mtorc2 inhibitor jr ab2 011  (MedChemExpress)


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    MedChemExpress mtorc2 inhibitor jr ab2 011
    miR-582 simultaneously targets <t>mTORC2/AKT</t> signaling to attenuate pre-B cell proliferation and survival. A Pre-B cells were infected with anti-miR-582 lentivirus and cultured for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4–5). B Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor <t>JR-AB2-011</t> for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4). C Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. Cell proliferation and apoptosis were evaluated by CFSE labeling and Annexin V + and 7-AAD + , respectively, followed by flow cytometry, and quantitatively compared ( n = 3). D The signaling pathway of miR-582 regulate the proliferation and survival of pre-B cell. Bars represent means ± SEM, * P
    Mtorc2 Inhibitor Jr Ab2 011, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mtorc2 inhibitor jr ab2 011/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mtorc2 inhibitor jr ab2 011 - by Bioz Stars, 2022-05
    94/100 stars

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    1) Product Images from "miR-582 negatively regulates pre-B cell proliferation and survival through targeting Hif1α and Rictor"

    Article Title: miR-582 negatively regulates pre-B cell proliferation and survival through targeting Hif1α and Rictor

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-022-04560-y

    miR-582 simultaneously targets mTORC2/AKT signaling to attenuate pre-B cell proliferation and survival. A Pre-B cells were infected with anti-miR-582 lentivirus and cultured for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4–5). B Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4). C Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. Cell proliferation and apoptosis were evaluated by CFSE labeling and Annexin V + and 7-AAD + , respectively, followed by flow cytometry, and quantitatively compared ( n = 3). D The signaling pathway of miR-582 regulate the proliferation and survival of pre-B cell. Bars represent means ± SEM, * P
    Figure Legend Snippet: miR-582 simultaneously targets mTORC2/AKT signaling to attenuate pre-B cell proliferation and survival. A Pre-B cells were infected with anti-miR-582 lentivirus and cultured for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4–5). B Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4). C Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. Cell proliferation and apoptosis were evaluated by CFSE labeling and Annexin V + and 7-AAD + , respectively, followed by flow cytometry, and quantitatively compared ( n = 3). D The signaling pathway of miR-582 regulate the proliferation and survival of pre-B cell. Bars represent means ± SEM, * P

    Techniques Used: Infection, Cell Culture, Western Blot, Labeling, Flow Cytometry

    2) Product Images from "RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy"

    Article Title: RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy

    Journal: Biomedicines

    doi: 10.3390/biomedicines9101498

    RAS interacts with RICTOR to promote resistance. ( A ) Cells were treated with DMSO, 1 μM of vemurafenib (V1), 3 μM (JR3) or 10 μM (JR10) of JR-AB2-011, or a combination of vemurafenib and JR-AB2-011, and the proliferation was analyzed after 3 days (data are represented as mean +/− SD). Significance was calculated using the Student’s t -test and showed that JR10 significantly inhibited proliferation of all 3 cell lines even when combined with V1 ( p
    Figure Legend Snippet: RAS interacts with RICTOR to promote resistance. ( A ) Cells were treated with DMSO, 1 μM of vemurafenib (V1), 3 μM (JR3) or 10 μM (JR10) of JR-AB2-011, or a combination of vemurafenib and JR-AB2-011, and the proliferation was analyzed after 3 days (data are represented as mean +/− SD). Significance was calculated using the Student’s t -test and showed that JR10 significantly inhibited proliferation of all 3 cell lines even when combined with V1 ( p

    Techniques Used:

    3) Product Images from "FLCN Regulates HIF2α Nuclear Import and Proliferation of Clear Cell Renal Cell Carcinoma"

    Article Title: FLCN Regulates HIF2α Nuclear Import and Proliferation of Clear Cell Renal Cell Carcinoma

