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phosphorylated ca2 calmodulin dependent protein kinase ii  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated ca2 calmodulin dependent protein kinase ii
    Phosphorylated Ca2 Calmodulin Dependent Protein Kinase Ii, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 625 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phosphorylated+ca2+calmodulin+dependent+protein+kinase+ii/Phospho-CaMKII+(Thr286)+Rabbit+mAb/pm41750618-87-89-98
    Average 96 stars, based on 625 article reviews
    phosphorylated ca2 calmodulin dependent protein kinase ii - by Bioz Stars, 2026-10
    96/100 stars

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    Control:

    Article Title: Stigmasterol Is Associated with Alterations in nNOS-PSD95/CAPON Signaling and Synaptic Plasticity in a PTSD Model.
    Article Snippet: .. Primary antibodies employed in this study included postsynaptic density protein 95 (PSD95; mouse, 1:1000; #sc-32290, Santa Cruz Biotechnology, Dallas, TX, USA), brain-derived neurotrophic factor (BDNF; rabbit, 1:1000; #PA5-85730, Invitrogen, Waltham, MA, USA), phosphorylated extracellular signal–regulated kinase (pERK, Thr202/Tyr204; rabbit, 1:1000; #4370, Cell Signaling Technology, Danvers, MA, USA), total ERK (t-ERK; rabbit, 1:1000; #9102, Cell Signaling Technology), phosphorylated cAMP response element–binding protein (p-CREB, Ser133; rabbit, 1:1000; #ab32096, Abcam, Cambridge, UK), total CREB (t-CREB; rabbit, 1:1000; #9197, Cell Signaling Technology), neuronal nitric oxide synthase (nNOS; mouse, 1:1000; #sc-5302, Santa Cruz Biotechnology), phosphorylated Ca2+/calmodulin-dependent protein kinase II (p-CaMKII; rabbit, 1:1000; #12716, Cell Signaling Technology), total CaMKII (t-CaMKII; rabbit, 1:1000; #3357, Cell Signaling Technology), carboxy-terminal PDZ ligand of nNOS (CAPON; mouse, 1:1000; #sc-374504, Santa Cruz Biotechnology), and α-tubulin (mouse, 1:5000; #MA5-31466, Invitrogen), which served as a loading control. ..



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    Expression of calpain-1 and p-CaMKII. Expression of calpain-1 and phosphorylated CaMKII were analyzed by western blot. (A) Representative images of calpain-1, p-CaMKII, and β-actin. (3d: 3 days after last injury; 5w: 5 weeks after last injury). (B) Semiquantitative analysis of calpain-1 3 days after injury. (C) Semi quantitative analysis of calpain-1 5 weeks after injury (*p < 0.05, NC-TBI vs. NC sham; #p < 0.05, NC-TBI vs. EE-TBI). (D) Semiquantitative analysis of p-CaMKII 3 days after injury and (E) semiquantitative analysis of p-CaMKII, 5 weeks after injury, using densitometry. β-actin was used as the control. Relative expression of each molecule was compared to β-actin expression (#p < 0.05, NC-TBI vs. EE-TBI; **p < 0.01, NC-TBI vs. NC-sham). (E) There was no significant difference in p-CaMKII expression in the cortex and hippocampus between each group, 5 weeks after last injury. EE, environmental enrichment; NC, normal condition; p-CaMKII, phosphorylated <t>Ca2+/calmodulin-dependent</t> protein kinase II; TBI, repetitive mild traumatic brain injury.
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    Image Search Results


    Expression of calpain-1 and p-CaMKII. Expression of calpain-1 and phosphorylated CaMKII were analyzed by western blot. (A) Representative images of calpain-1, p-CaMKII, and β-actin. (3d: 3 days after last injury; 5w: 5 weeks after last injury). (B) Semiquantitative analysis of calpain-1 3 days after injury. (C) Semi quantitative analysis of calpain-1 5 weeks after injury (*p < 0.05, NC-TBI vs. NC sham; #p < 0.05, NC-TBI vs. EE-TBI). (D) Semiquantitative analysis of p-CaMKII 3 days after injury and (E) semiquantitative analysis of p-CaMKII, 5 weeks after injury, using densitometry. β-actin was used as the control. Relative expression of each molecule was compared to β-actin expression (#p < 0.05, NC-TBI vs. EE-TBI; **p < 0.01, NC-TBI vs. NC-sham). (E) There was no significant difference in p-CaMKII expression in the cortex and hippocampus between each group, 5 weeks after last injury. EE, environmental enrichment; NC, normal condition; p-CaMKII, phosphorylated Ca2+/calmodulin-dependent protein kinase II; TBI, repetitive mild traumatic brain injury.

    Journal: Journal of Neurotrauma

    Article Title: Environmental Enrichment Mitigates Deficits after Repetitive Mild Traumatic Brain Injury

    doi: 10.1089/neu.2016.4823

    Figure Lengend Snippet: Expression of calpain-1 and p-CaMKII. Expression of calpain-1 and phosphorylated CaMKII were analyzed by western blot. (A) Representative images of calpain-1, p-CaMKII, and β-actin. (3d: 3 days after last injury; 5w: 5 weeks after last injury). (B) Semiquantitative analysis of calpain-1 3 days after injury. (C) Semi quantitative analysis of calpain-1 5 weeks after injury (*p < 0.05, NC-TBI vs. NC sham; #p < 0.05, NC-TBI vs. EE-TBI). (D) Semiquantitative analysis of p-CaMKII 3 days after injury and (E) semiquantitative analysis of p-CaMKII, 5 weeks after injury, using densitometry. β-actin was used as the control. Relative expression of each molecule was compared to β-actin expression (#p < 0.05, NC-TBI vs. EE-TBI; **p < 0.01, NC-TBI vs. NC-sham). (E) There was no significant difference in p-CaMKII expression in the cortex and hippocampus between each group, 5 weeks after last injury. EE, environmental enrichment; NC, normal condition; p-CaMKII, phosphorylated Ca2+/calmodulin-dependent protein kinase II; TBI, repetitive mild traumatic brain injury.

    Article Snippet: After blocking, proteins were incubated overnight at 4°C with antibodies targeting proteins glutamate receptor 1 (GluR1; 1: 1000; Cell Signaling Technology, Boston, MA), phosphorylated GluR1 (p-GluR1; [s845]; 1:1000; Cell Signaling Technology), p-GluR1 (s831; 1:1000; Abcam, Cambridge, MA), β-actin (1:5000; Abcam), nuclear receptor 1 (NR1; 1:1000; Abcam), N-methyl- d -aspartate (NMDA) receptor subunit 2A (NR2A; 1:1000; Millipore, Billerica, MA), NMDA receptor subunit 2B (NR2B; 1:1000; Abcam), amyloid precursor protein (APP; 1:1000; Millipore), phosphorylated Ca 2+ /calmodulin-dependent protein kinase II (p-CaMKII; 1:2000; Cell signaling Technology), calpain-1 (1:1000; Abcam, Cambridge, UK), postsynaptic density protein 95 (PSD-95; 1:1000; Cell Signaling Technology), and sodium potassium ATPaes (Na/K-ATPase; 1:1000; Millipore).

    Techniques: Expressing, Western Blot