Anti-CaMKII alpha antibody

• WB

Unknown

Western blot - Anti-CaMKII alpha antibody (AB87597)

All lanes:

Western blot - Anti-CaMKII alpha antibody (ab87597) at 0.1 µg/mL

All lanes:

mouse brain lysate at 35 µg

Predicted band size: 54 kDa

Observed band size: 55 kDa,65 kDa

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• WB

CiteAb

Western blot - Anti-CaMKII alpha antibody (AB87597)

CaMKII alpha western blot using anti-CaMKII alpha antibody ab87597. Publication image and figure legend from De La Rossa, A., Laporte, M. H., et al., 2022, Elife, PubMed 35188099.

ab87597 was used in this publication in western blot. This may not be the same as the application(s) guaranteed by Abcam. For a full list of applications guaranteed by Abcam for ab87597 please see the product overview.

Generation of mice with an inducible deletion of the MPC1 gene in adult glutamatergic neurons.(A) Strategies used to generate CamKIIaCreERT2-Mpc1flox/flox mice. Upon Tamoxifen injection, expression of the Cre recombinase in CamKIIα glutamatergic neurons drives deletion of the MPC1 gene. These mice are referred to as neuro-MPC1-KO or neuro-MPC1-WT when they are Cre- (1. Glutamatergic neuron; 2. Astrocytes; 3. Inhibitory neuron). (B) Immunostaining of MPC1 (red) in cortical sections from neuro-MPC1-WT and neuro-MPC1-KO mice (scale bar : 100 μm). (C) Western blot analysis of whole cortex, synaptosome lysates and heavy organelles (mainly mitochondria), obtained from brains of neuro-MPC1-WT and neuro-MPC1-KO mice using neuronal (Synaptophysin, tyrosine hydroxylase, CamKIIα) and astroglial markers (GFAP) as well as mitochondrial markers (MPC1, MPC2 and VDAC). Note that synaptosomes are enriched for CamKIIα, a marker of excitatory neurons. Quantification (right panel) shows that except for MPC1 and MPC2, the content of these markers is similar in WT and KO preparations. N = 6 independent neuro-MPC1-WT and neuro-MPC1-KO mice. Mann-Whitney test ((6) neuro-MPC1-WT vs neuro-MPC1-KO p = 0.0286, (7) neuro-MPC1-WT vs neuro-MPC1-KO p = 0.0152).Metabolic effects of MPC deletion in excitatory neurons in vitro and behavioural consequences in neuro-MPC1-WT and KO animals.(A) Profile and quantification of oxygen consumption rates (OCR) of synaptosomes purified from neuro-MPC1-WT and neuro-MPC1-KO mice. Data were obtained using the Seahorse XF analyzer. Assays were performed in the presence of pyruvate (5 mM) and glucose (5 mM) as carbon sources. Left panel : the following compounds were injected at the time indicated by vertical lines : Oligomycin, fCCP, Rotenone and Antimycin A. Right panel : quantification of basal and maximal OCR is expressed as a ratio of the WT for each condition. N = 10 independent mice for each condition. One-way ANOVA followed by Holm Sidak post hoc test (neuro-MPC1-WT vs neuro-MPC1-KO p = 0.0001). (B) 2-NBDG uptake in synaptosomes purified from neuro-MPC1-WT and neuro-MPC1-KO mice showing an increase of glucose import in neuro-MPC1-KO synaptosome compared to WT. N = 6 independent mice for each condition. Mann Whitney test (neuro-MPC1-WT vs neuro-MPC1-KO p = 0.0022). (C) Coronal sections of cortex and hippocampus P70 of neuro-MPC1-WT and neuro-MPC1-KO mice stained for apoptotic cells using TUNEL assay (TUNEL positive cells are indicated with a red arrowhead)(scale bar : 500 μm). (D) Quantification of total cell number in cortical L2/3 from neuro-MPC1-WT mice and neuro-MPC1-KO. N = 3 independent mice for each condition. Mann Whitney test (neuro-MPC1-WT vs neuro-MPC1-KO p = 0.2061). (E–J) Effect of the inducible MPC1-depletion in body weight (E), fat mass percentage (F), elevated plus maze (EPM) (G), open field (OF) (H), social preference (SP) (I) and forced swim test (FST) (J). N = 6–10 animals/group. Unpaired t test, ((E,F,I,J) neuro-MPC1-WT vs neuro-MPC1-KO p > 0.9; (G) neuro-MPC1-WT vs neuro-MPC1-KO p = 0.054; (H) neuro-MPC1-WT vs neuro-MPC1-KO, p = 0.073).

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