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ru265 (sml2991)  (Millipore)


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    Structured Review

    Millipore ru265 (sml2991)
    Inhibiting intracellular calcium release prevents the loss in mitochondrial mass in RHO overexpressed cells. The 661w cells were transfected with WT RHO and its mutants. (A) Mitochondrial and cellular calcium levels were determined by measuring the MFI of Rhod-2 AM and eFluor 514 with flow cytometry at 48 hours after transfection, and the MFI of Rhod-2 AM was further normalized to that of MitoTracker Green FM in the same group. (B) <t>Ru265</t> (10 µM), a selective mitochondrial calcium uniporter inhibitor, was applied to cells after transfection, and mitochondrial mass and mitochondrial and cellular calcium levels were detected at 48 hours. (C) After transfection, either the culture medium was changed to calcium-free DMEM to prevent calcium influx or 2-APB (10 µM) was applied to cells to inhibit intracellular calcium release, and cellular calcium levels were detected at 48 hours. Mitochondrial mass was also assayed after 48 hours of 2-APB treatment. (D) Cellular energy status, cell apoptosis, and cyto c release from mitochondria were tested at 48 hours of 2-APB treatment. * P < 0.05, ** P < 0.01 compared with the control group ( n = 4).
    Ru265 (Sml2991), supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ru265+(sml2991)/ru265++sml2991+/pmc09730732-12-18-27
    Average 90 stars, based on 1 article reviews
    ru265 (sml2991) - by Bioz Stars, 2026-10
    90/100 stars

    Images

    1) Product Images from "Overexpression of Rhodopsin or Its Mutants Leads to Energy Metabolism Dysfunction in 661w Cells"

    Article Title: Overexpression of Rhodopsin or Its Mutants Leads to Energy Metabolism Dysfunction in 661w Cells

    Journal: Investigative Ophthalmology & Visual Science

    doi: 10.1167/iovs.63.13.2

    Inhibiting intracellular calcium release prevents the loss in mitochondrial mass in RHO overexpressed cells. The 661w cells were transfected with WT RHO and its mutants. (A) Mitochondrial and cellular calcium levels were determined by measuring the MFI of Rhod-2 AM and eFluor 514 with flow cytometry at 48 hours after transfection, and the MFI of Rhod-2 AM was further normalized to that of MitoTracker Green FM in the same group. (B) Ru265 (10 µM), a selective mitochondrial calcium uniporter inhibitor, was applied to cells after transfection, and mitochondrial mass and mitochondrial and cellular calcium levels were detected at 48 hours. (C) After transfection, either the culture medium was changed to calcium-free DMEM to prevent calcium influx or 2-APB (10 µM) was applied to cells to inhibit intracellular calcium release, and cellular calcium levels were detected at 48 hours. Mitochondrial mass was also assayed after 48 hours of 2-APB treatment. (D) Cellular energy status, cell apoptosis, and cyto c release from mitochondria were tested at 48 hours of 2-APB treatment. * P < 0.05, ** P < 0.01 compared with the control group ( n = 4).
    Figure Legend Snippet: Inhibiting intracellular calcium release prevents the loss in mitochondrial mass in RHO overexpressed cells. The 661w cells were transfected with WT RHO and its mutants. (A) Mitochondrial and cellular calcium levels were determined by measuring the MFI of Rhod-2 AM and eFluor 514 with flow cytometry at 48 hours after transfection, and the MFI of Rhod-2 AM was further normalized to that of MitoTracker Green FM in the same group. (B) Ru265 (10 µM), a selective mitochondrial calcium uniporter inhibitor, was applied to cells after transfection, and mitochondrial mass and mitochondrial and cellular calcium levels were detected at 48 hours. (C) After transfection, either the culture medium was changed to calcium-free DMEM to prevent calcium influx or 2-APB (10 µM) was applied to cells to inhibit intracellular calcium release, and cellular calcium levels were detected at 48 hours. Mitochondrial mass was also assayed after 48 hours of 2-APB treatment. (D) Cellular energy status, cell apoptosis, and cyto c release from mitochondria were tested at 48 hours of 2-APB treatment. * P < 0.05, ** P < 0.01 compared with the control group ( n = 4).

    Techniques Used: Transfection, Flow Cytometry

    Related Articles

    Transfection:

    Article Title: Overexpression of Rhodopsin or Its Mutants Leads to Energy Metabolism Dysfunction in 661w Cells
    Article Snippet: N -acetylcysteine (NAC, S1623) and 2-aminoethyl diphenylborinate (2-APB, S6657) were purchased from Selleck Chemicals (Houston, TX, USA), and Ru265 (SML2991) and Compound C (P5499) were obtained from Sigma-Aldrich (St. Louis, MO, USA).