    Journal: Frontiers in Molecular Biosciences

    doi: 10.3389/fmolb.2020.00121

    Folliculin (FLCN) regulates clear cell renal cell carcinoma (ccRCC) invasion via the PI3K/mTORC2/HIF2α signaling pathway. (A,B) Western blotting analysis of MMP9 protein expression in 786-O (A) and ACHN (B) cell lines. The cells were co-transfected with siFLCN and siHIF2α or FLCN and EPAS1 overexpression plasmid for 48 h. (C) RT-qPCR analysis of MMP9 mRNA expression in ccRCC cell lines. ccRCC cell lines, including 786-O and ACHN, were used in this experiment. The normal renal tubular epithelium cell line HK-2 was used as control. (D) The 786-O cells were incubated with JR-AB2-011 (RICTOR inhibitor, 2 μM) for 24 h; the protein levels of RICTOR, HIF2α, FLCN, P-AKT, and AKT were examined. (E) The 786-O cells were transfected with control siRNA or siFLCN; the protein levels of p-AKT were detected. (F–I) The 786-O cells were incubated with LY294002 (PI3K inhibitor, 10 μM), KU0063794 (mTORC inhibitor, 10 μM), MK2206 (AKT inhibitor, 5 μM), and rapamycin (mTORC1 inhibitor, 10 μM) for 0–120 min; the protein levels of FLCN, P-AKT, and AKT were examined. The data are from three independently repeated experiments. * P
    Figure Legend Snippet: Folliculin (FLCN) regulates clear cell renal cell carcinoma (ccRCC) invasion via the PI3K/mTORC2/HIF2α signaling pathway. (A,B) Western blotting analysis of MMP9 protein expression in 786-O (A) and ACHN (B) cell lines. The cells were co-transfected with siFLCN and siHIF2α or FLCN and EPAS1 overexpression plasmid for 48 h. (C) RT-qPCR analysis of MMP9 mRNA expression in ccRCC cell lines. ccRCC cell lines, including 786-O and ACHN, were used in this experiment. The normal renal tubular epithelium cell line HK-2 was used as control. (D) The 786-O cells were incubated with JR-AB2-011 (RICTOR inhibitor, 2 μM) for 24 h; the protein levels of RICTOR, HIF2α, FLCN, P-AKT, and AKT were examined. (E) The 786-O cells were transfected with control siRNA or siFLCN; the protein levels of p-AKT were detected. (F–I) The 786-O cells were incubated with LY294002 (PI3K inhibitor, 10 μM), KU0063794 (mTORC inhibitor, 10 μM), MK2206 (AKT inhibitor, 5 μM), and rapamycin (mTORC1 inhibitor, 10 μM) for 0–120 min; the protein levels of FLCN, P-AKT, and AKT were examined. The data are from three independently repeated experiments. * P

    Techniques Used: Western Blot, Expressing, Transfection, Over Expression, Plasmid Preparation, Quantitative RT-PCR, Incubation

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    MedChemExpress mtorc2 inhibitor jr ab2 011
    miR-582 simultaneously targets <t>mTORC2/AKT</t> signaling to attenuate pre-B cell proliferation and survival. A Pre-B cells were infected with anti-miR-582 lentivirus and cultured for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4–5). B Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor <t>JR-AB2-011</t> for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4). C Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. Cell proliferation and apoptosis were evaluated by CFSE labeling and Annexin V + and 7-AAD + , respectively, followed by flow cytometry, and quantitatively compared ( n = 3). D The signaling pathway of miR-582 regulate the proliferation and survival of pre-B cell. Bars represent means ± SEM, * P
    Mtorc2 Inhibitor Jr Ab2 011, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mtorc2 inhibitor jr ab2 011/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    mtorc2 inhibitor jr ab2 011 - by Bioz Stars, 2022-05
    94/100 stars
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    miR-582 simultaneously targets mTORC2/AKT signaling to attenuate pre-B cell proliferation and survival. A Pre-B cells were infected with anti-miR-582 lentivirus and cultured for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4–5). B Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4). C Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. Cell proliferation and apoptosis were evaluated by CFSE labeling and Annexin V + and 7-AAD + , respectively, followed by flow cytometry, and quantitatively compared ( n = 3). D The signaling pathway of miR-582 regulate the proliferation and survival of pre-B cell. Bars represent means ± SEM, * P

    Journal: Cell Death & Disease

    Article Title: miR-582 negatively regulates pre-B cell proliferation and survival through targeting Hif1α and Rictor

    doi: 10.1038/s41419-022-04560-y

    Figure Lengend Snippet: miR-582 simultaneously targets mTORC2/AKT signaling to attenuate pre-B cell proliferation and survival. A Pre-B cells were infected with anti-miR-582 lentivirus and cultured for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4–5). B Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. The level of p-AKT, AKT, p-FoxO1, and FoxO1 was determined by Western blotting with β-actin as a reference control ( n = 4). C Pre-B cells were infected with anti-miR-582 lentivirus and cultured in the presence of the mTORC2 inhibitor JR-AB2-011 for 72 h. Cell proliferation and apoptosis were evaluated by CFSE labeling and Annexin V + and 7-AAD + , respectively, followed by flow cytometry, and quantitatively compared ( n = 3). D The signaling pathway of miR-582 regulate the proliferation and survival of pre-B cell. Bars represent means ± SEM, * P

    Article Snippet: In some experiments, Hif1α inhibitor Echinomycin (2 nM, Abcam, Cambridge, MA, USA) or mTORC2 inhibitor JR-AB2-011 (1 μM, MedChemexpress, Shanghai, China) were added in culture.

