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96 well plates  (MedChemExpress)


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    MedChemExpress 96 well plates
    96 Well Plates, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 90/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/96 well plates/product/MedChemExpress
    Average 90 stars, based on 3 article reviews
    96 well plates - by Bioz Stars, 2026-02
    90/100 stars

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    pi828  (MedChemExpress)
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    Representative recordings of intracellular Ca 2+ in individual Fluo-8-loaded cells stimulated by aminergic agonists in control and in the presence of <t>PI828.</t> PI828 (10 – 50 μM) inhibited Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells (A), 2 μM histamine in C6 cells (B), and 1 nM serotonin in CHO/5HT 2C cells (C). Note that PI828 did not inhibit cell responsiveness to the purinergic agonist ATP (3 μM) (A–C). (D) Representative recording from a HEK-293 cell demonstrating that unlike ACh responses, Ca 2+ responses to 3 μM norepinephrine (NE) were not inhibited by 50 μM PI828. Here and in the below figures: applications of compounds are indicated by the straight-line segments above the experimental traces; the data are presented as ΔF/F 0 , where ΔF = F–F 0 , F is the instant intensity of cell fluorescence, F 0 is the intensity of cell fluorescence obtained in the very beginning of a recording and averaged over a 20 s interval.
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    Representative recordings of intracellular Ca 2+ in individual Fluo-8-loaded cells stimulated by aminergic agonists in control and in the presence of PI828. PI828 (10 – 50 μM) inhibited Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells (A), 2 μM histamine in C6 cells (B), and 1 nM serotonin in CHO/5HT 2C cells (C). Note that PI828 did not inhibit cell responsiveness to the purinergic agonist ATP (3 μM) (A–C). (D) Representative recording from a HEK-293 cell demonstrating that unlike ACh responses, Ca 2+ responses to 3 μM norepinephrine (NE) were not inhibited by 50 μM PI828. Here and in the below figures: applications of compounds are indicated by the straight-line segments above the experimental traces; the data are presented as ΔF/F 0 , where ΔF = F–F 0 , F is the instant intensity of cell fluorescence, F 0 is the intensity of cell fluorescence obtained in the very beginning of a recording and averaged over a 20 s interval.

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: Representative recordings of intracellular Ca 2+ in individual Fluo-8-loaded cells stimulated by aminergic agonists in control and in the presence of PI828. PI828 (10 – 50 μM) inhibited Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells (A), 2 μM histamine in C6 cells (B), and 1 nM serotonin in CHO/5HT 2C cells (C). Note that PI828 did not inhibit cell responsiveness to the purinergic agonist ATP (3 μM) (A–C). (D) Representative recording from a HEK-293 cell demonstrating that unlike ACh responses, Ca 2+ responses to 3 μM norepinephrine (NE) were not inhibited by 50 μM PI828. Here and in the below figures: applications of compounds are indicated by the straight-line segments above the experimental traces; the data are presented as ΔF/F 0 , where ΔF = F–F 0 , F is the instant intensity of cell fluorescence, F 0 is the intensity of cell fluorescence obtained in the very beginning of a recording and averaged over a 20 s interval.

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques: Control, Fluorescence

    (A–C) Representative responses of cells to aminergic agonists in control and in the presence of wortmannin or PI828. Unlike PI828 (10 – 20 μM), wortmannin (10 μM) did not affect Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells (A), 2 μM histamine in C6 cells (B), and 1 nM serotonin in CHO/5HT 2C cells (C).

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: (A–C) Representative responses of cells to aminergic agonists in control and in the presence of wortmannin or PI828. Unlike PI828 (10 – 20 μM), wortmannin (10 μM) did not affect Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells (A), 2 μM histamine in C6 cells (B), and 1 nM serotonin in CHO/5HT 2C cells (C).

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques: Control

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet:

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques:

    (A) Experimental protocol timing. The applications of wortmannin, PI828, and insulin during recordings are indicated by the line segments above the time axis; the moments of image capturing are indicated by the arrows. (B, C) Representative sequential images of HEK/R-GECO1/PH(Akt)-Venus cells were obtained with SIM-microscopy at the moments indicated in (A). The left panels, control images of two cells obtained right before drug application demonstrate the virtually homogeneous distribution of PH(Akt)-Venus fluorescence over cell bodies. The middle panels, the cell stimulation with 100 nM insulin negligibly affected sensor distribution in the presence of 10 μM wortmannin (B) or 30 μM PI828 (C). The weak decrease in cell fluorescence was presumably arisen from photobleaching. The right panels, after the rinse of PI3K inhibitors, 100 nM insulin initiated a drop in the fluorescence of the cell cytosol and the appearance of detectable stripe-like fluorescent zones (arrows in the right panels), the phenomenon suggesting the insulin-induced accumulation of the PH(Akt)-Venus sensor in the plasmalemma.

