akt inhibitor Search Results


akt kinase inhibitor  (MedChemExpress)
94
MedChemExpress akt kinase inhibitor
YTHDF2 regulated the activity of endometrial cell via targeting IRS1. ( A , B ) qRT-PCR and immunoblot analysis of IRS1 in HEC-1-A transfected with negative control (NC), IRS1 siRNA #1 or #2 as indicated for 48 h. ( C , E-H ) qRT-PCR analysis of MMP9 mRNA in HEC-1-A transfected with siRNA ( C,F ), plasmids ( E,G ) or treated with <t>AKT</t> <t>inhibitor</t> ( H ) as indicated, and stimulated with IGF for 6 h. ( D ) Immunoblot analysis of IRS1 in HEC-1-A transfected with the IRS1 plasmids for 48 h. ns: not significant; *p<0.05 (Student's t-test). Data are representative of three independent experiments (mean and s.d. of technical triplicates ( A,C,E-H ).
Akt Kinase Inhibitor, 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
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akt inhibitor rapamycin  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology akt inhibitor rapamycin
YTHDF2 regulated the activity of endometrial cell via targeting IRS1. ( A , B ) qRT-PCR and immunoblot analysis of IRS1 in HEC-1-A transfected with negative control (NC), IRS1 siRNA #1 or #2 as indicated for 48 h. ( C , E-H ) qRT-PCR analysis of MMP9 mRNA in HEC-1-A transfected with siRNA ( C,F ), plasmids ( E,G ) or treated with <t>AKT</t> <t>inhibitor</t> ( H ) as indicated, and stimulated with IGF for 6 h. ( D ) Immunoblot analysis of IRS1 in HEC-1-A transfected with the IRS1 plasmids for 48 h. ns: not significant; *p<0.05 (Student's t-test). Data are representative of three independent experiments (mean and s.d. of technical triplicates ( A,C,E-H ).
Akt Inhibitor Rapamycin, 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
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akt viii  (MedChemExpress)
96
MedChemExpress akt viii
RABV infection is mutually regulated with EGFR-Rac1 in the early stage. (A and B) After transfected with the WT or the DN mutant forms of Rho A, Rac1, or Cdc42 for 24 h, N2a cells were infected with CVS-11 (MOI = 10) for 1 h at 4°C ( A ) and then shifted to 37°C. At 0 h (binding) ( A ) or 2 h (entry) ( B ) p.i., the cell cultures were harvested, and the mRNA levels of RABV N and P were quantified. ( C–E ) N2a cells were, respectively, treated with increasing concentrations of <t>AKT</t> <t>VIII</t> (0, 2.5, 5, 10, and 20 µM) ( C ), Wortmannin (0, 1, 2, 5, and 10 µM) ( D ), or AG-1478 (0, 5, 10, 20, and 40 µM) ( E ). MTT assay was performed to exclude cytotoxic side effects upon drug treatment. ( F–M ) N2a cells were pretreated with indicated concentration of drugs, namely CCG-1423 (10 µM) ( C ), ML141 (8 µM) ( D ), NSC23766 (100 µM) ( E ), AKT VIII (20 µM) ( F ), Wortmannin (10 µM) ( G ), AG-1478 (40 µM) ( H ), Jasp (4 µM) ( I ), and Lat A (5 µM) ( J ), at 37°C for 1 h, inoculated with CVS-11 (MOI = 10) at 4°C for 1 h, and then shifted to 37°C. At 0 h (binding) or 2 h (entry) p.i., the cell cultures were harvested for RT-qPCR. ( K–M ) N2a cells were inoculated with CVS-11 (MOI = 10) at 4°C for 1 h and then transferred to 37°C for indicated time. Cells were lysed and processed for G-lisa assay to detect Rac1 activity ( K ). The p-EGFR, EGFR, p-PI3K, PI3K, p-Akt, Akt p-Pak1, Pak1, p-Limk1, Limk-1, p-Cofilin1, and Cofilin1 were immunoblotted ( L ). N2a cells were inoculated with CVS-11 (MOI = 10) at 1 h and then transferred to 37°C for 0, 30, 60, and 120 min p.i.. The F-actin and G-actin fractions were prepared and subjected to western blot analysis. G, G-actin from supernatant fraction; F, F-actin from pellet fraction ( M ). Results are represented as mean ± SD of three independent experiments. Statistical significances of the differences are indicated. Student’s t test, P < 0.05 (*); P < 0.01 (**); P < 0.001 (***).
Akt Viii, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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akt1 2 kinase inhibitor  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology akt1 2 kinase inhibitor
