rabbit anti mglur5  (Alomone Labs)


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    Name:
    Anti mGluR5 extracellular Antibody
    Description:
    Anti mGluR5 extracellular Antibody AGC 007 is a highly specific antibody directed against an extracelluar epitope of rat mGluR5 The antibody can be used in western blot immunohistochemistry live cell imaging and indirect live cell flow cytometry applications It has been designed to recognize mGluR5 from rat mouse and human samples
    Catalog Number:
    AGC-007
    Price:
    397.0
    Category:
    Primary Antibody
    Applications:
    Immunocytochemistry, Immunofluorescence, Immunohistochemistry, Live Cell Imaging, Western Blot
    Purity:
    Affinity purified on immobilized antigen.
    Immunogen:
    Synthetic peptide
    Size:
    25 mcl
    Antibody Type:
    Polyclonal Primary Antibodies
    Format:
    Lyophilized Powder
    Host:
    Rabbit
    Isotype:
    Rabbit IgG
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    Structured Review

    Alomone Labs rabbit anti mglur5
    Anti mGluR5 extracellular Antibody
    Anti mGluR5 extracellular Antibody AGC 007 is a highly specific antibody directed against an extracelluar epitope of rat mGluR5 The antibody can be used in western blot immunohistochemistry live cell imaging and indirect live cell flow cytometry applications It has been designed to recognize mGluR5 from rat mouse and human samples
    https://www.bioz.com/result/rabbit anti mglur5/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti mglur5 - by Bioz Stars, 2021-09
    92/100 stars

    Images

    1) Product Images from "Ablation of SNX6 leads to defects in synaptic function of CA1 pyramidal neurons and spatial memory"

    Article Title: Ablation of SNX6 leads to defects in synaptic function of CA1 pyramidal neurons and spatial memory

    Journal: eLife

    doi: 10.7554/eLife.20991

    Homer1a overexpression increases surface mGluR5 expression. This experiment serves as a control for Figure 9—figure supplement 2 and is in agreement with previous reports ( Ango et al., 2002 ). ( A ) Hippocampal neurons were co-transfected with pLL3.7.1 and EGFP-Homer1a or EGFP construct on DIV13, and fixed on DIV18. Surface mGluR5 expressions were immunostained with antibodies to mGluR5. ( B ) Quantification of surface mGluR5 signal in ( A ) (mean ± SEM, n = 30 cells, N = 3). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.035
    Figure Legend Snippet: Homer1a overexpression increases surface mGluR5 expression. This experiment serves as a control for Figure 9—figure supplement 2 and is in agreement with previous reports ( Ango et al., 2002 ). ( A ) Hippocampal neurons were co-transfected with pLL3.7.1 and EGFP-Homer1a or EGFP construct on DIV13, and fixed on DIV18. Surface mGluR5 expressions were immunostained with antibodies to mGluR5. ( B ) Quantification of surface mGluR5 signal in ( A ) (mean ± SEM, n = 30 cells, N = 3). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.035

    Techniques Used: Over Expression, Expressing, Transfection, Construct

    Ablation of SNX6 causes an increase in surface expression of mGluR5 in hippocampal neurons, which is rescued by SNX6 or Homer1c. ( A ) DIV13 neurons were transfected with constructs expressing DsRed and EGFP, EGFP-SNX6, mEmerald-Homer1c-FL or EGFP-Homer1c-C, fixed on DIV18 and immunostained with antibodies to surface-expressed mGluR5. ( B ) Quantification of surface mGluR5 fluorescence intensity per μm 2 (mean ± SEM, n = 30, N = 3, the exact p values are indicated in the bar graph). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.034
    Figure Legend Snippet: Ablation of SNX6 causes an increase in surface expression of mGluR5 in hippocampal neurons, which is rescued by SNX6 or Homer1c. ( A ) DIV13 neurons were transfected with constructs expressing DsRed and EGFP, EGFP-SNX6, mEmerald-Homer1c-FL or EGFP-Homer1c-C, fixed on DIV18 and immunostained with antibodies to surface-expressed mGluR5. ( B ) Quantification of surface mGluR5 fluorescence intensity per μm 2 (mean ± SEM, n = 30, N = 3, the exact p values are indicated in the bar graph). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.034

    Techniques Used: Expressing, Transfection, Construct, Fluorescence

    2) Product Images from "Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours"

