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rap1 sirna mouse  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology rap1 sirna mouse
    Fig. 3. mTORC2 inactivation in C2C12 myoblasts leads to a similar toxicity as treatment with simvastatin. C2C12 myoblasts were transfected for 24 h with control <t>siRNA</t> or 60 pmol Rictor siRNA and treated with 10 μM simvastatin and/or 100 ng/mL insulin and/or 100 µM mevalonate and/or 50 µM geranylgeraniol and/or 50 µM farnesol. DMSO 0.1% was used as negative control and 1% Triton-X 100 as positive control (not shown). A. Membrane toxicity (AK release) in transfected cells treated for 24 h. B. Intracellular ATP in transfected cells treated for 24 h. C. Quantification for Rictor, P-Akt Ser473 and P-S6rp 235/236 based on the immunoblots 3D and 3E. D and E. Representative immunoblots of Rictor, P-Akt and P-S6rp. Data represent the mean ± SEM of at least three independent experiments. F. Expression of Ki-67 mRNA. *P < 0.05 versus 0.1 % respective DMSO control sample; +P < 0.05 versus respective 10 μM simvastatin sample. #P < 0.05 Rictor siRNA samples versus respective control siRNA samples. SMV: simvastatin, INS: insulin, MEVA: mevalonate, GGOH: geranylgeraniol, FOH: farnesol.
    Rap1 Sirna Mouse, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rap1+sirna+mouse/RAP1+siRNA/pm34461118-104-0-12
    Average 92 stars, based on 20 article reviews
    rap1 sirna mouse - by Bioz Stars, 2026-10
    92/100 stars

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    1) Product Images from "mTORC2 is an important target for simvastatin-associated toxicity in C2C12 cells and mouse skeletal muscle - Roles of Rap1 geranylgeranylation and mitochondrial dysfunction."

    Article Title: mTORC2 is an important target for simvastatin-associated toxicity in C2C12 cells and mouse skeletal muscle - Roles of Rap1 geranylgeranylation and mitochondrial dysfunction.

    Journal: Biochemical pharmacology

    doi: 10.1016/j.bcp.2021.114750

    Fig. 3. mTORC2 inactivation in C2C12 myoblasts leads to a similar toxicity as treatment with simvastatin. C2C12 myoblasts were transfected for 24 h with control siRNA or 60 pmol Rictor siRNA and treated with 10 μM simvastatin and/or 100 ng/mL insulin and/or 100 µM mevalonate and/or 50 µM geranylgeraniol and/or 50 µM farnesol. DMSO 0.1% was used as negative control and 1% Triton-X 100 as positive control (not shown). A. Membrane toxicity (AK release) in transfected cells treated for 24 h. B. Intracellular ATP in transfected cells treated for 24 h. C. Quantification for Rictor, P-Akt Ser473 and P-S6rp 235/236 based on the immunoblots 3D and 3E. D and E. Representative immunoblots of Rictor, P-Akt and P-S6rp. Data represent the mean ± SEM of at least three independent experiments. F. Expression of Ki-67 mRNA. *P < 0.05 versus 0.1 % respective DMSO control sample; +P < 0.05 versus respective 10 μM simvastatin sample. #P < 0.05 Rictor siRNA samples versus respective control siRNA samples. SMV: simvastatin, INS: insulin, MEVA: mevalonate, GGOH: geranylgeraniol, FOH: farnesol.
    Figure Legend Snippet: Fig. 3. mTORC2 inactivation in C2C12 myoblasts leads to a similar toxicity as treatment with simvastatin. C2C12 myoblasts were transfected for 24 h with control siRNA or 60 pmol Rictor siRNA and treated with 10 μM simvastatin and/or 100 ng/mL insulin and/or 100 µM mevalonate and/or 50 µM geranylgeraniol and/or 50 µM farnesol. DMSO 0.1% was used as negative control and 1% Triton-X 100 as positive control (not shown). A. Membrane toxicity (AK release) in transfected cells treated for 24 h. B. Intracellular ATP in transfected cells treated for 24 h. C. Quantification for Rictor, P-Akt Ser473 and P-S6rp 235/236 based on the immunoblots 3D and 3E. D and E. Representative immunoblots of Rictor, P-Akt and P-S6rp. Data represent the mean ± SEM of at least three independent experiments. F. Expression of Ki-67 mRNA. *P < 0.05 versus 0.1 % respective DMSO control sample; +P < 0.05 versus respective 10 μM simvastatin sample. #P < 0.05 Rictor siRNA samples versus respective control siRNA samples. SMV: simvastatin, INS: insulin, MEVA: mevalonate, GGOH: geranylgeraniol, FOH: farnesol.