RABV infection is mutually regulated with EGFR-Rac1 in the early stage. (A and B) After transfected with the WT or the DN mutant forms of Rho A, Rac1, or Cdc42 for 24 h, N2a cells were infected with CVS-11 (MOI = 10) for 1 h at 4°C ( A ) and then shifted to 37°C. At 0 h (binding) ( A ) or 2 h (entry) ( B ) p.i., the cell cultures were harvested, and the mRNA levels of RABV N and P were quantified. ( C–E ) N2a cells were, respectively, treated with increasing concentrations of <t>AKT</t> <t>VIII</t> (0, 2.5, 5, 10, and 20 µM) ( C ), Wortmannin (0, 1, 2, 5, and 10 µM) ( D ), or AG-1478 (0, 5, 10, 20, and 40 µM) ( E ). MTT assay was performed to exclude cytotoxic side effects upon drug treatment. ( F–M ) N2a cells were pretreated with indicated concentration of drugs, namely CCG-1423 (10 µM) ( C ), ML141 (8 µM) ( D ), NSC23766 (100 µM) ( E ), AKT VIII (20 µM) ( F ), Wortmannin (10 µM) ( G ), AG-1478 (40 µM) ( H ), Jasp (4 µM) ( I ), and Lat A (5 µM) ( J ), at 37°C for 1 h, inoculated with CVS-11 (MOI = 10) at 4°C for 1 h, and then shifted to 37°C. At 0 h (binding) or 2 h (entry) p.i., the cell cultures were harvested for RT-qPCR. ( K–M ) N2a cells were inoculated with CVS-11 (MOI = 10) at 4°C for 1 h and then transferred to 37°C for indicated time. Cells were lysed and processed for G-lisa assay to detect Rac1 activity ( K ). The p-EGFR, EGFR, p-PI3K, PI3K, p-Akt, Akt p-Pak1, Pak1, p-Limk1, Limk-1, p-Cofilin1, and Cofilin1 were immunoblotted ( L ). N2a cells were inoculated with CVS-11 (MOI = 10) at 1 h and then transferred to 37°C for 0, 30, 60, and 120 min p.i.. The F-actin and G-actin fractions were prepared and subjected to western blot analysis. G, G-actin from supernatant fraction; F, F-actin from pellet fraction ( M ). Results are represented as mean ± SD of three independent experiments. Statistical significances of the differences are indicated. Student’s t test, P < 0.05 (*); P < 0.01 (**); P < 0.001 (***).
Akt1 2 Kinase Inhibitor, 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/akt+inhibitor/Akt1%2F2+kinase+Inhibitor/pmc06456923-129-5-66
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akt inhibitor iv  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology akt inhibitor iv
RABV infection is mutually regulated with EGFR-Rac1 in the early stage. (A and B) After transfected with the WT or the DN mutant forms of Rho A, Rac1, or Cdc42 for 24 h, N2a cells were infected with CVS-11 (MOI = 10) for 1 h at 4°C ( A ) and then shifted to 37°C. At 0 h (binding) ( A ) or 2 h (entry) ( B ) p.i., the cell cultures were harvested, and the mRNA levels of RABV N and P were quantified. ( C–E ) N2a cells were, respectively, treated with increasing concentrations of <t>AKT</t> <t>VIII</t> (0, 2.5, 5, 10, and 20 µM) ( C ), Wortmannin (0, 1, 2, 5, and 10 µM) ( D ), or AG-1478 (0, 5, 10, 20, and 40 µM) ( E ). MTT assay was performed to exclude cytotoxic side effects upon drug treatment. ( F–M ) N2a cells were pretreated with indicated concentration of drugs, namely CCG-1423 (10 µM) ( C ), ML141 (8 µM) ( D ), NSC23766 (100 µM) ( E ), AKT VIII (20 µM) ( F ), Wortmannin (10 µM) ( G ), AG-1478 (40 µM) ( H ), Jasp (4 µM) ( I ), and Lat A (5 µM) ( J ), at 37°C for 1 h, inoculated with CVS-11 (MOI = 10) at 4°C for 1 h, and then shifted to 37°C. At 0 h (binding) or 2 h (entry) p.i., the cell cultures were harvested for RT-qPCR. ( K–M ) N2a cells were inoculated with CVS-11 (MOI = 10) at 4°C for 1 h and then transferred to 37°C for indicated time. Cells were lysed and processed for G-lisa assay to detect Rac1 activity ( K ). The p-EGFR, EGFR, p-PI3K, PI3K, p-Akt, Akt p-Pak1, Pak1, p-Limk1, Limk-1, p-Cofilin1, and Cofilin1 were immunoblotted ( L ). N2a cells were inoculated with CVS-11 (MOI = 10) at 1 h and then transferred to 37°C for 0, 30, 60, and 120 min p.i.. The F-actin and G-actin fractions were prepared and subjected to western blot analysis. G, G-actin from supernatant fraction; F, F-actin from pellet fraction ( M ). Results are represented as mean ± SD of three independent experiments. Statistical significances of the differences are indicated. Student’s t test, P < 0.05 (*); P < 0.01 (**); P < 0.001 (***).
Akt Inhibitor Iv, 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/akt+inhibitor/Akt+Inhibitor+IV/pm23886627-27-2-8
Average 93 stars, based on 1 article reviews
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akt inhibitor x  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology akt inhibitor x
RABV infection is mutually regulated with EGFR-Rac1 in the early stage. (A and B) After transfected with the WT or the DN mutant forms of Rho A, Rac1, or Cdc42 for 24 h, N2a cells were infected with CVS-11 (MOI = 10) for 1 h at 4°C ( A ) and then shifted to 37°C. At 0 h (binding) ( A ) or 2 h (entry) ( B ) p.i., the cell cultures were harvested, and the mRNA levels of RABV N and P were quantified. ( C–E ) N2a cells were, respectively, treated with increasing concentrations of <t>AKT</t> <t>VIII</t> (0, 2.5, 5, 10, and 20 µM) ( C ), Wortmannin (0, 1, 2, 5, and 10 µM) ( D ), or AG-1478 (0, 5, 10, 20, and 40 µM) ( E ). MTT assay was performed to exclude cytotoxic side effects upon drug treatment. ( F–M ) N2a cells were pretreated with indicated concentration of drugs, namely CCG-1423 (10 µM) ( C ), ML141 (8 µM) ( D ), NSC23766 (100 µM) ( E ), AKT VIII (20 µM) ( F ), Wortmannin (10 µM) ( G ), AG-1478 (40 µM) ( H ), Jasp (4 µM) ( I ), and Lat A (5 µM) ( J ), at 37°C for 1 h, inoculated with CVS-11 (MOI = 10) at 4°C for 1 h, and then shifted to 37°C. At 0 h (binding) or 2 h (entry) p.i., the cell cultures were harvested for RT-qPCR. ( K–M ) N2a cells were inoculated with CVS-11 (MOI = 10) at 4°C for 1 h and then transferred to 37°C for indicated time. Cells were lysed and processed for G-lisa assay to detect Rac1 activity ( K ). The p-EGFR, EGFR, p-PI3K, PI3K, p-Akt, Akt p-Pak1, Pak1, p-Limk1, Limk-1, p-Cofilin1, and Cofilin1 were immunoblotted ( L ). N2a cells were inoculated with CVS-11 (MOI = 10) at 1 h and then transferred to 37°C for 0, 30, 60, and 120 min p.i.. The F-actin and G-actin fractions were prepared and subjected to western blot analysis. G, G-actin from supernatant fraction; F, F-actin from pellet fraction ( M ). Results are represented as mean ± SD of three independent experiments. Statistical significances of the differences are indicated. Student’s t test, P < 0.05 (*); P < 0.01 (**); P < 0.001 (***).
Akt Inhibitor X, 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
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akt inhibitor viii  (Santa Cruz Biotechnology)
94
Santa Cruz Biotechnology akt inhibitor viii
Activation of PI3K and Akt pathway and its role in FMRP production and cell viability . ETO-treated HeLa cells were analyzed using Western blot to investigate the activation of PI3K (A) and Akt (B). Western blot against total protein was used as a loading control. (C) An inhibitor of Akt phosphorylation, LY294002 (10 μM, LY) was pretreated and the level of FMRP was determined by Western blot. (D) After LY treatment, cell viability was measured by MTT assay, inhibition of Akt phosphorylation further decreased cell viability. (E) The level of BcL-xL after LY treatment. Increased BcL-xL expression induced <t>by</t> <t>etoposide</t> treatment was prevented by LY294002 treatment. (F) Another inhibitor of Akt, inhibitor <t>VIII</t> (0, 5, 10 μM, VIII) pretreatment also decreased activity and expression of Akt and Bcl-xL, respectively, in a concentration dependent manner. At the same time, cellular viability was also reduced by VIII treatment. The bar graphs represent the quantification of band intensity. Data represent mean ± S.E.M. * significantly different as compared with control and # significantly different as compared with ETO alone treated sample (p < 0.01, n = 4).
Akt Inhibitor Viii, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pi3k inhibitor  (Selleck Chemicals)
95
Selleck Chemicals pi3k inhibitor
SERPIND1 regulated the EMT of ovarian cancer cells via the <t>PI3K/AKT</t> pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Pi3k Inhibitor, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/akt+inhibitor/PI3K%2FAkt+Inhibitor+Library/pmc06788328-98-10-15
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hy 19712 akt inhibitor iv tocris  (Tocris)
93
Tocris hy 19712 akt inhibitor iv tocris
SERPIND1 regulated the EMT of ovarian cancer cells via the <t>PI3K/AKT</t> pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Hy 19712 Akt Inhibitor Iv Tocris, supplied by Tocris, 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/akt+inhibitor/AKT+Inhibitor+IV/pm37683605-579-262-266
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cells  (Novus Biologicals)
90
Novus Biologicals cells
SERPIND1 regulated the EMT of ovarian cancer cells via the <t>PI3K/AKT</t> pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Cells, supplied by Novus Biologicals, 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/akt+inhibitor/AKT1%2F2%2F3+Inhibitor+Peptide+Set/pm29928668-77-4-15
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cells - by Bioz Stars, 2026-09
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pi3k akt mtor pathway inhibitor  (Selleck Chemicals)
92
Selleck Chemicals pi3k akt mtor pathway inhibitor
SERPIND1 regulated the EMT of ovarian cancer cells via the <t>PI3K/AKT</t> pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Pi3k Akt Mtor Pathway Inhibitor, supplied by Selleck Chemicals, 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/akt+inhibitor/PI3K%2FAkt%2FmTOR+Pathway+Inhibitor+Kit/pmc08290725-88-84-88
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akt inhibitor xi  (Santa Cruz Biotechnology)
86
Santa Cruz Biotechnology akt inhibitor xi
SERPIND1 regulated the EMT of ovarian cancer cells via the <t>PI3K/AKT</t> pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.
Akt Inhibitor Xi, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