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    Journal: Nature biomedical engineering

    doi: 10.1038/s41551-018-0252-8

    mGluR5–CRISPR successfully promotes mGluR5 gene editing in the striatum of wild-type and Fmr1 knockout mice. a , Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b , RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., *** P
    Figure Legend Snippet: mGluR5–CRISPR successfully promotes mGluR5 gene editing in the striatum of wild-type and Fmr1 knockout mice. a , Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b , RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., *** P

    Techniques Used: CRISPR, Knock-Out, Mouse Assay, Injection, Amplification, Quantitative RT-PCR

    Knocking out mGluR5 using mGluR5–CRISPR significantly rescues the increased repetitive behaviours in Fmr1 knockout mice. a–c , Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay ( a ) or the empty cage observation test ( b , c ) was performed. a , Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping ( b ) and line crossing behaviours ( c ) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., * P
    Figure Legend Snippet: Knocking out mGluR5 using mGluR5–CRISPR significantly rescues the increased repetitive behaviours in Fmr1 knockout mice. a–c , Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay ( a ) or the empty cage observation test ( b , c ) was performed. a , Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping ( b ) and line crossing behaviours ( c ) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., * P

    Techniques Used: CRISPR, Knock-Out, Mouse Assay, Injection

    Related Articles

    Immunostaining:

    Article Title: Receptor-selective diffusion barrier enhances sensitivity of astrocytic processes to metabotropic glutamate receptor stimulation.
    Article Snippet: .. Metabotropic glutamate receptor (mGluR)-dependent calcium ion (Ca²+) signaling in astrocytic processes regulates synaptic transmission and local blood flow essential for brain function.. However, because of difficulties in imaging astrocytic processes, the subcellular spatial organization of mGluR-dependent Ca²+ signaling is not well characterized and its regulatory mechanism remains unclear. ..

    Incubation:

    Article Title: Receptor-selective diffusion barrier enhances sensitivity of astrocytic processes to metabotropic glutamate receptor stimulation.
    Article Snippet: .. Metabotropic glutamate receptor (mGluR)-dependent calcium ion (Ca²+) signaling in astrocytic processes regulates synaptic transmission and local blood flow essential for brain function.. However, because of difficulties in imaging astrocytic processes, the subcellular spatial organization of mGluR-dependent Ca²+ signaling is not well characterized and its regulatory mechanism remains unclear. ..

    Article Title: Abnormal mGluR-mediated synaptic plasticity and autism-like behaviours in Gprasp2 mutant mice
    Article Snippet: .. Neurons were fixed and incubated o.n. with the mGluR5 intracellular N-terminus antibody (AGC-007, 1:100, Alomone Labs). ..

    Blocking Assay:

    Article Title: Receptor-selective diffusion barrier enhances sensitivity of astrocytic processes to metabotropic glutamate receptor stimulation.
    Article Snippet: .. Metabotropic glutamate receptor (mGluR)-dependent calcium ion (Ca²+) signaling in astrocytic processes regulates synaptic transmission and local blood flow essential for brain function.. However, because of difficulties in imaging astrocytic processes, the subcellular spatial organization of mGluR-dependent Ca²+ signaling is not well characterized and its regulatory mechanism remains unclear. ..

    other:

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours
    Article Snippet: The mouse monoclonal RFP antibody (6G6) was purchased from ChromoTek, the chicken polyclonal GFP antibody (GFP-1020) from Aves Labs (Tigard), the rabbit polyclonal GFAP antibody (AB5804) and the mouse monoclonal NeuN antibody (MAB377) from Millipore, the rabbit polyclonal IBA1 antibody (019–19741) from Wako Chemicals, and the rabbit polyclonal mGluR5 antibody (AGC-007) was from Alomone Labs.