    Techniques Used: Transfection, Control, Negative Control, Positive Control, Membrane, Western Blot, Expressing

    Fig. 7. Simvastatin increases mitochondrial ROS production, which can be mitigated by antioxidants and which contributes to impaired function of mTORC2 and cytotoxicity. C2C12 myoblasts or myotubes were treated for 24 h with 10 μM simvastatin and/or 10 to 20 μM MitoTEMPO and/or 10 to 50 µM geranylgeraniol. MitoSOX Red dye was used to quantify mitochondrial superoxide production. DMSO 0.1% was used as a negative control and 100 μM antimycin A as a positive control (1 h exposure) A. Mitochondrial O2 •- accumulation in C2C12 myoblasts transfected with control siRNA or Rap1 siRNA. B. Mitochondrial O2 •- accumulation in C2C12 myotubes treated with simvastatin or antimycin A. C. Membrane integrity (AK release) of C2C12 myotubes treated with simvastatin, MitoTEMPO, or anti mycin A. D. Intracellular ATP of C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. E. mTORC2 activity assessed by phosphorylation levels of Akt (Ser473) in C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. F. Quantification of Akt (Ser473) phosphorylation shown in E. Data represent the mean ± SEM of at least three independent experiments. *P < 0.05 versus the respective DMSO control; +P < 0.05 versus 10 μM simvastatin or 100 μM antimycin A. SMV: simvastatin, GGOH: geranylgeraniol, MITOT: MitoTEMPO, ANT.A: antimycin A.
    Figure Legend Snippet: Fig. 7. Simvastatin increases mitochondrial ROS production, which can be mitigated by antioxidants and which contributes to impaired function of mTORC2 and cytotoxicity. C2C12 myoblasts or myotubes were treated for 24 h with 10 μM simvastatin and/or 10 to 20 μM MitoTEMPO and/or 10 to 50 µM geranylgeraniol. MitoSOX Red dye was used to quantify mitochondrial superoxide production. DMSO 0.1% was used as a negative control and 100 μM antimycin A as a positive control (1 h exposure) A. Mitochondrial O2 •- accumulation in C2C12 myoblasts transfected with control siRNA or Rap1 siRNA. B. Mitochondrial O2 •- accumulation in C2C12 myotubes treated with simvastatin or antimycin A. C. Membrane integrity (AK release) of C2C12 myotubes treated with simvastatin, MitoTEMPO, or anti mycin A. D. Intracellular ATP of C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. E. mTORC2 activity assessed by phosphorylation levels of Akt (Ser473) in C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. F. Quantification of Akt (Ser473) phosphorylation shown in E. Data represent the mean ± SEM of at least three independent experiments. *P < 0.05 versus the respective DMSO control; +P < 0.05 versus 10 μM simvastatin or 100 μM antimycin A. SMV: simvastatin, GGOH: geranylgeraniol, MITOT: MitoTEMPO, ANT.A: antimycin A.