YTHDF2 regulated the activity of endometrial cell via targeting IRS1. ( A , B ) qRT-PCR and immunoblot analysis of IRS1 in HEC-1-A transfected with negative control (NC), IRS1 siRNA #1 or #2 as indicated for 48 h. ( C , E-H ) qRT-PCR analysis of MMP9 mRNA in HEC-1-A transfected with siRNA ( C,F ), plasmids ( E,G ) or treated with AKT inhibitor ( H ) as indicated, and stimulated with IGF for 6 h. ( D ) Immunoblot analysis of IRS1 in HEC-1-A transfected with the IRS1 plasmids for 48 h. ns: not significant; *p<0.05 (Student's t-test). Data are representative of three independent experiments (mean and s.d. of technical triplicates ( A,C,E-H ).

Journal: Journal of Cancer

Article Title: YTHDF2 inhibit the tumorigenicity of endometrial cancer via downregulating the expression of IRS1 methylated with m 6 A

doi: 10.7150/jca.54527

Figure Lengend Snippet: YTHDF2 regulated the activity of endometrial cell via targeting IRS1. ( A , B ) qRT-PCR and immunoblot analysis of IRS1 in HEC-1-A transfected with negative control (NC), IRS1 siRNA #1 or #2 as indicated for 48 h. ( C , E-H ) qRT-PCR analysis of MMP9 mRNA in HEC-1-A transfected with siRNA ( C,F ), plasmids ( E,G ) or treated with AKT inhibitor ( H ) as indicated, and stimulated with IGF for 6 h. ( D ) Immunoblot analysis of IRS1 in HEC-1-A transfected with the IRS1 plasmids for 48 h. ns: not significant; *p<0.05 (Student's t-test). Data are representative of three independent experiments (mean and s.d. of technical triplicates ( A,C,E-H ).

Article Snippet: AKT kinase inhibitor (HY-10249A) was from MCE (USA).