    Article Title: Ablation of SNX6 leads to defects in synaptic function of CA1 pyramidal neurons and spatial memory
    Article Snippet: Antibodies Antibodies used in this study are: mouse anti-GluA1 (MAB2263), mouse anti-GluA2 (MAB397), mouse anti-Tau1 (MAB3420), and mouse anti-MAP2 (MAB3418) from Millipore (Billerica, MA); mouse anti-SYP (D-4) (sc-17750), mouse anti-PSD95 (6G6) (sc-32291), mouse anti-DIC (74-1) (sc-13524), goat anti-Homer1a (M-13) (sc-8922), rabbit anti-Homer1b/c (H-174) (sc-20807), mouse anti-SNX6 (D-5) (sc-365965), goat anti-SNX6 (N-19) (sc-8679), and rabbit anti-Rab5B (A-20) (sc-598) from Santa Cruz Biotechnology (Santa Cruz, CA); mouse anti-p150Glued (610474), mouse anti-EEA1 (610457) from BD Biosciences (San Diego, CA); rabbit anti-clathrin (ab21679), rabbit anti-TGN46 (ab50595), rat anti-CTIP2 (ab18465), rabbit anti-SNX1 (ab134126) and rabbit anti-Rab4 (ab109009) from Abcam; rabbit anti-GluN1 (D65B7) from Cell Signaling Technology (Mississauga, ON, Canada); rabbit anti-GluN2B (AGC-003) and rabbit anti-mGluR5 (AGC-007) from Alomone labs (Jerusalem, Israel); rabbit and mouse anti-GFP (MBL598, D153-3), rabbit and mouse anti-RFP (PM005, M155-3) from Medical and Biological Laboratories (Naka-kuNagoya, Japan); mouse anti-β-actin (A5441) (Sigma-Aldrich, St. Louis, MO); mouse anti-Golgi97 (A21270) from Invitrogen (Carlsbad, CA); goat anti-VPS35 (PAB7499) from Abnova (Taipei, Taiwan) and rabbit anti-GluN2A (612–401-D89) from Rockland Immunochemicals (Limerick, PA); rabbit anti-Rab7 (#9367) from Cell Signaling Technology (Mississauga, ON, Canada); rabbit anti-Rab11 (3H18L, 700184) from Life Technologies (Carlsbad, CA); Rabbit anti-SNX6 was described previously ( ).

    Staining:

    Article Title: Sapap3 deletion anomalously activates short-term endocannabinoid-mediated synaptic plasticity
    Article Snippet: .. Cultures were stained with anti-mGluR5 N-terminus rabbit polyclonal antibodies (1:50, Alomone Labs AGC-007) overnight at 4°C. ..

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  • 92
    Alomone Labs rabbit anti mglur5
    Homer1a overexpression increases surface <t>mGluR5</t> expression. This experiment serves as a control for Figure 9—figure supplement 2 and is in agreement with previous reports ( Ango et al., 2002 ). ( A ) Hippocampal neurons were co-transfected with pLL3.7.1 and EGFP-Homer1a or EGFP construct on DIV13, and fixed on DIV18. Surface mGluR5 expressions were immunostained with antibodies to mGluR5. ( B ) Quantification of surface mGluR5 signal in ( A ) (mean ± SEM, n = 30 cells, N = 3). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.035
    Rabbit Anti Mglur5, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti mglur5/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti mglur5 - by Bioz Stars, 2021-09
    92/100 stars
      Buy from Supplier

    Image Search Results


    Homer1a overexpression increases surface mGluR5 expression. This experiment serves as a control for Figure 9—figure supplement 2 and is in agreement with previous reports ( Ango et al., 2002 ). ( A ) Hippocampal neurons were co-transfected with pLL3.7.1 and EGFP-Homer1a or EGFP construct on DIV13, and fixed on DIV18. Surface mGluR5 expressions were immunostained with antibodies to mGluR5. ( B ) Quantification of surface mGluR5 signal in ( A ) (mean ± SEM, n = 30 cells, N = 3). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.035

    Journal: eLife

    Article Title: Ablation of SNX6 leads to defects in synaptic function of CA1 pyramidal neurons and spatial memory

    doi: 10.7554/eLife.20991

    Figure Lengend Snippet: Homer1a overexpression increases surface mGluR5 expression. This experiment serves as a control for Figure 9—figure supplement 2 and is in agreement with previous reports ( Ango et al., 2002 ). ( A ) Hippocampal neurons were co-transfected with pLL3.7.1 and EGFP-Homer1a or EGFP construct on DIV13, and fixed on DIV18. Surface mGluR5 expressions were immunostained with antibodies to mGluR5. ( B ) Quantification of surface mGluR5 signal in ( A ) (mean ± SEM, n = 30 cells, N = 3). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.035

