rap1 sirna mouse Search Results


rap1 sirna mouse  (Santa Cruz Biotechnology)
92
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
  Buy from Supplier
control sirna a  (Santa Cruz Biotechnology)
96
Santa Cruz Biotechnology control sirna a
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.
Control Sirna A, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/Control+siRNA-A/ppr0356476-88-7-12
Average 96 stars, based on 1 article reviews
control sirna a - by Bioz Stars, 2026-10
96/100 stars
  Buy from Supplier
rictor sirna mouse  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology rictor 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.
Rictor Sirna Mouse, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/Rictor+siRNA/ppr0356476-88-3-12
Average 93 stars, based on 1 article reviews
rictor sirna mouse - by Bioz Stars, 2026-10
93/100 stars
  Buy from Supplier
rabbit polyclonal anti glyceraldehyde 3 phosphate dehydrogenase  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc rabbit polyclonal anti glyceraldehyde 3 phosphate dehydrogenase
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.
Rabbit Polyclonal Anti Glyceraldehyde 3 Phosphate Dehydrogenase, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/GAPDH+Rabbit+mAb/pmc05383783-424-32-39
Average 99 stars, based on 1 article reviews
rabbit polyclonal anti glyceraldehyde 3 phosphate dehydrogenase - by Bioz Stars, 2026-10
99/100 stars
  Buy from Supplier
fugene hd  (Promega)
90
Promega fugene hd
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.
Fugene Hd, supplied by Promega, 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/rap1+sirna+mouse/fugene+hd/pmc07521479__mmc4-168-132-134
Average 90 stars, based on 1 article reviews
fugene hd - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier
pll-g-peg  (Susos AG)
90
Susos AG pll-g-peg
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.
Pll G Peg, supplied by Susos AG, 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/rap1+sirna+mouse/pll+g+peg/pmc07521479__mmc4-168-168-169
Average 90 stars, based on 1 article reviews
pll-g-peg - by Bioz Stars, 2026-10
90/100 stars
  Buy from Supplier
ac001 alexafluor 488 igg mouse  (ABclonal Biotechnology)
98
ABclonal Biotechnology ac001 alexafluor 488 igg 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.
Ac001 Alexafluor 488 Igg Mouse, supplied by ABclonal Biotechnology, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/GAPDH+Rabbit+pAb/pm35702948-34-210-208
Average 98 stars, based on 1 article reviews
ac001 alexafluor 488 igg mouse - by Bioz Stars, 2026-10
98/100 stars
  Buy from Supplier
2250 mouse, monoclonal  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc 2250 mouse, monoclonal
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.
2250 Mouse, Monoclonal, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/c-Fos+Rabbit+mAb/pm35702948-34-175-174
Average 98 stars, based on 1 article reviews
2250 mouse, monoclonal - by Bioz Stars, 2026-10
98/100 stars
  Buy from Supplier
anti akt antibody  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc anti akt antibody
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.
Anti Akt Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/Akt+Antibody/pmc02793292-30-39-43
Average 99 stars, based on 1 article reviews
anti akt antibody - by Bioz Stars, 2026-10
99/100 stars
  Buy from Supplier
rabgef1  (Proteintech)
93
Proteintech rabgef1
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.
Rabgef1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rap1+sirna+mouse/RabGEF1+Antibody/pm41364502-135-228-233
Average 93 stars, based on 1 article reviews
rabgef1 - by Bioz Stars, 2026-10
93/100 stars
  Buy from Supplier

Image Search Results


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