    Flow Cytometry:

    Article Title: Overexpression of Rhodopsin or Its Mutants Leads to Energy Metabolism Dysfunction in 661w Cells
    Article Snippet: N -acetylcysteine (NAC, S1623) and 2-aminoethyl diphenylborinate (2-APB, S6657) were purchased from Selleck Chemicals (Houston, TX, USA), and Ru265 (SML2991) and Compound C (P5499) were obtained from Sigma-Aldrich (St. Louis, MO, USA).



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    Millipore ru265 (sml2991)
    Inhibiting intracellular calcium release prevents the loss in mitochondrial mass in RHO overexpressed cells. The 661w cells were transfected with WT RHO and its mutants. (A) Mitochondrial and cellular calcium levels were determined by measuring the MFI of Rhod-2 AM and eFluor 514 with flow cytometry at 48 hours after transfection, and the MFI of Rhod-2 AM was further normalized to that of MitoTracker Green FM in the same group. (B) <t>Ru265</t> (10 µM), a selective mitochondrial calcium uniporter inhibitor, was applied to cells after transfection, and mitochondrial mass and mitochondrial and cellular calcium levels were detected at 48 hours. (C) After transfection, either the culture medium was changed to calcium-free DMEM to prevent calcium influx or 2-APB (10 µM) was applied to cells to inhibit intracellular calcium release, and cellular calcium levels were detected at 48 hours. Mitochondrial mass was also assayed after 48 hours of 2-APB treatment. (D) Cellular energy status, cell apoptosis, and cyto c release from mitochondria were tested at 48 hours of 2-APB treatment. * P < 0.05, ** P < 0.01 compared with the control group ( n = 4).
    Ru265 (Sml2991), supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ru265+(sml2991)/ru265++sml2991+/pmc09730732-12-18-27
    Average 90 stars, based on 1 article reviews
    ru265 (sml2991) - by Bioz Stars, 2026-10
    90/100 stars
      Buy from Supplier

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    Inhibiting intracellular calcium release prevents the loss in mitochondrial mass in RHO overexpressed cells. The 661w cells were transfected with WT RHO and its mutants. (A) Mitochondrial and cellular calcium levels were determined by measuring the MFI of Rhod-2 AM and eFluor 514 with flow cytometry at 48 hours after transfection, and the MFI of Rhod-2 AM was further normalized to that of MitoTracker Green FM in the same group. (B) Ru265 (10 µM), a selective mitochondrial calcium uniporter inhibitor, was applied to cells after transfection, and mitochondrial mass and mitochondrial and cellular calcium levels were detected at 48 hours. (C) After transfection, either the culture medium was changed to calcium-free DMEM to prevent calcium influx or 2-APB (10 µM) was applied to cells to inhibit intracellular calcium release, and cellular calcium levels were detected at 48 hours. Mitochondrial mass was also assayed after 48 hours of 2-APB treatment. (D) Cellular energy status, cell apoptosis, and cyto c release from mitochondria were tested at 48 hours of 2-APB treatment. * P < 0.05, ** P < 0.01 compared with the control group ( n = 4).

    Journal: Investigative Ophthalmology & Visual Science

    Article Title: Overexpression of Rhodopsin or Its Mutants Leads to Energy Metabolism Dysfunction in 661w Cells

    doi: 10.1167/iovs.63.13.2

    Figure Lengend Snippet: Inhibiting intracellular calcium release prevents the loss in mitochondrial mass in RHO overexpressed cells. The 661w cells were transfected with WT RHO and its mutants. (A) Mitochondrial and cellular calcium levels were determined by measuring the MFI of Rhod-2 AM and eFluor 514 with flow cytometry at 48 hours after transfection, and the MFI of Rhod-2 AM was further normalized to that of MitoTracker Green FM in the same group. (B) Ru265 (10 µM), a selective mitochondrial calcium uniporter inhibitor, was applied to cells after transfection, and mitochondrial mass and mitochondrial and cellular calcium levels were detected at 48 hours. (C) After transfection, either the culture medium was changed to calcium-free DMEM to prevent calcium influx or 2-APB (10 µM) was applied to cells to inhibit intracellular calcium release, and cellular calcium levels were detected at 48 hours. Mitochondrial mass was also assayed after 48 hours of 2-APB treatment. (D) Cellular energy status, cell apoptosis, and cyto c release from mitochondria were tested at 48 hours of 2-APB treatment. * P < 0.05, ** P < 0.01 compared with the control group ( n = 4).

    Article Snippet: N -acetylcysteine (NAC, S1623) and 2-aminoethyl diphenylborinate (2-APB, S6657) were purchased from Selleck Chemicals (Houston, TX, USA), and Ru265 (SML2991) and Compound C (P5499) were obtained from Sigma-Aldrich (St. Louis, MO, USA).

    Techniques: Transfection, Flow Cytometry