Techniques: Activity Assay, Quantitative RT-PCR, Western Blot, Transfection, Negative Control

RABV infection is mutually regulated with EGFR-Rac1 in the early stage. (A and B) After transfected with the WT or the DN mutant forms of Rho A, Rac1, or Cdc42 for 24 h, N2a cells were infected with CVS-11 (MOI = 10) for 1 h at 4°C ( A ) and then shifted to 37°C. At 0 h (binding) ( A ) or 2 h (entry) ( B ) p.i., the cell cultures were harvested, and the mRNA levels of RABV N and P were quantified. ( C–E ) N2a cells were, respectively, treated with increasing concentrations of AKT VIII (0, 2.5, 5, 10, and 20 µM) ( C ), Wortmannin (0, 1, 2, 5, and 10 µM) ( D ), or AG-1478 (0, 5, 10, 20, and 40 µM) ( E ). MTT assay was performed to exclude cytotoxic side effects upon drug treatment. ( F–M ) N2a cells were pretreated with indicated concentration of drugs, namely CCG-1423 (10 µM) ( C ), ML141 (8 µM) ( D ), NSC23766 (100 µM) ( E ), AKT VIII (20 µM) ( F ), Wortmannin (10 µM) ( G ), AG-1478 (40 µM) ( H ), Jasp (4 µM) ( I ), and Lat A (5 µM) ( J ), at 37°C for 1 h, inoculated with CVS-11 (MOI = 10) at 4°C for 1 h, and then shifted to 37°C. At 0 h (binding) or 2 h (entry) p.i., the cell cultures were harvested for RT-qPCR. ( K–M ) N2a cells were inoculated with CVS-11 (MOI = 10) at 4°C for 1 h and then transferred to 37°C for indicated time. Cells were lysed and processed for G-lisa assay to detect Rac1 activity ( K ). The p-EGFR, EGFR, p-PI3K, PI3K, p-Akt, Akt p-Pak1, Pak1, p-Limk1, Limk-1, p-Cofilin1, and Cofilin1 were immunoblotted ( L ). N2a cells were inoculated with CVS-11 (MOI = 10) at 1 h and then transferred to 37°C for 0, 30, 60, and 120 min p.i.. The F-actin and G-actin fractions were prepared and subjected to western blot analysis. G, G-actin from supernatant fraction; F, F-actin from pellet fraction ( M ). Results are represented as mean ± SD of three independent experiments. Statistical significances of the differences are indicated. Student’s t test, P < 0.05 (*); P < 0.01 (**); P < 0.001 (***).

Journal: Journal of Virology

Article Title: RABV induces biphasic actin cytoskeletal rearrangement through Rac1 activity modulation

doi: 10.1128/jvi.00606-24

Figure Lengend Snippet: RABV infection is mutually regulated with EGFR-Rac1 in the early stage. (A and B) After transfected with the WT or the DN mutant forms of Rho A, Rac1, or Cdc42 for 24 h, N2a cells were infected with CVS-11 (MOI = 10) for 1 h at 4°C ( A ) and then shifted to 37°C. At 0 h (binding) ( A ) or 2 h (entry) ( B ) p.i., the cell cultures were harvested, and the mRNA levels of RABV N and P were quantified. ( C–E ) N2a cells were, respectively, treated with increasing concentrations of AKT VIII (0, 2.5, 5, 10, and 20 µM) ( C ), Wortmannin (0, 1, 2, 5, and 10 µM) ( D ), or AG-1478 (0, 5, 10, 20, and 40 µM) ( E ). MTT assay was performed to exclude cytotoxic side effects upon drug treatment. ( F–M ) N2a cells were pretreated with indicated concentration of drugs, namely CCG-1423 (10 µM) ( C ), ML141 (8 µM) ( D ), NSC23766 (100 µM) ( E ), AKT VIII (20 µM) ( F ), Wortmannin (10 µM) ( G ), AG-1478 (40 µM) ( H ), Jasp (4 µM) ( I ), and Lat A (5 µM) ( J ), at 37°C for 1 h, inoculated with CVS-11 (MOI = 10) at 4°C for 1 h, and then shifted to 37°C. At 0 h (binding) or 2 h (entry) p.i., the cell cultures were harvested for RT-qPCR. ( K–M ) N2a cells were inoculated with CVS-11 (MOI = 10) at 4°C for 1 h and then transferred to 37°C for indicated time. Cells were lysed and processed for G-lisa assay to detect Rac1 activity ( K ). The p-EGFR, EGFR, p-PI3K, PI3K, p-Akt, Akt p-Pak1, Pak1, p-Limk1, Limk-1, p-Cofilin1, and Cofilin1 were immunoblotted ( L ). N2a cells were inoculated with CVS-11 (MOI = 10) at 1 h and then transferred to 37°C for 0, 30, 60, and 120 min p.i.. The F-actin and G-actin fractions were prepared and subjected to western blot analysis. G, G-actin from supernatant fraction; F, F-actin from pellet fraction ( M ). Results are represented as mean ± SD of three independent experiments. Statistical significances of the differences are indicated. Student’s t test, P < 0.05 (*); P < 0.01 (**); P < 0.001 (***).

