (p-CaMKII) (Thr286) rabbit polyclonal antibody (1:1000 dilution) (Cell Signaling Technology, USA), anti-CREB (48H2) rabbit monoclonal antibody (1:1000 dilution), anti-phospho-CREB (p-CREB) (Ser133) rabbit monoclonal antibody (1:1000 dilution), anti-BDNF (Tyr951) rabbit polyclonal antibody (1:500 dilution), anti-VEGF (A-20: sc-152) rabbit polyclonal antibody (1:1000 dilution) (Santa Cruz Biotechnology, USA), and anti-VEGFR2 (Ab-951) rabbit polyclonal antibody (1:1000 dilution) (Signalway Antibody, USA) and anti-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mouse monoclonal antibody (1:2000 dilution) (Chemicon, USA) at 4°C for 24 hours.

    Techniques: Expressing

    ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) phosphorylated-CaMKII, and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. p-CaMKII, Phosphorylated calcium/calmodulin-dependent protein kinase type II.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: ANKRD22 Drives Rapid Proliferation of Lgr5 + Cells and Acts as a Promising Therapeutic Target in Gastric Mucosal Injury

    doi: 10.1016/j.jcmgh.2021.06.020

    Figure Lengend Snippet: ANKRD22 deletion suppresses the noncanonical Wnt-Ca 2+ pathway. ( A ) Effect of Ankrd22 knockout on the Wnt pathway in mouse gastric epithelium after mucosal injury detected by Western blot. ( B ) Effect of ANKRD22 on the Wnt pathway in cultured cells detected by Western blot. ( C ) Ankrd22 knockout reduced the intracellular Ca 2+ levels in mouse gastric epithelial cells detected by Fluo-4–based FCM. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl or saline solution (Ctrl) (n = 4). ( D ) ANKRD22 increased the intracellular Ca 2+ levels in gastric cancer cells. ( E ) Mitochondrial colocalization of the exogenous-expressing ANKRD22 in the organoid-enriched gastric cancer cells detected by confocal microscopy. ( F and G ) Ankrd22 knockout reduced the mitochondrial Ca 2+ level in mouse gastric epithelium. Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl (n = 3). Confocal microscopy was used to compare the fluorescence intensity and colocalization with mitochondria. The fluorescence intensity was detected by Rhod-2–based FCM. ( H ) Inhibition of the Wnt-Ca 2+ pathway increased the canonical Wnt pathway activity in the gastric cancer cells detected by Western blot. ( I ) Inhibition of the Wnt-Ca 2+ pathway increased the number of organoid-enriched primary mouse gastric EPCs. ( H and I ) The cells were cultured for 24 hours in medium with or without (Ctrl) 10 μmol/L FK506 or KN93. ( J–L ) Ankrd22 knockout decreased the levels of diacylglycerol (DAG) phosphorylated-CaMKII, and NFAT in the mouse gastric epithelium after mucosal injury detected by Western blot (n = 3). ( M ) Expression of NFAT1 in the Ankrd22 +/+ and Ankrd22 -/- mouse gastric epithelium after mucosal injury detected by IHC staining. Normal mouse IgG was used as a negative control (Ctrl). Ankrd22 +/+ and Ankrd22 -/- mice were subjected to subsequent detection at 24 hours after intragastric administration of EtOH/HCl. The data were analyzed by the Student t test and are presented as means ± SD. ∗ P < .05 and ∗∗ P < .01. p-CaMKII, Phosphorylated calcium/calmodulin-dependent protein kinase type II.

    Article Snippet: The following primary antibodies were used: β-tubulin (HuaBio), c-Myc (Cell Signaling Technology, Danvers, MA), AXIN2 (Cell Signaling Technology), NFAT1 (Proteintech, Wuhan, Hubei, China), NFAT2 (Cell Signaling Technology), NFAT3 (Abcam, Cambridge, UK), NFAT4 (GeneTex, Irvine, CA), diacylglycerol (LifeSpan BioSciences, Seattle, WA), phospho-CaMKII (Thr286; Cell Signaling Technology), and CaMKII (GeneTex).

    Techniques: Knock-Out, Western Blot, Cell Culture, Expressing, Confocal Microscopy, Fluorescence, Inhibition, Activity Assay, Immunohistochemistry, Negative Control