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mglur i agonist dhpg  (MedChemExpress)


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    Structured Review

    MedChemExpress mglur i agonist dhpg
    Mglur I Agonist Dhpg, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mglur i agonist dhpg/product/MedChemExpress
    Average 93 stars, based on 4 article reviews
    mglur i agonist dhpg - by Bioz Stars, 2026-02
    93/100 stars

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    (A–D). QMI maps showing network biosignatures for A. 100 μM glutamate, B. 1μM glutamate, C. <t>100μM</t> NMDA+10μm Glycine, D. 100μm <t>DHPG</t> for N=4–8 biological replicates. (E) Principal component analysis showing separation of NMDA <t>and</t> <t>mGluR</t> treatment along opposing axes, with glutamate intermediate. (F) Topological overlap matrix with significant modules boxed as in Figure 4. (G) Module-trait matrix showing Turquoise module correlated with NMDA stimulation, and the Brown module correlated with DHPG.
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    (A–D). QMI maps showing network biosignatures for A. 100 μM glutamate, B. 1μM glutamate, C. <t>100μM</t> NMDA+10μm Glycine, D. 100μm <t>DHPG</t> for N=4–8 biological replicates. (E) Principal component analysis showing separation of NMDA <t>and</t> <t>mGluR</t> treatment along opposing axes, with glutamate intermediate. (F) Topological overlap matrix with significant modules boxed as in Figure 4. (G) Module-trait matrix showing Turquoise module correlated with NMDA stimulation, and the Brown module correlated with DHPG.
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    (A–D). QMI maps showing network biosignatures for A. 100 μM glutamate, B. 1μM glutamate, C. <t>100μM</t> NMDA+10μm Glycine, D. 100μm <t>DHPG</t> for N=4–8 biological replicates. (E) Principal component analysis showing separation of NMDA <t>and</t> <t>mGluR</t> treatment along opposing axes, with glutamate intermediate. (F) Topological overlap matrix with significant modules boxed as in Figure 4. (G) Module-trait matrix showing Turquoise module correlated with NMDA stimulation, and the Brown module correlated with DHPG.
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    (A–D). QMI maps showing network biosignatures for A. 100 μM glutamate, B. 1μM glutamate, C. <t>100μM</t> NMDA+10μm Glycine, D. 100μm <t>DHPG</t> for N=4–8 biological replicates. (E) Principal component analysis showing separation of NMDA <t>and</t> <t>mGluR</t> treatment along opposing axes, with glutamate intermediate. (F) Topological overlap matrix with significant modules boxed as in Figure 4. (G) Module-trait matrix showing Turquoise module correlated with NMDA stimulation, and the Brown module correlated with DHPG.
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    Tocris s)-3,5,-dhpg (mglur i agonist
    Released glutamate from PSMA-processed glutamate folate activates mGluR I and up-regulates cytoplasmic calcium levels. (A) PSMA activates Akt in a p110b-dependent fashion, using glutamate as the molecular messenger. PC3-Ctrl cells grown on 96-well plates were supplemented with Glu-Fol, recombinant PSMA, and inhibitors for 2 h. The change in 700-nm fluorescence intensity emission of the Akt-specific substrate LS456 was calculated based on unstimulated cells ( n = 12 per treatment). (B) The released glutamate by PSMA engages mGluR I, mobilizing calcium to the cytoplasm. PC3-Ctrl cells were incubated in basal medium deprived of serum, folate, and glutamate for 4 h at 37°C, 5% CO 2 (mGluR I agonist: ( S <t>)-3,5,-DHPG;</t> n = 8 per condition). Detection was achieved with the Fluo-4 Direct calcium kit. (C) Intracellular calcium levels upon stimulation of cells expressing wild-type (PSMA wt ) and enzymatically inactive PSMA (PSMA mut ). Changes in [Ca 2+ ] were calculated with respect to nonstimulated PC3-PSMA wt or PC3-PSMA mut cells grown in basal RPMI medium, as mentioned above for panel B of this figure (mGluR I agonist: ( S )-3,5,-DHPG; n = 8 per condition). Graphs show mean ± SEM. *, P < 0.05, ***, P < 0.001; ****, P < 0.0001 (ordinary one-way ANOVA).
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    Image Search Results


    (A–D). QMI maps showing network biosignatures for A. 100 μM glutamate, B. 1μM glutamate, C. 100μM NMDA+10μm Glycine, D. 100μm DHPG for N=4–8 biological replicates. (E) Principal component analysis showing separation of NMDA and mGluR treatment along opposing axes, with glutamate intermediate. (F) Topological overlap matrix with significant modules boxed as in Figure 4. (G) Module-trait matrix showing Turquoise module correlated with NMDA stimulation, and the Brown module correlated with DHPG.