    Techniques Used: Negative Control, Positive Control, Transfection, Control, Membrane, Activity Assay, Phospho-proteomics

    Fig. 8. Effects of simvastatin on mTORC1 and mTORC2. Simvastatin impairs the function of mTORC2 by inhibition of Rap1 and by mitochondrial damage. Impaired function of mTORC2 reduces the function of Akt (impaired phosphorylation of Ser473), which limits the function of mTORC1 and increases the expression of atrogin- 1. Impaired function of mTORC1 reduces the activity of S6rp. Cell death associated with simvastatin can be explained by apoptosis (via inhibition of Akt and mitochondrial damage) and necrosis (mitochondrial damage).
    Figure Legend Snippet: Fig. 8. Effects of simvastatin on mTORC1 and mTORC2. Simvastatin impairs the function of mTORC2 by inhibition of Rap1 and by mitochondrial damage. Impaired function of mTORC2 reduces the function of Akt (impaired phosphorylation of Ser473), which limits the function of mTORC1 and increases the expression of atrogin- 1. Impaired function of mTORC1 reduces the activity of S6rp. Cell death associated with simvastatin can be explained by apoptosis (via inhibition of Akt and mitochondrial damage) and necrosis (mitochondrial damage).

    Techniques Used: Inhibition, Phospho-proteomics, Expressing, Activity Assay

    Related Articles

    Control:

    Article Title: mTORC2 is the Primary Target for Simvastatin-Associated Toxicity in C2C12 Cells and in Mouse Skeletal Muscle
    Article Snippet: .. Rap1 siRNA (mouse), Rictor siRNA (mouse) and Control siRNA-A were purchased from Santa Cruz Biotechnology (sc-61479 and sc-37007, respectively; USA). .. The transfection was done using Lipofectamine RNAiMAX (Invitrogen) in accordance with the manufacturer’s instructions.

    Article Title: mTORC2 is an important target for simvastatin-associated toxicity in C2C12 cells and mouse skeletal muscle - Roles of Rap1 geranylgeranylation and mitochondrial dysfunction.
    Article Snippet: .. Rap1 siRNA (mouse), Rictor siRNA (mouse) and Control siRNA-A were purchased from Santa Cruz Biotechnology (sc-61479 and sc-37007, respectively; USA). .. The transfection was done using Lipofectamine RNAiMAX (Invitrogen) in accordance with the manufacturer’s instructions.



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    rap1 sirna mouse  (Santa Cruz Biotechnology)
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    Santa Cruz Biotechnology rap1 sirna mouse
    Fig. 3. mTORC2 inactivation in C2C12 myoblasts leads to a similar toxicity as treatment with simvastatin. C2C12 myoblasts were transfected for 24 h with control <t>siRNA</t> or 60 pmol Rictor siRNA and treated with 10 μM simvastatin and/or 100 ng/mL insulin and/or 100 µM mevalonate and/or 50 µM geranylgeraniol and/or 50 µM farnesol. DMSO 0.1% was used as negative control and 1% Triton-X 100 as positive control (not shown). A. Membrane toxicity (AK release) in transfected cells treated for 24 h. B. Intracellular ATP in transfected cells treated for 24 h. C. Quantification for Rictor, P-Akt Ser473 and P-S6rp 235/236 based on the immunoblots 3D and 3E. D and E. Representative immunoblots of Rictor, P-Akt and P-S6rp. Data represent the mean ± SEM of at least three independent experiments. F. Expression of Ki-67 mRNA. *P < 0.05 versus 0.1 % respective DMSO control sample; +P < 0.05 versus respective 10 μM simvastatin sample. #P < 0.05 Rictor siRNA samples versus respective control siRNA samples. SMV: simvastatin, INS: insulin, MEVA: mevalonate, GGOH: geranylgeraniol, FOH: farnesol.
    Rap1 Sirna Mouse, supplied by Santa Cruz Biotechnology, 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/product/rap1+sirna+mouse/RAP1+siRNA/pm34461118-104-0-12
    Average 92 stars, based on 1 article reviews
    rap1 sirna mouse - by Bioz Stars, 2026-10
    92/100 stars
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    Fig. 3. mTORC2 inactivation in C2C12 myoblasts leads to a similar toxicity as treatment with simvastatin. C2C12 myoblasts were transfected for 24 h with control siRNA or 60 pmol Rictor siRNA and treated with 10 μM simvastatin and/or 100 ng/mL insulin and/or 100 µM mevalonate and/or 50 µM geranylgeraniol and/or 50 µM farnesol. DMSO 0.1% was used as negative control and 1% Triton-X 100 as positive control (not shown). A. Membrane toxicity (AK release) in transfected cells treated for 24 h. B. Intracellular ATP in transfected cells treated for 24 h. C. Quantification for Rictor, P-Akt Ser473 and P-S6rp 235/236 based on the immunoblots 3D and 3E. D and E. Representative immunoblots of Rictor, P-Akt and P-S6rp. Data represent the mean ± SEM of at least three independent experiments. F. Expression of Ki-67 mRNA. *P < 0.05 versus 0.1 % respective DMSO control sample; +P < 0.05 versus respective 10 μM simvastatin sample. #P < 0.05 Rictor siRNA samples versus respective control siRNA samples. SMV: simvastatin, INS: insulin, MEVA: mevalonate, GGOH: geranylgeraniol, FOH: farnesol.

