Glur2

Manufactured by Merck Group

GluR2 is a laboratory equipment product manufactured by Merck Group. It is a receptor protein that plays a key role in the function of the central nervous system. The core function of GluR2 is to mediate excitatory neurotransmission through the binding of the neurotransmitter glutamate.

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Lab products found in correlation

Glur1, by Merck Group (4 mentions) Flag tag (flag), by Merck Group (3 mentions) Anti psd95, by Merck Group (1 mentions) Infrared dye conjugated secondary antibody, by LI COR (1 mentions) Synaptophysin, by Merck Group (1 mentions) Secondary antibody conjugated to horseradish peroxidase, by GE Healthcare (1 mentions) Synaptotagmin 1, by Synaptic Systems (1 mentions) Syntaxin 1, by Merck Group (1 mentions) Vamp2, by Synaptic Systems (1 mentions) Na k pump, by Abcam (1 mentions) Lamp1, by Developmental Studies Hybridoma Bank (1 mentions) Snap25, by Synaptic Systems (1 mentions) Glur1, by Cell Signaling Technology (1 mentions) Dy light 660 anti rabbit secondary antibody, by Thermo Fisher Scientific (1 mentions) Fla 5100 scanner, by Fujifilm (1 mentions) Psd 95, by Thermo Fisher Scientific (1 mentions) Erk1 2, by Cell Signaling Technology (1 mentions) Odyssey fc, by LI COR (1 mentions) Phospho erk1 2, by Cell Signaling Technology (1 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (1 mentions)

Close spelling variants of this product

Anti-GluR2 (6 citations) GluR2/3 (5 citations) Mouse anti-GluR2 (3 citations) Anti-GluR2/3 (3 citations) Monoclonal mouse anti-GluR2 antibody (2 citations)

7 protocols using glur2

Generating Rabbit Polyclonal VPS35 Antibody

Cited 2 times

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Rabbit polyclonal anti-vps35 antibody was generated by using the antigen of GST–VPS35D1 fusion protein as described [14 (link), 17 (link)]. Rabbit polyclonal anti-Synapsin 1a/1b (Santa Cruz), GluR1 (Millipore), GFP (Santa Cruz) antibodies and mouse monoclonal anti-PSD95 (Millipore), GluR1 (Millipore), GluR2 (Millipore), β-actin (Upstate), Flag (Sigma), and TfR (Abcam) antibodies were used.
VPS35 mutant mice were generated by injection of mutant embryonic stem (ES) cells obtained from Bay Genomics as described previously [17 (link), 20 (link)]. All experimental procedures were approved by the Animal Subjects Committee at the Georgia Regents University, according to US National Institutes of Health guidelines.

Tian Y., Tang F.L., Sun X., Wen L., Mei L., Tang B.S, & Xiong W.C. (2015). VPS35-deficiency results in an impaired AMPA receptor trafficking and decreased dendritic spine maturation. Molecular Brain, 8, 70.

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Comprehensive Synaptic Protein Expression

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We used the following antibodies at the titer indicated: VGLUT1 (1:2000), VGLUT2 (1:1000), VGAT (1:2000), SV2 (Developmental Studies Hybridoma Bank, 1:1000), synaptophysin (Sigma, 1:2000), synaptotagmin 1 (Synaptic Systems, 1:1000), VAMP2 (Synaptic Systems, 1:1000), syntaxin 1 (Sigma, 1:1000), SNAP25 (Synaptic Systems, 1:1000), munc18 (BD Biosciences, 1:500), GluR1 (Millipore 1:1000), GluR2 (Millipore, 1:500), NR1 (BD Biosciences, 1:1000), PSD-95 (Neuromab, 1:1000), TfR (Invitrogen, 1:500), rab3 (Synaptic Systems, 1:500), rab5 (Synaptic Systems, 1:500), rab7 (Sigma, 1:500), LAMP1 (Developmental Studies Hybridoma Bank, 1:500), V-ATPase H subunit (Santa Cruz, 1:100), Na⁺/K⁺ pump (Abcam, 1:1000), α-ATP synthase (Abcam, 1:1000), GFAP (Zymed, 1:250), CPE-c term (P. Loh, at 1:500), actin (Millipore, 1:1000), FLAG (Sigma, 1:2000), voltage-gated calcium channel subunit α₁A (Synaptic Systems, 1:500), voltage-gated calcium channel subunit α₂δ-1 (Sigma, 1:1000), EAAT1 (Synaptic Systems, 1:1000) and PrPc (S. Prusiner D13, 1:1000). Infrared dye-conjugated secondary antibodies (LI-COR) were used for western blotting at 1:50,000 with the exception of the calcium channel subunit α₁A and PrPc, which required chemiluminescence detection using secondary antibody conjugated to horseradish peroxidase at 1:5000 (GE Healthcare).