Article Snippet: Latrunculin A (Lat A; ab144290, Abcam), Jasplakinolide (Jasp; 141409, Abcam), CCG-1423(S7719, Selleck), ML141(HY-12755, MCE), AG-1478 (HY-13524, MCE), Wortmannin (HY-10197, MCE), AKT VIII (HY-10355, MCE), NSC23766 (S8031, Selleck), and IPA-3 (HY-15663, MCE) were employed.

Techniques: Infection, Transfection, Mutagenesis, Binding Assay, MTT Assay, Concentration Assay, Quantitative RT-PCR, Activity Assay, Western Blot

Activation of PI3K and Akt pathway and its role in FMRP production and cell viability . ETO-treated HeLa cells were analyzed using Western blot to investigate the activation of PI3K (A) and Akt (B). Western blot against total protein was used as a loading control. (C) An inhibitor of Akt phosphorylation, LY294002 (10 μM, LY) was pretreated and the level of FMRP was determined by Western blot. (D) After LY treatment, cell viability was measured by MTT assay, inhibition of Akt phosphorylation further decreased cell viability. (E) The level of BcL-xL after LY treatment. Increased BcL-xL expression induced by etoposide treatment was prevented by LY294002 treatment. (F) Another inhibitor of Akt, inhibitor VIII (0, 5, 10 μM, VIII) pretreatment also decreased activity and expression of Akt and Bcl-xL, respectively, in a concentration dependent manner. At the same time, cellular viability was also reduced by VIII treatment. The bar graphs represent the quantification of band intensity. Data represent mean ± S.E.M. * significantly different as compared with control and # significantly different as compared with ETO alone treated sample (p < 0.01, n = 4).

Journal: Journal of Biomedical Science

Article Title: Cellular stress-induced up-regulation of FMRP promotes cell survival by modulating PI3K-Akt phosphorylation cascades

doi: 10.1186/1423-0127-18-17

Figure Lengend Snippet: Activation of PI3K and Akt pathway and its role in FMRP production and cell viability . ETO-treated HeLa cells were analyzed using Western blot to investigate the activation of PI3K (A) and Akt (B). Western blot against total protein was used as a loading control. (C) An inhibitor of Akt phosphorylation, LY294002 (10 μM, LY) was pretreated and the level of FMRP was determined by Western blot. (D) After LY treatment, cell viability was measured by MTT assay, inhibition of Akt phosphorylation further decreased cell viability. (E) The level of BcL-xL after LY treatment. Increased BcL-xL expression induced by etoposide treatment was prevented by LY294002 treatment. (F) Another inhibitor of Akt, inhibitor VIII (0, 5, 10 μM, VIII) pretreatment also decreased activity and expression of Akt and Bcl-xL, respectively, in a concentration dependent manner. At the same time, cellular viability was also reduced by VIII treatment. The bar graphs represent the quantification of band intensity. Data represent mean ± S.E.M. * significantly different as compared with control and # significantly different as compared with ETO alone treated sample (p < 0.01, n = 4).

Article Snippet: To verify the role of Akt pathway in the regulation of FMRP induction and cell survival in etoposide treated cells, we used another inhibitor of Akt such as Akt inhibitor VIII (sc-202048, Santa Cruz Biotechnology, CA, USA) before etoposide treatment (Figure ).

Techniques: Activation Assay, Western Blot, Control, Phospho-proteomics, MTT Assay, Inhibition, Expressing, Activity Assay, Concentration Assay

The potentiation of PI3K-Akt phosphorylation and Bcl-xL expression by the overexpression of FMRP . Cells transfected with wither eGFP- or eGFP-FMRP were treated with ETO (20 μM, 3 hr) and analyzed using Western blot. ETO-induced PI3K (A) and Akt (B) phosphorylation as well as Bcl-xL (C) expression were potentiated as compared with control. * significantly different as compared with control, # significantly different as compared with eGFP transfected cells. (D) A specific Akt inhibitor VIII reduced activation of Akt as well as induction of Bcl-xL in a concentration dependent manner. Graphs represent the densitometric quantification of the band intensity. * significantly different as compared with ETO treated cells, # significantly different as compared with eGFP transfected cells (p < 0.01, n = 4). eGFP denotes HeLa cells transfected with eGFP-empty vector, eGFP-FMRP indicates cells transfected with eGFP-FMRP vector.

