- PA5-14315 - Invitrogen Antibodies CAMK2A antibody

Submitted references Dyrk1a gene dosage in glutamatergic neurons has key effects in cognitive deficits observed in mouse models of MRD7 and Down syndrome.

Brault V, Nguyen TL, Flores-Gutiérrez J, Iacono G, Birling MC, Lalanne V, Meziane H, Manousopoulou A, Pavlovic G, Lindner L, Selloum M, Sorg T, Yu E, Garbis SD, Hérault Y
PLoS genetics 2021 Sep;17(9):e1009777

Changes in GABA and glutamate receptors on auditory cortical excitatory neurons in a rat model of salicylate-induced tinnitus.

Wu C, Wu X, Yi B, Cui M, Wang X, Wang Q, Wu H, Huang Z
American journal of translational research 2018;10(12):3941-3955

Correction of cognitive deficits in mouse models of Down syndrome by a pharmacological inhibitor of DYRK1A.

Nguyen TL, Duchon A, Manousopoulou A, Loaëc N, Villiers B, Pani G, Karatas M, Mechling AE, Harsan LA, Limanton E, Bazureau JP, Carreaux F, Garbis SD, Meijer L, Herault Y
Disease models & mechanisms 2018 Sep 27;11(9)

Homeostatic Changes in GABA and Glutamate Receptors on Excitatory Cortical Neurons during Sleep Deprivation and Recovery.

Del Cid-Pellitero E, Plavski A, Mainville L, Jones BE
Frontiers in systems neuroscience 2017;11:17

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Immunohistochemistry analysis of CaMKII alpha in formalin-fixed and paraffin-embedded human brain tissue. Samples were incubated with CaMKII alpha polyclonal antibody (Product # PA5-14315) which was peroxidase-conjugated to the secondary antibody, followed by DAB staining. This data demonstrates the use of this antibody for immunohistochemistry; clinical relevance has not been evaluated.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 9. Direct interaction of DYRK1A and SYN1, phosphorylation of SYN1 by DYRK1A. (A) DYRK1A and SYN1 were immunoblotted following immunoprecipitation from wt mice brain extracts. DYRK1A or SYN1 present in the starting material (Input) were recovered in the IPs. SYN1 (74 kDa) was present in the DYRK1A IP and DYRK1A (85 kDa) was detected in the SYN1 IP, suggesting that these two proteins interact directly. Positive control of the SYN1 IP was performed using an anti-CAMKII antibody. As expected, CAMKII (50 kDa) was present in the SYN1 IP. DYRK1A IP also brought down CAMKII, suggesting complexes between SYN1, CAMKII and DYRK1A. (B) Sequence of SYN1 in the vicinity of Ser551 matches with the consensus DYRK1A phosphorylation site. Based on this sequence, three peptides were synthesized and used as potential substrates: SYN1, SYN1-S551A and SYN1-S553A. (C) Kinase activity of recombinant DYRK1A towards the three different SYN1peptides. SYN1 and SYN1-S553A peptides were phosphorylated at the same level as Woodtide by recombinant DYRK1A (71.7%+-5.2%, 70.1% and 78.4%+-11.4%, respectively). No significant catalytic activity was measured with the SYN1-S551A peptide (7.9%+-1.2%).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Figure 7 GABA A Rs on CaMKIIalpha+ pyramidal cells following SD and SR. Confocal images of sections dual-immunostained for (the beta2-3 subunits of the) GABA A R (red) and CaMKIIalpha (green) in the layer V of the barrel cortex contralateral to the whisker stimulation. (A) In SC mouse, GABA A R immunostaining is apparent along portions of the plasma membrane in some CaMKIIalpha+ pyramidal cells (arrowhead). (B) In SD2 mouse, GABA A R immunostaining is apparent in high intensity along the entire plasma membrane of multiple CaMKIIalpha+ neurons (arrowheads). (C) In SD4 mouse, GABA A R immunostaining is still evident in high intensity along the entire membrane of CaMKIIalpha+ neurons (arrowheads). (D) In SR mice, GABA A R immunostaining is of relatively low intensity and apparent along portions of few CaMKIIalpha+ cells (arrowhead). Cells indicated with large arrowhead enlarged to right. Scale bars, 10 mum. Thickness, 1440 nm.

PA5-14315

Antibody data