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: (A) Experimental protocol timing. The applications of wortmannin, PI828, and insulin during recordings are indicated by the line segments above the time axis; the moments of image capturing are indicated by the arrows. (B, C) Representative sequential images of HEK/R-GECO1/PH(Akt)-Venus cells were obtained with SIM-microscopy at the moments indicated in (A). The left panels, control images of two cells obtained right before drug application demonstrate the virtually homogeneous distribution of PH(Akt)-Venus fluorescence over cell bodies. The middle panels, the cell stimulation with 100 nM insulin negligibly affected sensor distribution in the presence of 10 μM wortmannin (B) or 30 μM PI828 (C). The weak decrease in cell fluorescence was presumably arisen from photobleaching. The right panels, after the rinse of PI3K inhibitors, 100 nM insulin initiated a drop in the fluorescence of the cell cytosol and the appearance of detectable stripe-like fluorescent zones (arrows in the right panels), the phenomenon suggesting the insulin-induced accumulation of the PH(Akt)-Venus sensor in the plasmalemma.

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques: Microscopy, Control, Fluorescence, Cell Stimulation

    Docking-predicted conformations of the muscarinic M3 receptor in complex with 4-DAMP (A), wortmannin (B), PI828 (C). The left panels represent the overall view of the receptor; the right panels illustrate the extracellular loop region and the orthosteric site. TM1, TM3, TM5, and TM6 are as in . As shown, 4-DAMP localizes in the orthosteric site, while wortmannin and PI828 occupy the extracellular loops region.

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: Docking-predicted conformations of the muscarinic M3 receptor in complex with 4-DAMP (A), wortmannin (B), PI828 (C). The left panels represent the overall view of the receptor; the right panels illustrate the extracellular loop region and the orthosteric site. TM1, TM3, TM5, and TM6 are as in . As shown, 4-DAMP localizes in the orthosteric site, while wortmannin and PI828 occupy the extracellular loops region.

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques:

    Snapshots are taken from representative MD trajectories at 25, 50, 75, and 100 ns. The MD simulations for 4-DAMP (A), wortmannin (B), and PI828 (C), started from the conformations shown in , respectively. The compounds are shown as spheres colored according to element (carbon – cyan, orange, and yellow in 4-DAMP, wortmannin, and PI828, correspondingly; nitrogen – blue; oxygen – red; hydrogen – white). As demonstrated, 4-DAMP and wortmannin did not leave the orthosteric site and the vestibule, respectively, within 100 ns. At the same time, PI828 was capable of moving from its docking-predicted location in the vestibule towards the orthosteric site already after 25 ns.

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: Snapshots are taken from representative MD trajectories at 25, 50, 75, and 100 ns. The MD simulations for 4-DAMP (A), wortmannin (B), and PI828 (C), started from the conformations shown in , respectively. The compounds are shown as spheres colored according to element (carbon – cyan, orange, and yellow in 4-DAMP, wortmannin, and PI828, correspondingly; nitrogen – blue; oxygen – red; hydrogen – white). As demonstrated, 4-DAMP and wortmannin did not leave the orthosteric site and the vestibule, respectively, within 100 ns. At the same time, PI828 was capable of moving from its docking-predicted location in the vestibule towards the orthosteric site already after 25 ns.

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques:

    Snapshots of PI828-M3 receptor complex obtained with representative MD-simulation. Positions of PI828 (yellow) in the receptor vestibule predicted by docking (A) and obtained from over 100 ns-long trajectory showing its passage toward the orthosteric site (B); here ACh (green) is shown in its position at the orthosteric site of the receptor for reference. (C) Transformation of the tyrosine lid opening the passage for PI828. Tyrosines 148 and 506 are rendered as sticks, the muscarinic M3 receptor in docking-predicted conformation is shown in orange and after molecular dynamics simulation – in green. Note the displacement of the tyrosine terminal oxygen atoms shown in red.

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: Snapshots of PI828-M3 receptor complex obtained with representative MD-simulation. Positions of PI828 (yellow) in the receptor vestibule predicted by docking (A) and obtained from over 100 ns-long trajectory showing its passage toward the orthosteric site (B); here ACh (green) is shown in its position at the orthosteric site of the receptor for reference. (C) Transformation of the tyrosine lid opening the passage for PI828. Tyrosines 148 and 506 are rendered as sticks, the muscarinic M3 receptor in docking-predicted conformation is shown in orange and after molecular dynamics simulation – in green. Note the displacement of the tyrosine terminal oxygen atoms shown in red.

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques: Transformation Assay

    Representative Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells in control and in the presence of hemantein (100 μM) or PI828 (20 μM).

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: Representative Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells in control and in the presence of hemantein (100 μM) or PI828 (20 μM).

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques: Control

    (A) Structural formulas of PI3K inhibitors and ketanserin. (B) Representative Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells in control and in the presence of ketanserin (20 μM) or PI828 (20 μM).

    Journal: bioRxiv

    Article Title: PI3 kinase inhibitor PI828 uncouples aminergic GPCRs and Ca 2+ mobilization irrespectively of its primary target

    doi: 10.1101/2024.01.17.576005

    Figure Lengend Snippet: (A) Structural formulas of PI3K inhibitors and ketanserin. (B) Representative Ca 2+ transients elicited by 1 μM ACh in HEK-293 cells in control and in the presence of ketanserin (20 μM) or PI828 (20 μM).

    Article Snippet: The used ACh, histamine, serotonin, insulin, PI828, U73122, and 4-DAMP were purchased from Tocris Bioscience; norepinephrine was from Calbiochem Biochemicals; ATP and wortmannin were from Sigma-Aldrich; hematein and ketanserin were from MedChemExpress.

    Techniques: Control