Journal: Journal of Biomedical Science

Article Title: Cellular stress-induced up-regulation of FMRP promotes cell survival by modulating PI3K-Akt phosphorylation cascades

doi: 10.1186/1423-0127-18-17

Figure Lengend Snippet: The potentiation of PI3K-Akt phosphorylation and Bcl-xL expression by the overexpression of FMRP . Cells transfected with wither eGFP- or eGFP-FMRP were treated with ETO (20 μM, 3 hr) and analyzed using Western blot. ETO-induced PI3K (A) and Akt (B) phosphorylation as well as Bcl-xL (C) expression were potentiated as compared with control. * significantly different as compared with control, # significantly different as compared with eGFP transfected cells. (D) A specific Akt inhibitor VIII reduced activation of Akt as well as induction of Bcl-xL in a concentration dependent manner. Graphs represent the densitometric quantification of the band intensity. * significantly different as compared with ETO treated cells, # significantly different as compared with eGFP transfected cells (p < 0.01, n = 4). eGFP denotes HeLa cells transfected with eGFP-empty vector, eGFP-FMRP indicates cells transfected with eGFP-FMRP vector.

Article Snippet: To verify the role of Akt pathway in the regulation of FMRP induction and cell survival in etoposide treated cells, we used another inhibitor of Akt such as Akt inhibitor VIII (sc-202048, Santa Cruz Biotechnology, CA, USA) before etoposide treatment (Figure ).

Techniques: Phospho-proteomics, Expressing, Over Expression, Transfection, Western Blot, Control, Activation Assay, Concentration Assay, Plasmid Preparation

Akt activation is necessary for the pro-survival effects of FMRP overexpression in ETO treated HeLa cells . Cells transfected with wither eGFP- or eGFP-FMRP were incubated with Akt inhibitor VIII (10 μM, 1 hr) before ETO (20 μM, 3 hr) treatment and analyzed by PI staining. (A) Red fluorescence represents PI positive cells and green fluorescence represents GFP positive cells. White arrows indicate yellow spots which represent double positive for PI and GFP. (B) Graphs represent the quantification of the PI/GFP double-positive cell number. * significantly different as compared with eGFP transfected cells, # significantly different as compared with ETO treated HeLa cells (p < 0.01, n = 4). eGFP denotes HeLa cells transfected with eGFP-empty vector, eGFP-FMRP indicates cells transfected with eGFP-FMRP vector.

Journal: Journal of Biomedical Science

Article Title: Cellular stress-induced up-regulation of FMRP promotes cell survival by modulating PI3K-Akt phosphorylation cascades

doi: 10.1186/1423-0127-18-17

Figure Lengend Snippet: Akt activation is necessary for the pro-survival effects of FMRP overexpression in ETO treated HeLa cells . Cells transfected with wither eGFP- or eGFP-FMRP were incubated with Akt inhibitor VIII (10 μM, 1 hr) before ETO (20 μM, 3 hr) treatment and analyzed by PI staining. (A) Red fluorescence represents PI positive cells and green fluorescence represents GFP positive cells. White arrows indicate yellow spots which represent double positive for PI and GFP. (B) Graphs represent the quantification of the PI/GFP double-positive cell number. * significantly different as compared with eGFP transfected cells, # significantly different as compared with ETO treated HeLa cells (p < 0.01, n = 4). eGFP denotes HeLa cells transfected with eGFP-empty vector, eGFP-FMRP indicates cells transfected with eGFP-FMRP vector.

Article Snippet: To verify the role of Akt pathway in the regulation of FMRP induction and cell survival in etoposide treated cells, we used another inhibitor of Akt such as Akt inhibitor VIII (sc-202048, Santa Cruz Biotechnology, CA, USA) before etoposide treatment (Figure ).

Techniques: Activation Assay, Over Expression, Transfection, Incubation, Staining, Fluorescence, Plasmid Preparation

SERPIND1 regulated the EMT of ovarian cancer cells via the PI3K/AKT pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.

Journal: Frontiers in Oncology

Article Title: SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study

doi: 10.3389/fonc.2019.00954

Figure Lengend Snippet: SERPIND1 regulated the EMT of ovarian cancer cells via the PI3K/AKT pathway. (A) SERPIND1 overexpression in ES-2 cells resulted in a significant reduction in E-cadherin expression and increased expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (B) Inhibition of SERPIND1 expression in CAOV3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. (C) Inhibition of SERPIND1 expression in OVCAR3 cells resulted in increased E-cadherin expression and reduced expressions of N-cadherin, Vimentin, MMP2, MMP9, p-PI3K, and p-AKT. SERPIND1, serpin family D member 1; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B.