    Journal: Journal of neurochemistry

    Article Title: Synaptic activity induces input-specific rearrangements in a targeted synaptic protein interaction network

    doi: 10.1111/jnc.14466

    Figure Lengend Snippet: (A–D). QMI maps showing network biosignatures for A. 100 μM glutamate, B. 1μM glutamate, C. 100μM NMDA+10μm Glycine, D. 100μm DHPG for N=4–8 biological replicates. (E) Principal component analysis showing separation of NMDA and mGluR treatment along opposing axes, with glutamate intermediate. (F) Topological overlap matrix with significant modules boxed as in Figure 4. (G) Module-trait matrix showing Turquoise module correlated with NMDA stimulation, and the Brown module correlated with DHPG.

    Article Snippet: Type I mGluR agonist DHPG (Tocris, 0805; 100μM) was dissolved in HEPES-aCSF in the presence of non-mGluR glutamate receptor blockers (CNQX, Tocris, 0190, 40μM; Nimodipine, Tocris, 0600, 1μM; APV, Sigma, A5282, 50μM).

    Techniques:

    Released glutamate from PSMA-processed glutamate folate activates mGluR I and up-regulates cytoplasmic calcium levels. (A) PSMA activates Akt in a p110b-dependent fashion, using glutamate as the molecular messenger. PC3-Ctrl cells grown on 96-well plates were supplemented with Glu-Fol, recombinant PSMA, and inhibitors for 2 h. The change in 700-nm fluorescence intensity emission of the Akt-specific substrate LS456 was calculated based on unstimulated cells ( n = 12 per treatment). (B) The released glutamate by PSMA engages mGluR I, mobilizing calcium to the cytoplasm. PC3-Ctrl cells were incubated in basal medium deprived of serum, folate, and glutamate for 4 h at 37°C, 5% CO 2 (mGluR I agonist: ( S )-3,5,-DHPG; n = 8 per condition). Detection was achieved with the Fluo-4 Direct calcium kit. (C) Intracellular calcium levels upon stimulation of cells expressing wild-type (PSMA wt ) and enzymatically inactive PSMA (PSMA mut ). Changes in [Ca 2+ ] were calculated with respect to nonstimulated PC3-PSMA wt or PC3-PSMA mut cells grown in basal RPMI medium, as mentioned above for panel B of this figure (mGluR I agonist: ( S )-3,5,-DHPG; n = 8 per condition). Graphs show mean ± SEM. *, P < 0.05, ***, P < 0.001; ****, P < 0.0001 (ordinary one-way ANOVA).

    Journal: The Journal of Experimental Medicine

    Article Title: Prostate-specific membrane antigen cleavage of vitamin B9 stimulates oncogenic signaling through metabotropic glutamate receptors

    doi: 10.1084/jem.20171052

    Figure Lengend Snippet: Released glutamate from PSMA-processed glutamate folate activates mGluR I and up-regulates cytoplasmic calcium levels. (A) PSMA activates Akt in a p110b-dependent fashion, using glutamate as the molecular messenger. PC3-Ctrl cells grown on 96-well plates were supplemented with Glu-Fol, recombinant PSMA, and inhibitors for 2 h. The change in 700-nm fluorescence intensity emission of the Akt-specific substrate LS456 was calculated based on unstimulated cells ( n = 12 per treatment). (B) The released glutamate by PSMA engages mGluR I, mobilizing calcium to the cytoplasm. PC3-Ctrl cells were incubated in basal medium deprived of serum, folate, and glutamate for 4 h at 37°C, 5% CO 2 (mGluR I agonist: ( S )-3,5,-DHPG; n = 8 per condition). Detection was achieved with the Fluo-4 Direct calcium kit. (C) Intracellular calcium levels upon stimulation of cells expressing wild-type (PSMA wt ) and enzymatically inactive PSMA (PSMA mut ). Changes in [Ca 2+ ] were calculated with respect to nonstimulated PC3-PSMA wt or PC3-PSMA mut cells grown in basal RPMI medium, as mentioned above for panel B of this figure (mGluR I agonist: ( S )-3,5,-DHPG; n = 8 per condition). Graphs show mean ± SEM. *, P < 0.05, ***, P < 0.001; ****, P < 0.0001 (ordinary one-way ANOVA).

    Article Snippet: The following chemicals were acquired from Tocris: 2-PMPA (PSMA inhibitor), ( S )-3,5,-DHPG (mGluR I agonist), l -quisqualic acid (mGluR I agonist), L-AP3 (mGluR I antagonist), U73122 (phospholipase C inhibitor), IEM 1460 (AMPAR blocker), D-AP5 (NMDA receptor antagonist), and NPS 2390 (mGluR I antagonist).

    Techniques: Recombinant, Fluorescence, Incubation, Expressing