    Article Snippet: Antibodies Antibodies used in this study are: mouse anti-GluA1 (MAB2263), mouse anti-GluA2 (MAB397), mouse anti-Tau1 (MAB3420), and mouse anti-MAP2 (MAB3418) from Millipore (Billerica, MA); mouse anti-SYP (D-4) (sc-17750), mouse anti-PSD95 (6G6) (sc-32291), mouse anti-DIC (74-1) (sc-13524), goat anti-Homer1a (M-13) (sc-8922), rabbit anti-Homer1b/c (H-174) (sc-20807), mouse anti-SNX6 (D-5) (sc-365965), goat anti-SNX6 (N-19) (sc-8679), and rabbit anti-Rab5B (A-20) (sc-598) from Santa Cruz Biotechnology (Santa Cruz, CA); mouse anti-p150Glued (610474), mouse anti-EEA1 (610457) from BD Biosciences (San Diego, CA); rabbit anti-clathrin (ab21679), rabbit anti-TGN46 (ab50595), rat anti-CTIP2 (ab18465), rabbit anti-SNX1 (ab134126) and rabbit anti-Rab4 (ab109009) from Abcam; rabbit anti-GluN1 (D65B7) from Cell Signaling Technology (Mississauga, ON, Canada); rabbit anti-GluN2B (AGC-003) and rabbit anti-mGluR5 (AGC-007) from Alomone labs (Jerusalem, Israel); rabbit and mouse anti-GFP (MBL598, D153-3), rabbit and mouse anti-RFP (PM005, M155-3) from Medical and Biological Laboratories (Naka-kuNagoya, Japan); mouse anti-β-actin (A5441) (Sigma-Aldrich, St. Louis, MO); mouse anti-Golgi97 (A21270) from Invitrogen (Carlsbad, CA); goat anti-VPS35 (PAB7499) from Abnova (Taipei, Taiwan) and rabbit anti-GluN2A (612–401-D89) from Rockland Immunochemicals (Limerick, PA); rabbit anti-Rab7 (#9367) from Cell Signaling Technology (Mississauga, ON, Canada); rabbit anti-Rab11 (3H18L, 700184) from Life Technologies (Carlsbad, CA); Rabbit anti-SNX6 was described previously ( ).

    Techniques: Over Expression, Expressing, Transfection, Construct

    Ablation of SNX6 causes an increase in surface expression of mGluR5 in hippocampal neurons, which is rescued by SNX6 or Homer1c. ( A ) DIV13 neurons were transfected with constructs expressing DsRed and EGFP, EGFP-SNX6, mEmerald-Homer1c-FL or EGFP-Homer1c-C, fixed on DIV18 and immunostained with antibodies to surface-expressed mGluR5. ( B ) Quantification of surface mGluR5 fluorescence intensity per μm 2 (mean ± SEM, n = 30, N = 3, the exact p values are indicated in the bar graph). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.034

    Journal: eLife

    Article Title: Ablation of SNX6 leads to defects in synaptic function of CA1 pyramidal neurons and spatial memory

    doi: 10.7554/eLife.20991

    Figure Lengend Snippet: Ablation of SNX6 causes an increase in surface expression of mGluR5 in hippocampal neurons, which is rescued by SNX6 or Homer1c. ( A ) DIV13 neurons were transfected with constructs expressing DsRed and EGFP, EGFP-SNX6, mEmerald-Homer1c-FL or EGFP-Homer1c-C, fixed on DIV18 and immunostained with antibodies to surface-expressed mGluR5. ( B ) Quantification of surface mGluR5 fluorescence intensity per μm 2 (mean ± SEM, n = 30, N = 3, the exact p values are indicated in the bar graph). Bar: 2 μm. DOI: http://dx.doi.org/10.7554/eLife.20991.034

    Article Snippet: Antibodies Antibodies used in this study are: mouse anti-GluA1 (MAB2263), mouse anti-GluA2 (MAB397), mouse anti-Tau1 (MAB3420), and mouse anti-MAP2 (MAB3418) from Millipore (Billerica, MA); mouse anti-SYP (D-4) (sc-17750), mouse anti-PSD95 (6G6) (sc-32291), mouse anti-DIC (74-1) (sc-13524), goat anti-Homer1a (M-13) (sc-8922), rabbit anti-Homer1b/c (H-174) (sc-20807), mouse anti-SNX6 (D-5) (sc-365965), goat anti-SNX6 (N-19) (sc-8679), and rabbit anti-Rab5B (A-20) (sc-598) from Santa Cruz Biotechnology (Santa Cruz, CA); mouse anti-p150Glued (610474), mouse anti-EEA1 (610457) from BD Biosciences (San Diego, CA); rabbit anti-clathrin (ab21679), rabbit anti-TGN46 (ab50595), rat anti-CTIP2 (ab18465), rabbit anti-SNX1 (ab134126) and rabbit anti-Rab4 (ab109009) from Abcam; rabbit anti-GluN1 (D65B7) from Cell Signaling Technology (Mississauga, ON, Canada); rabbit anti-GluN2B (AGC-003) and rabbit anti-mGluR5 (AGC-007) from Alomone labs (Jerusalem, Israel); rabbit and mouse anti-GFP (MBL598, D153-3), rabbit and mouse anti-RFP (PM005, M155-3) from Medical and Biological Laboratories (Naka-kuNagoya, Japan); mouse anti-β-actin (A5441) (Sigma-Aldrich, St. Louis, MO); mouse anti-Golgi97 (A21270) from Invitrogen (Carlsbad, CA); goat anti-VPS35 (PAB7499) from Abnova (Taipei, Taiwan) and rabbit anti-GluN2A (612–401-D89) from Rockland Immunochemicals (Limerick, PA); rabbit anti-Rab7 (#9367) from Cell Signaling Technology (Mississauga, ON, Canada); rabbit anti-Rab11 (3H18L, 700184) from Life Technologies (Carlsbad, CA); Rabbit anti-SNX6 was described previously ( ).