Article Snippet: To inhibit PI3K/AKT signaling, the cells were treated with a PI3K inhibitor, LY294002 (10 μM; Selleck, Houston, USA) for 48 h.

Techniques: Over Expression, Expressing, Inhibition

The transcription factor NF-κB1 could regulate SERPIND1 expression, which in turn could activate the PI3K/AKT signaling pathway. (A) The PI3K/AKT pathway inhibitor LY294002 inhibited the promoting effect of SERPIND1 on the migration capacity of ovarian cancer cells. (B) LY294002 inhibited the promoting effect of SERPIND1 on the invasion capacity of ovarian cancer cells. (C) After the addition of LY294002, the SERPIND1-overexpressing ES-2 cells exhibited a reduced proportion of S-phase cells. (D) LY294002 inhibited the promoting effect of SERPIND1 on the proliferation capacity of ovarian cancer cells. (E) After the addition of LY294002, the SERPIND1-overexpressing ES-2 cells exhibited a significantly increased apoptotic rate. (F) A schematic diagram showing the proposed mechanism of NF-κB1 binding to the promoter region of SERPIND1. (G) NF-κB1 could bind to the promoter region of SERPIND1 at the −258 to −248 (GGTGTTTTCCA) and +131 to +141 (AGGCCTTCCTC) loci. (H) After inhibiting NF-κB1 expression, SERPIND1 expression was also reduced. Data are presented as mean ± standard deviation from three independent experiments. * P < 0.05. Scale bar: 100 μm. NF-κB1, nuclear factor kappa B1; SERPIND1, serpin family D member 1.

Journal: Frontiers in Oncology

Article Title: SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study

doi: 10.3389/fonc.2019.00954

Figure Lengend Snippet: The transcription factor NF-κB1 could regulate SERPIND1 expression, which in turn could activate the PI3K/AKT signaling pathway. (A) The PI3K/AKT pathway inhibitor LY294002 inhibited the promoting effect of SERPIND1 on the migration capacity of ovarian cancer cells. (B) LY294002 inhibited the promoting effect of SERPIND1 on the invasion capacity of ovarian cancer cells. (C) After the addition of LY294002, the SERPIND1-overexpressing ES-2 cells exhibited a reduced proportion of S-phase cells. (D) LY294002 inhibited the promoting effect of SERPIND1 on the proliferation capacity of ovarian cancer cells. (E) After the addition of LY294002, the SERPIND1-overexpressing ES-2 cells exhibited a significantly increased apoptotic rate. (F) A schematic diagram showing the proposed mechanism of NF-κB1 binding to the promoter region of SERPIND1. (G) NF-κB1 could bind to the promoter region of SERPIND1 at the −258 to −248 (GGTGTTTTCCA) and +131 to +141 (AGGCCTTCCTC) loci. (H) After inhibiting NF-κB1 expression, SERPIND1 expression was also reduced. Data are presented as mean ± standard deviation from three independent experiments. * P < 0.05. Scale bar: 100 μm. NF-κB1, nuclear factor kappa B1; SERPIND1, serpin family D member 1.

Article Snippet: To inhibit PI3K/AKT signaling, the cells were treated with a PI3K inhibitor, LY294002 (10 μM; Selleck, Houston, USA) for 48 h.

Techniques: Expressing, Migration, Binding Assay, Standard Deviation

Schematic model showing: When the cells are subjected to external stimuli, NF-κB1 could enter the nucleus and exert its transcription factor function. The transcription factor NF-κB1 could bind to the promoter region of SERPIND1 and regulate SERPIND1 expression, which in turn could affect the PI3K/AKT pathway and promote the malignant biological behavior of ovarian cancer cells.

Journal: Frontiers in Oncology

Article Title: SERPIND1 Affects the Malignant Biological Behavior of Epithelial Ovarian Cancer via the PI3K/AKT Pathway: A Mechanistic Study

doi: 10.3389/fonc.2019.00954

Figure Lengend Snippet: Schematic model showing: When the cells are subjected to external stimuli, NF-κB1 could enter the nucleus and exert its transcription factor function. The transcription factor NF-κB1 could bind to the promoter region of SERPIND1 and regulate SERPIND1 expression, which in turn could affect the PI3K/AKT pathway and promote the malignant biological behavior of ovarian cancer cells.

Article Snippet: To inhibit PI3K/AKT signaling, the cells were treated with a PI3K inhibitor, LY294002 (10 μM; Selleck, Houston, USA) for 48 h.

Techniques: Expressing