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pan-akt1/2/3 inhibitor (mk2206  (Merck & Co)
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Merck & Co pan-akt1/2/3 inhibitor (mk2206
Genomic and proteomic profiling of ovarian cancer cell lines. A, Probe-level (blue dots) and segmentation data (red lines) from Agilent 244K arrays identifying representative focal amplification (KRAS in SKOV-8) and focal homozygous deletion (RB1 in SKOV-433) events. The vertical green line crosses the x-axis at the chromosomal position of the gene. Y-axis indicates log2 copy-number signal. B, Immunoblot analysis of the ovarian cancer cell line panel for expression of <t>AKT1/2/3,</t> phosphorylated AKT (Ser473), and activation and abundance of key downstream targets. Cells were arranged based upon the presence of PI3K/AKT (red) or RAS/RAF-pathway alterations (blue) and RB1 loss (green).
Pan Akt1/2/3 Inhibitor (Mk2206, supplied by Merck & Co, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Genomic and proteomic profiling of ovarian cancer cell lines. A, Probe-level (blue dots) and segmentation data (red lines) from Agilent 244K arrays identifying representative focal amplification (KRAS in SKOV-8) and focal homozygous deletion (RB1 in SKOV-433) events. The vertical green line crosses the x-axis at the chromosomal position of the gene. Y-axis indicates log2 copy-number signal. B, Immunoblot analysis of the ovarian cancer cell line panel for expression of AKT1/2/3, phosphorylated AKT (Ser473), and activation and abundance of key downstream targets. Cells were arranged based upon the presence of PI3K/AKT (red) or RAS/RAF-pathway alterations (blue) and RB1 loss (green).

Journal: Cancer discovery

Article Title: Genomic complexity and AKT dependence in serous ovarian cancer

doi: 10.1158/2159-8290.CD-11-0170

Figure Lengend Snippet: Genomic and proteomic profiling of ovarian cancer cell lines. A, Probe-level (blue dots) and segmentation data (red lines) from Agilent 244K arrays identifying representative focal amplification (KRAS in SKOV-8) and focal homozygous deletion (RB1 in SKOV-433) events. The vertical green line crosses the x-axis at the chromosomal position of the gene. Y-axis indicates log2 copy-number signal. B, Immunoblot analysis of the ovarian cancer cell line panel for expression of AKT1/2/3, phosphorylated AKT (Ser473), and activation and abundance of key downstream targets. Cells were arranged based upon the presence of PI3K/AKT (red) or RAS/RAF-pathway alterations (blue) and RB1 loss (green).

Article Snippet: Cell Lines and Culture Conditions AKT1/2 inhibitor (AKTi-1/2, compound 17) ( 15 ) and pan-AKT1/2/3 inhibitor (MK2206) ( 16 , 17 ) were obtained from Merck.

Techniques: Amplification, Western Blot, Expressing, Activation Assay

AKT dependence of ovarian cancer cell lines. A, IC50/90 values for the AKT-1/2 inhibitor (AKTi-1/2) and panAKT-1/2/3 inhibitor (MK2206) were calculated following treatment with 0–10 µM of each inhibitor for 5 days. Drug concentrations are represented by color block gradations from dark red (0–0.3 µM) to bright red (0.3–1.7 µM), dark pink (1.7–3 µM), pale pink (3–10 µM), and white (>10 µM). Cells with detectable AKT3 expression are indicated by black boxes. Cell lines are colored based upon the presence of PI3K/AKT (red) or RAS/RAF-pathway (blue) alterations and RB1 loss (green) as in Fig. 1B. B, Cells were treated for 0–24 h with AKTi-1/2 or MK2206 (2 µM) and lysates immunoblotted for p-AKT S473 and total AKT. C, Day 5 dose response plots of three representative cell lines (IGROV-1, hypersensitive to AKT inhibition, red; OVCAR-5, heightened sensitivity to pan-AKT inhibition, blue; SKOV-433, resistant to AKT inhibition, green).

Journal: Cancer discovery

Article Title: Genomic complexity and AKT dependence in serous ovarian cancer

doi: 10.1158/2159-8290.CD-11-0170

Figure Lengend Snippet: AKT dependence of ovarian cancer cell lines. A, IC50/90 values for the AKT-1/2 inhibitor (AKTi-1/2) and panAKT-1/2/3 inhibitor (MK2206) were calculated following treatment with 0–10 µM of each inhibitor for 5 days. Drug concentrations are represented by color block gradations from dark red (0–0.3 µM) to bright red (0.3–1.7 µM), dark pink (1.7–3 µM), pale pink (3–10 µM), and white (>10 µM). Cells with detectable AKT3 expression are indicated by black boxes. Cell lines are colored based upon the presence of PI3K/AKT (red) or RAS/RAF-pathway (blue) alterations and RB1 loss (green) as in Fig. 1B. B, Cells were treated for 0–24 h with AKTi-1/2 or MK2206 (2 µM) and lysates immunoblotted for p-AKT S473 and total AKT. C, Day 5 dose response plots of three representative cell lines (IGROV-1, hypersensitive to AKT inhibition, red; OVCAR-5, heightened sensitivity to pan-AKT inhibition, blue; SKOV-433, resistant to AKT inhibition, green).