    Techniques: Expressing, Transfection, Construct, Fluorescence

    mGluR5–CRISPR successfully promotes mGluR5 gene editing in the striatum of wild-type and Fmr1 knockout mice. a , Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b , RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., *** P

    Journal: Nature biomedical engineering

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    doi: 10.1038/s41551-018-0252-8

    Figure Lengend Snippet: mGluR5–CRISPR successfully promotes mGluR5 gene editing in the striatum of wild-type and Fmr1 knockout mice. a , Upper: schematic of the injection process for mGluR5–CRISPR into the striatum of wild-type (WT) and Fmr1 knockout (KO) mice. Saline or mGluR5–CRISPR was injected into the striatum (Bregma: 0.26 mm, 3 injection sites per hemisphere are indicated as blue dots, 0.4-mm interval) of WT or Fmr1 KO mice. Lower: schematic of the target sequences of Cas9 RNPs and the protospacer adjacent motif (PAM) for Grm5 knockout. b , RNA was extracted from the saline-injected control side (control) or from the mGluR5–CRISPR-injected side (mGluR5–CRISPR) of WT or Fmr1 KO mice 11 weeks after stereotaxic injections. mRNA levels of Grm5 were amplified and analysed by RT-qPCR. Fold-change of Grm5 mRNA levels are shown after normalization against PPIA mRNA levels. n = 4–6, mean ± s.e.m., *** P

    Article Snippet: The mouse monoclonal RFP antibody (6G6) was purchased from ChromoTek, the chicken polyclonal GFP antibody (GFP-1020) from Aves Labs (Tigard), the rabbit polyclonal GFAP antibody (AB5804) and the mouse monoclonal NeuN antibody (MAB377) from Millipore, the rabbit polyclonal IBA1 antibody (019–19741) from Wako Chemicals, and the rabbit polyclonal mGluR5 antibody (AGC-007) was from Alomone Labs.

    Techniques: CRISPR, Knock-Out, Mouse Assay, Injection, Amplification, Quantitative RT-PCR

    Knocking out mGluR5 using mGluR5–CRISPR significantly rescues the increased repetitive behaviours in Fmr1 knockout mice. a–c , Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay ( a ) or the empty cage observation test ( b , c ) was performed. a , Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping ( b ) and line crossing behaviours ( c ) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., * P

    Journal: Nature biomedical engineering

    Article Title: Nanoparticle delivery of CRISPR into the brain rescues a mouse model of fragile X syndrome from exaggerated repetitive behaviours

    doi: 10.1038/s41551-018-0252-8

    Figure Lengend Snippet: Knocking out mGluR5 using mGluR5–CRISPR significantly rescues the increased repetitive behaviours in Fmr1 knockout mice. a–c , Three weeks after stereotaxic injection of either saline (control) or mGluR5–CRISPR into the striatum of WT and Fmr1 KO mice, the marble-burying assay ( a ) or the empty cage observation test ( b , c ) was performed. a , Left: percentage of marbles buried after 30 min of the marble-burying test. Right: representative images after marble-burying assay for 30 min. Jumping ( b ) and line crossing behaviours ( c ) were scored during 10 min of an empty cage observation test. n = 10–12 for each group, mean ± s.e.m., * P

    Article Snippet: The mouse monoclonal RFP antibody (6G6) was purchased from ChromoTek, the chicken polyclonal GFP antibody (GFP-1020) from Aves Labs (Tigard), the rabbit polyclonal GFAP antibody (AB5804) and the mouse monoclonal NeuN antibody (MAB377) from Millipore, the rabbit polyclonal IBA1 antibody (019–19741) from Wako Chemicals, and the rabbit polyclonal mGluR5 antibody (AGC-007) was from Alomone Labs.

    Techniques: CRISPR, Knock-Out, Mouse Assay, Injection