    Techniques: Infection, Cell Culture, Western Blot, Labeling, Flow Cytometry

    RAS interacts with RICTOR to promote resistance. ( A ) Cells were treated with DMSO, 1 μM of vemurafenib (V1), 3 μM (JR3) or 10 μM (JR10) of JR-AB2-011, or a combination of vemurafenib and JR-AB2-011, and the proliferation was analyzed after 3 days (data are represented as mean +/− SD). Significance was calculated using the Student’s t -test and showed that JR10 significantly inhibited proliferation of all 3 cell lines even when combined with V1 ( p

    Journal: Biomedicines

    Article Title: RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy

    doi: 10.3390/biomedicines9101498

    Figure Lengend Snippet: RAS interacts with RICTOR to promote resistance. ( A ) Cells were treated with DMSO, 1 μM of vemurafenib (V1), 3 μM (JR3) or 10 μM (JR10) of JR-AB2-011, or a combination of vemurafenib and JR-AB2-011, and the proliferation was analyzed after 3 days (data are represented as mean +/− SD). Significance was calculated using the Student’s t -test and showed that JR10 significantly inhibited proliferation of all 3 cell lines even when combined with V1 ( p

    Article Snippet: JR-AB2-011 (mTORC2 inhibitor) was from MedChemExpress (Monmouth Junction, NJ, USA).

    Techniques:

    Folliculin (FLCN) regulates clear cell renal cell carcinoma (ccRCC) invasion via the PI3K/mTORC2/HIF2α signaling pathway. (A,B) Western blotting analysis of MMP9 protein expression in 786-O (A) and ACHN (B) cell lines. The cells were co-transfected with siFLCN and siHIF2α or FLCN and EPAS1 overexpression plasmid for 48 h. (C) RT-qPCR analysis of MMP9 mRNA expression in ccRCC cell lines. ccRCC cell lines, including 786-O and ACHN, were used in this experiment. The normal renal tubular epithelium cell line HK-2 was used as control. (D) The 786-O cells were incubated with JR-AB2-011 (RICTOR inhibitor, 2 μM) for 24 h; the protein levels of RICTOR, HIF2α, FLCN, P-AKT, and AKT were examined. (E) The 786-O cells were transfected with control siRNA or siFLCN; the protein levels of p-AKT were detected. (F–I) The 786-O cells were incubated with LY294002 (PI3K inhibitor, 10 μM), KU0063794 (mTORC inhibitor, 10 μM), MK2206 (AKT inhibitor, 5 μM), and rapamycin (mTORC1 inhibitor, 10 μM) for 0–120 min; the protein levels of FLCN, P-AKT, and AKT were examined. The data are from three independently repeated experiments. * P

    Journal: Frontiers in Molecular Biosciences

    Article Title: FLCN Regulates HIF2α Nuclear Import and Proliferation of Clear Cell Renal Cell Carcinoma

    doi: 10.3389/fmolb.2020.00121

    Figure Lengend Snippet: Folliculin (FLCN) regulates clear cell renal cell carcinoma (ccRCC) invasion via the PI3K/mTORC2/HIF2α signaling pathway. (A,B) Western blotting analysis of MMP9 protein expression in 786-O (A) and ACHN (B) cell lines. The cells were co-transfected with siFLCN and siHIF2α or FLCN and EPAS1 overexpression plasmid for 48 h. (C) RT-qPCR analysis of MMP9 mRNA expression in ccRCC cell lines. ccRCC cell lines, including 786-O and ACHN, were used in this experiment. The normal renal tubular epithelium cell line HK-2 was used as control. (D) The 786-O cells were incubated with JR-AB2-011 (RICTOR inhibitor, 2 μM) for 24 h; the protein levels of RICTOR, HIF2α, FLCN, P-AKT, and AKT were examined. (E) The 786-O cells were transfected with control siRNA or siFLCN; the protein levels of p-AKT were detected. (F–I) The 786-O cells were incubated with LY294002 (PI3K inhibitor, 10 μM), KU0063794 (mTORC inhibitor, 10 μM), MK2206 (AKT inhibitor, 5 μM), and rapamycin (mTORC1 inhibitor, 10 μM) for 0–120 min; the protein levels of FLCN, P-AKT, and AKT were examined. The data are from three independently repeated experiments. * P

    Article Snippet: JR-AB2-011 was purchased from MedChenExpress.

    Techniques: Western Blot, Expressing, Transfection, Over Expression, Plasmid Preparation, Quantitative RT-PCR, Incubation