    Journal: Biochemical pharmacology

    Article Title: mTORC2 is an important target for simvastatin-associated toxicity in C2C12 cells and mouse skeletal muscle - Roles of Rap1 geranylgeranylation and mitochondrial dysfunction.

    doi: 10.1016/j.bcp.2021.114750

    Figure Lengend Snippet: Fig. 3. mTORC2 inactivation in C2C12 myoblasts leads to a similar toxicity as treatment with simvastatin. C2C12 myoblasts were transfected for 24 h with control siRNA or 60 pmol Rictor siRNA and treated with 10 μM simvastatin and/or 100 ng/mL insulin and/or 100 µM mevalonate and/or 50 µM geranylgeraniol and/or 50 µM farnesol. DMSO 0.1% was used as negative control and 1% Triton-X 100 as positive control (not shown). A. Membrane toxicity (AK release) in transfected cells treated for 24 h. B. Intracellular ATP in transfected cells treated for 24 h. C. Quantification for Rictor, P-Akt Ser473 and P-S6rp 235/236 based on the immunoblots 3D and 3E. D and E. Representative immunoblots of Rictor, P-Akt and P-S6rp. Data represent the mean ± SEM of at least three independent experiments. F. Expression of Ki-67 mRNA. *P < 0.05 versus 0.1 % respective DMSO control sample; +P < 0.05 versus respective 10 μM simvastatin sample. #P < 0.05 Rictor siRNA samples versus respective control siRNA samples. SMV: simvastatin, INS: insulin, MEVA: mevalonate, GGOH: geranylgeraniol, FOH: farnesol.

    Article Snippet: Rap1 siRNA (mouse), Rictor siRNA (mouse) and Control siRNA-A were purchased from Santa Cruz Biotechnology (sc-61479 and sc-37007, respectively; USA).

    Techniques: Transfection, Control, Negative Control, Positive Control, Membrane, Western Blot, Expressing

    Fig. 7. Simvastatin increases mitochondrial ROS production, which can be mitigated by antioxidants and which contributes to impaired function of mTORC2 and cytotoxicity. C2C12 myoblasts or myotubes were treated for 24 h with 10 μM simvastatin and/or 10 to 20 μM MitoTEMPO and/or 10 to 50 µM geranylgeraniol. MitoSOX Red dye was used to quantify mitochondrial superoxide production. DMSO 0.1% was used as a negative control and 100 μM antimycin A as a positive control (1 h exposure) A. Mitochondrial O2 •- accumulation in C2C12 myoblasts transfected with control siRNA or Rap1 siRNA. B. Mitochondrial O2 •- accumulation in C2C12 myotubes treated with simvastatin or antimycin A. C. Membrane integrity (AK release) of C2C12 myotubes treated with simvastatin, MitoTEMPO, or anti mycin A. D. Intracellular ATP of C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. E. mTORC2 activity assessed by phosphorylation levels of Akt (Ser473) in C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. F. Quantification of Akt (Ser473) phosphorylation shown in E. Data represent the mean ± SEM of at least three independent experiments. *P < 0.05 versus the respective DMSO control; +P < 0.05 versus 10 μM simvastatin or 100 μM antimycin A. SMV: simvastatin, GGOH: geranylgeraniol, MITOT: MitoTEMPO, ANT.A: antimycin A.

