pf-573228 Search Results


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(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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ApexBio fak inhibitors pf-562271
(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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ChemScene llc fak inhibitor pf- 573228
(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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Merck KGaA emd57970
(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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Topscience Co Ltd pf-573228
(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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Beyotime p-fak inhibitor pf-573228
(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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Absource Diagnostics GmbH fak inhibitor pf573228
(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor <t>PF573228,</t> the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.
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Image Search Results


(A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor PF573228, the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.

Journal: Oncogene

Article Title: Integrin β5 contributes to the tumorigenic potential of breast cancer cells through Src-FAK and MEK-ERK signaling pathways

doi: 10.1038/onc.2012.320

Figure Lengend Snippet: (A) Anchorage-independent growth analysis of MDA-MB-231 cells treated with the FAK inhibitor PF573228, the Src inhibitor Dasatinib, or the MEK inhibitor U0126 at the indicated concentration. Statistical analysis by Student t -Test is provided (* p < 0.05; ** p <0.001). (B) MDA-MB-231 cells were treated with the FAK inhibitor PF573228 or the MEK inhibitor U0126 for 24h at the indicated concentrations. Immunoblotting was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, ERK1/2, and phospho-ERK1/2. (C) Immunoblot analysis of whole-cell protein extracts from control and siRNA to FAK treated MDA-MB-231 cells that were treated with 2ng/ml TGF-β1 for 2h and 24h. Membranes were probed with antibodies for FAK, phospho-Smad2, Smad2, phospho-ERK1/2, and GAPDH as loading control. (D) MDA-MB-231 cells were treated with the Src inhibitor Dasatinib at 100nM for the indicated times. Immunoblot analysis was performed on whole-cell extracts probing for FAK, phospho-FAK-Tyr397, phospho-FAK-Tyr861, phospho-FAK-Tyr925, phospho-paxillin-Tyr31, paxillin, ERK1/2, phospho-ERK1/2 and α-tubulin.

Article Snippet: The FAK inhibitor PF573228 was from Tocris (Ellisville, MO); U0126 and AG1478 were from EMD Bioscience-Calbiochem (La Jolla, CA); Dasatinib was a gift of Dr. Yahao Bu (Kinex Pharmaceutical, Buffalo, NY).

Techniques: Concentration Assay, Western Blot, Control