Ullman J.C., Yang J., Sullivan M., Bendor J., Levy J., Pham E., Silm K., Seifikar H., Sohal V.S., Nicoll R.A, & Edwards R.H. (2018). A mouse model of autism implicates endosome pH in the regulation of presynaptic calcium entry. Nature Communications, 9, 330.

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PSD-95 Interactome Analysis in Hippocampus

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The PSD95 immunoprecipitation assay was probed with PSD-95 rabbit primary antibody (1:1000, Cell Signaling) to check for presence of PSD-95 pulled down. Equal amounts of sample were loaded to probe interaction of PSD-95 with GluR2 (Millipore), GluR1, and ILK with rabbit primary antibodies (1:1000, Cell Signaling). Whole hippocampal protein lysates were probed for BDNF or proBDNF, and GSK3β to total GSK3β, using their respective primary antibodies at 1:1000 (Cell Signaling). All blots were probed with Dy-Light 660 anti-rabbit secondary antibody (1:10000, Thermo Scientific) using a Fuji FLA 5100 scanner. They are presented as means ± SEM. Significance was determined using a two-tailed Student's t-test.

Bhattacharya D., Dunaway E.P., Bhattacharya S., Bloemer J., Buabeid M., Escobar M., Suppiramaniam V, & Dhanasekaran M. (2015). Impaired ILK Function Is Associated with Deficits in Hippocampal Based Memory and Synaptic Plasticity in a FASD Rat Model. PLoS ONE, 10(8), e0135700.

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Western Blot Analysis of Hippocampal Proteins

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Brains of mice were removed followed by dissection of the hippocampus, which were homogenized using a dounce homogenizer. Tissue extracts were sonicated and centrifuged at 1000rpm. Supernatants were collected and a BCA assay was performed to measure protein levels. Bis-Tris polyacrylamide gels (4–12%) were loaded with 15–20ug of protein. Protein was transferred to PVDF membranes overnight. Membranes were then blocked in 5% milk or 5% BSA for 1hr at room temperature. After blocking, the membranes were incubated in primary antibody overnight at 4°C. Antibodies used: phospho-ERK1/2 (Cell Signaling, 1:3000), ERK1/2 (Cell Signaling, 1:3000), PSD95 (Thermo, 1:5000), GluR1 (Millipore, 1:1000), GluR2 (Millipore, 1:1000), NR2A (Millipore, 1:1000), NR2B (Millipore, 1:1000). Blots were washed and then incubated in HRP-conjugated secondary antibodies. The blots were then washed, treated with chemiluminescent substrate and imaged on the LI-COR Odyssey Fc. Densitometry analysis was performed using Odyssey imaging software and statistically analyzed using Graphpad Prism. Densitometry values for each sample were normalized to the average of the control animals and average densitometry of CKO animals were compared to control animals using t-tests.

Vithayathil J., Pucilowska J., Friel D, & Landreth G.E. (2017). Chronic impairment of ERK signaling in glutamatergic neurons of the forebrain does not affect spatial memory retention and LTP in the same manner as acute blockade of the ERK pathway. Hippocampus, 27(12), 1239-1249.

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Characterization of APP processing in HEK293 cells