Article Snippet: Cell Lines and Culture Conditions AKT1/2 inhibitor (AKTi-1/2, compound 17) ( 15 ) and pan-AKT1/2/3 inhibitor (MK2206) ( 16 , 17 ) were obtained from Merck.

Techniques: Blocking Assay, Expressing, Inhibition

Consequence of differential AKT isoform inhibition in PTEN-mutant IGROV-1 cells. A, IGROV-1 cells (PTEN-null) were treated with 0–10 µM of either AKTi-1/2 or MK2206 and viable cells counted at days 3 and 5. B, Cell cycle distribution was determined by FACS for IGROV-1 cells treated with AKTi-1/2 or MK2206 (2 µM) for 24 h. C, Immunoblots following treatment of IGROV-1 cells with either 2 µM of AKTi-1/2 or MK2206 for 0–72 h. Lysates were probed for p-AKT (S473 and T308), pPRAS40 (T246) and cell cycle and translation regulators as indicated. D, Control siRNA (siNTp) or siRNA against individual AKT isoforms, alone or in combination, were transfected into IGROV-1 cells followed by incubation for 64 h. Cells were collected for FACS analysis (asterisks indicates p≤0.0015, n≥3) or subjected to immunoblotting.

Journal: Cancer discovery

Article Title: Genomic complexity and AKT dependence in serous ovarian cancer

doi: 10.1158/2159-8290.CD-11-0170

Figure Lengend Snippet: Consequence of differential AKT isoform inhibition in PTEN-mutant IGROV-1 cells. A, IGROV-1 cells (PTEN-null) were treated with 0–10 µM of either AKTi-1/2 or MK2206 and viable cells counted at days 3 and 5. B, Cell cycle distribution was determined by FACS for IGROV-1 cells treated with AKTi-1/2 or MK2206 (2 µM) for 24 h. C, Immunoblots following treatment of IGROV-1 cells with either 2 µM of AKTi-1/2 or MK2206 for 0–72 h. Lysates were probed for p-AKT (S473 and T308), pPRAS40 (T246) and cell cycle and translation regulators as indicated. D, Control siRNA (siNTp) or siRNA against individual AKT isoforms, alone or in combination, were transfected into IGROV-1 cells followed by incubation for 64 h. Cells were collected for FACS analysis (asterisks indicates p≤0.0015, n≥3) or subjected to immunoblotting.

Article Snippet: Cell Lines and Culture Conditions AKT1/2 inhibitor (AKTi-1/2, compound 17) ( 15 ) and pan-AKT1/2/3 inhibitor (MK2206) ( 16 , 17 ) were obtained from Merck.

Techniques: Inhibition, Mutagenesis, Western Blot, Transfection, Incubation

RAS/RAF pathway-activated ovarian cancer cells exhibit MEK dependence and synergistic induction of apoptosis with combined MEK/AKT inhibition. A, Levels of activated RAS (RAS-GTP) were determined by pulldown of GTP-bound RAS using recombinant RAS binding domain of RAF. Input lysates were also immunoblotted as shown. B, IC50/90 values for the allosteric inhibitor of MEK1/2, PD0325901 (PD901) were calculated following treatment with 0–500 nM of inhibitor for 5 days. Immunoblots for p-ERK and ERK following treatment with PD901 (50 nM) for 0–24 h. C, Induction of cell death following combined treatment with 50 nM PD901 and increasing doses of either AKTi-1/2 or MK2206 (2 or 10 µM) was measured by FACS analysis at 72 h in OVCAR-5 cells. Maximal cell death was induced following co-treatment with PD901 and MK2206 (asterisk indicates p ≤ 0.0287 vs. all other treatments, n ≥3). D, OVCAR-5 cells were treated with PD901 (50 nM) or MK2206 (10 µM) alone or in combination for 48 h and lysates immunoblotted.

Journal: Cancer discovery

Article Title: Genomic complexity and AKT dependence in serous ovarian cancer

doi: 10.1158/2159-8290.CD-11-0170

Figure Lengend Snippet: RAS/RAF pathway-activated ovarian cancer cells exhibit MEK dependence and synergistic induction of apoptosis with combined MEK/AKT inhibition. A, Levels of activated RAS (RAS-GTP) were determined by pulldown of GTP-bound RAS using recombinant RAS binding domain of RAF. Input lysates were also immunoblotted as shown. B, IC50/90 values for the allosteric inhibitor of MEK1/2, PD0325901 (PD901) were calculated following treatment with 0–500 nM of inhibitor for 5 days. Immunoblots for p-ERK and ERK following treatment with PD901 (50 nM) for 0–24 h. C, Induction of cell death following combined treatment with 50 nM PD901 and increasing doses of either AKTi-1/2 or MK2206 (2 or 10 µM) was measured by FACS analysis at 72 h in OVCAR-5 cells. Maximal cell death was induced following co-treatment with PD901 and MK2206 (asterisk indicates p ≤ 0.0287 vs. all other treatments, n ≥3). D, OVCAR-5 cells were treated with PD901 (50 nM) or MK2206 (10 µM) alone or in combination for 48 h and lysates immunoblotted.

Article Snippet: Cell Lines and Culture Conditions AKT1/2 inhibitor (AKTi-1/2, compound 17) ( 15 ) and pan-AKT1/2/3 inhibitor (MK2206) ( 16 , 17 ) were obtained from Merck.

Techniques: Inhibition, Recombinant, Binding Assay, Western Blot