    Journal: Biochemical pharmacology

    Article Title: mTORC2 is an important target for simvastatin-associated toxicity in C2C12 cells and mouse skeletal muscle - Roles of Rap1 geranylgeranylation and mitochondrial dysfunction.

    doi: 10.1016/j.bcp.2021.114750

    Figure Lengend Snippet: Fig. 7. Simvastatin increases mitochondrial ROS production, which can be mitigated by antioxidants and which contributes to impaired function of mTORC2 and cytotoxicity. C2C12 myoblasts or myotubes were treated for 24 h with 10 μM simvastatin and/or 10 to 20 μM MitoTEMPO and/or 10 to 50 µM geranylgeraniol. MitoSOX Red dye was used to quantify mitochondrial superoxide production. DMSO 0.1% was used as a negative control and 100 μM antimycin A as a positive control (1 h exposure) A. Mitochondrial O2 •- accumulation in C2C12 myoblasts transfected with control siRNA or Rap1 siRNA. B. Mitochondrial O2 •- accumulation in C2C12 myotubes treated with simvastatin or antimycin A. C. Membrane integrity (AK release) of C2C12 myotubes treated with simvastatin, MitoTEMPO, or anti mycin A. D. Intracellular ATP of C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. E. mTORC2 activity assessed by phosphorylation levels of Akt (Ser473) in C2C12 myotubes treated with simvastatin, MitoTEMPO or antimycin A. F. Quantification of Akt (Ser473) phosphorylation shown in E. Data represent the mean ± SEM of at least three independent experiments. *P < 0.05 versus the respective DMSO control; +P < 0.05 versus 10 μM simvastatin or 100 μM antimycin A. SMV: simvastatin, GGOH: geranylgeraniol, MITOT: MitoTEMPO, ANT.A: antimycin A.

    Article Snippet: Rap1 siRNA (mouse), Rictor siRNA (mouse) and Control siRNA-A were purchased from Santa Cruz Biotechnology (sc-61479 and sc-37007, respectively; USA).

    Techniques: Negative Control, Positive Control, Transfection, Control, Membrane, Activity Assay, Phospho-proteomics

    Fig. 8. Effects of simvastatin on mTORC1 and mTORC2. Simvastatin impairs the function of mTORC2 by inhibition of Rap1 and by mitochondrial damage. Impaired function of mTORC2 reduces the function of Akt (impaired phosphorylation of Ser473), which limits the function of mTORC1 and increases the expression of atrogin- 1. Impaired function of mTORC1 reduces the activity of S6rp. Cell death associated with simvastatin can be explained by apoptosis (via inhibition of Akt and mitochondrial damage) and necrosis (mitochondrial damage).

    Journal: Biochemical pharmacology

    Article Title: mTORC2 is an important target for simvastatin-associated toxicity in C2C12 cells and mouse skeletal muscle - Roles of Rap1 geranylgeranylation and mitochondrial dysfunction.

    doi: 10.1016/j.bcp.2021.114750

    Figure Lengend Snippet: Fig. 8. Effects of simvastatin on mTORC1 and mTORC2. Simvastatin impairs the function of mTORC2 by inhibition of Rap1 and by mitochondrial damage. Impaired function of mTORC2 reduces the function of Akt (impaired phosphorylation of Ser473), which limits the function of mTORC1 and increases the expression of atrogin- 1. Impaired function of mTORC1 reduces the activity of S6rp. Cell death associated with simvastatin can be explained by apoptosis (via inhibition of Akt and mitochondrial damage) and necrosis (mitochondrial damage).

    Article Snippet: Rap1 siRNA (mouse), Rictor siRNA (mouse) and Control siRNA-A were purchased from Santa Cruz Biotechnology (sc-61479 and sc-37007, respectively; USA).

    Techniques: Inhibition, Phospho-proteomics, Expressing, Activity Assay