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HEK293 cells and HEK293 cells stably expressing human APP Swedish mutations (HEK293Swe) were cultured in DMEM (Hyclone) supplemented with 10% FBS (Gibco) and 1% penicillin/streptomycin (Gibco), in the absence and presence of 400 µg/mL G418 (Sigma), respectively.
Primary cortical neurons from embryonic day 17 (E17) rat pups were maintained in neurobasal medium supplemented with B27 and 0.8mM glutamine.
Antibodies used in these experiments include: NeuN (mouse mAb, Millipore), Nicastrin (mouse mAb, Abcam), Aph-1a (Invitrogen), Pen-2 (Abcam), Cleaved Notch1 (Val1744, Cell signaling), Anti-Notch1 intracellular domain antibody (rabbit pAb, Abcam), FLAG (mAb, clone M2, Sigma), GluR1 (mAb, Chemicon), GluR2 (pAb, Millipore), NR1 (mAb, BD Biosciences), α-tubulin (mAb, Sigma), β-actin (mAb, Sigma), Myc (9E10, Santa Cruz Biotechnology), Aβ (6E10, Covance); The rabbit polyclonal antibodies against PS1 loop (Thinakaran et al., 1996 (link)) and SNX27 (Balana et al., 2011 (link)) were described previously; The mouse monoclonal antibody (clone 3D5) against BACE1 was described previously (Zhao et al., 2007 (link)); The rabbit polyclonal antibody 369 against the APP C-terminus (Xu et al., 1997 (link)), Anti-Nicastrin (Ru716) and Anti-PS1 NTF antibody (Ab14) was developed in our laboratory.

Wang X., Huang T., Zhao Y., Zheng Q., Thompson R.C., Bu G., Zhang Y.W., Hong W, & Xu H. (2014). Sorting Nexin 27 Regulates Aβ Production through Modulating γ-secretase Activity. Cell reports, 9(3), 1023-1033.

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Hippocampal Protein Expression Analysis

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Western blotting was performed according to methods established in our laboratory^{46 (link)}. Hippocampus was removed and homogenized on ice with RIPA buffer (Bi Yuntian). The samples were separated by SDS-PAGE, transferred onto nitrocellulose membranes and then covered by 5% non-fat milk. After washings by Tween-TBS, the membranes were detected by primary antibodies overnight, and then by secondary antibodies conjugated to IRDyeTM (800CW) for 1 h. The visual blots were acquired from the Odyssey Infrared Imaging System (Licor biosciences, Lincoln, NE, USA). The full length blots are presented in Supplementary Information. The primary antibodies are displayed as follows: CREB (cell signaling, 1:1000), p-CREB (cell signaling, 1:1000), BDNF (SANTA CRUZ, 1:1000), GluN2A (abcam, 1:1000), GluN2B (abcam, 1:1000), GluR1 (Millipore, 1:500), GluR2 (Millipore, 1:500), PSD95 (cell signaling, 1:1000), anti-Synaptotagmin1 (abcam, 1:2000), anti-Synapsin1 (Millipore, 1:1000), PT231 (SAB, 1:500), PP1 (Millipore, 1:200), HT7 (Thermo, 1:500), β-actin (abcam, 1:1000), acetylated H3 (Millipore, 1:1000), acetylated H3K14 (Millipore, 1:1000), acetylated H3K9 (Millipore, 1:1000), Histone 3 (abcam, 1:1000).

Zhang S., Li X., Wang Z., Liu Y., Gao Y., Tan L., Liu E., Zhou Q., Xu C., Wang X., Liu G., Chen H, & Wang J.Z. (2017). Paternal spatial training enhances offspring’s cognitive performance and synaptic plasticity in wild-type but not improve memory deficit in Alzheimer’s mice. Scientific Reports, 7, 1521.

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Immunohistochemistry and Western Blot Analysis of Neuronal Markers

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Mice were perfused with 4% paraformaldehyde in PBS for 20 min and processed for histology. Immunofluorescence labeling and Western blot analysis were performed as previously described [12 (link)]. The primary antibodies used for immunohistochemistry and Western blot analysis were as follows: β-actin (Santa Cruz, sc-47778), ΔFosB (Cell signaling, #14695), SIRT2 (Millipore, 09-843), Egr1 (Cell signaling, #4153), Tuj1 (Covance, MMS-435P), GluR1 (Upstate, # 06-306), GluR2 (Millipore, AB1768-I), NR1 (Upstate, #06-311), PSD95 (abcam, ab18258), Synaptophysin (abcam, ab32127), Synapsin1 (Cell signaling, #5297), CoREST (Millipore, #07-455), and GFP (Roche Applied Sciences, 11 814 460 001).

Wang S.E., Ko S.Y., Jo S., Jo H.R., Han J., Kim Y.S, & Son H. (2019). Downregulation of SIRT2 by Chronic Stress Reduces Expression of Synaptic Plasticity-related Genes through the Upregulation of Ehmt2. Experimental Neurobiology, 28(4), 537-546.

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