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aag treatments  (MedChemExpress)


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    MedChemExpress aag treatments
    Aag Treatments, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 96/100, based on 96 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/aag+treatments/Tanespimycin/pmc12907857-248-1-13
    Average 96 stars, based on 96 article reviews
    aag treatments - by Bioz Stars, 2026-09
    96/100 stars

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    Isolation:

    Article Title: Large extracellular vesicles regulate endothelial angiogenic potential via paracrine and autocrine signaling.
    Article Snippet: For assays involving MIF neutralization, endothelial cells were incubated with isolated L-EVs, media was replaced and conditioned media was collected after 48 hours and used in combination with MIF neutralizing antibody (5g/mL; R&D Systems) in tube assays. .. For 17-AAG treatments, LOX cells were treated with 17-AAG inhibitor (500nM-1M; MCE) or an equivalent amount of DMSO in EV-free media and cells were allowed to shed for 24 hours before L-EV isolation. ..

    Article Title: Large extracellular vesicles regulate endothelial angiogenic potential via paracrine and autocrine signaling
    Article Snippet: For assays involving MIF neutralization, ECs were incubated with isolated L-EVs, media were replaced, and conditioned media were collected after 48 h and used in combination with MIF-neutralizing antibody (5 μg/ml; R&D Systems) in tube assays. .. For 17-AAG treatments, LOX cells were treated with 17-AAG inhibitor (500 nM–1 μM; MCE) or an equivalent amount of dimethyl sulfoxide in EV-free media, and cells were allowed to shed for 24 h before L-EV isolation. ..

    Article Title: Large extracellular vesicles regulate endothelial angiogenic potential via paracrine and autocrine signaling
    Article Snippet: For assays involving MIF neutralization, endothelial cells were incubated with isolated L-EVs, media was replaced and conditioned media was collected after 48 hours and used in combination with MIF neutralizing antibody (5μg/mL; R&D Systems) in tube assays. .. For 17-AAG treatments, LOX cells were treated with 17-AAG inhibitor (500nM-1μM; MCE) or an equivalent amount of DMSO in EV-free media and cells were allowed to shed for 24 hours before L-EV isolation. ..



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    aag treatments  (MedChemExpress)
    96
    MedChemExpress aag treatments
    Aag Treatments, 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
    https://www.bioz.com/product/aag+treatments/Tanespimycin/pmc12907857-248-1-13
    Average 96 stars, based on 1 article reviews
    aag treatments - by Bioz Stars, 2026-09
    96/100 stars
    		  Buy from Supplier
    aag treatment  (Cell Signaling Technology Inc)
    92
    Cell Signaling Technology Inc aag treatment
    Effects of c-Met TKI and Hsp90 inhibitor on induction of apoptosis. (A) H1993 cells were treated with SU11274 (2.5 μM) or <t>17-AAG</t> (0.5 μM) for the indicated times, and analyzed by immunoblotting using PARP antibody (lower band represents the cleaved PARP) and cleaved Caspase-3 antibody. α-tubulin was used as a loading control. (B) H1993 cells were treated with SU11274 or 17-AAG for the indicated times. Cells were stained with propidium iodide, and the extent of apoptosis was calculated as described in Methods.
    Aag Treatment, supplied by Cell Signaling Technology Inc, 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/aag+treatments/17-AAG/pmc07282701-99-4-42
    Average 92 stars, based on 1 article reviews
    aag treatment - by Bioz Stars, 2026-09
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    Effects of c-Met TKI and Hsp90 inhibitor on induction of apoptosis. (A) H1993 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using PARP antibody (lower band represents the cleaved PARP) and cleaved Caspase-3 antibody. α-tubulin was used as a loading control. (B) H1993 cells were treated with SU11274 or 17-AAG for the indicated times. Cells were stained with propidium iodide, and the extent of apoptosis was calculated as described in Methods.

    Journal: Cell cycle (Georgetown, Tex.)

    Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

    doi: 10.4161/cc.8.13.8861

    Figure Lengend Snippet: Effects of c-Met TKI and Hsp90 inhibitor on induction of apoptosis. (A) H1993 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using PARP antibody (lower band represents the cleaved PARP) and cleaved Caspase-3 antibody. α-tubulin was used as a loading control. (B) H1993 cells were treated with SU11274 or 17-AAG for the indicated times. Cells were stained with propidium iodide, and the extent of apoptosis was calculated as described in Methods.

    Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

    Techniques: Western Blot, Staining

    Effects of c-Met TKI and Hsp90 inhibitor on Akt and Erk signaling. H1993 cells were treated with SU11274 or 17-AAG for the indicated times and lysates were immunoblotted as shown. ‘C’ = untreated cells.

    Journal: Cell cycle (Georgetown, Tex.)

    Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

    doi: 10.4161/cc.8.13.8861

    Figure Lengend Snippet: Effects of c-Met TKI and Hsp90 inhibitor on Akt and Erk signaling. H1993 cells were treated with SU11274 or 17-AAG for the indicated times and lysates were immunoblotted as shown. ‘C’ = untreated cells.

    Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

    Techniques:

    Involvement of PKC δ in the reactivation of EGFR family members and downstream Akt and Erk signaling following prolonged c-Met TKI treatment. (A) H1993 cells were treated with SU11274 or 17-AAG for the indicated times and analyzed by immunoblotting using anti-PKC δ or anti-PKC δ (pS664) antibodies. Tubulin was used as a loading control. (B) H1993 cells were treated with SU1274 for 4 h (lane 2) or 48 h (lane 3–6). CI-1033 (1.5 μM, lane 4), rottlerin (10 μM, lane 5), or GO6976 (10 μM, lane 6) were added 4 hours before the cells were harvested. Untreated (lane 1) or treated cells were analyzed by immunobloting with the indicated antibodies. (C) H1993 cells were incubated continuously with DMSO (◆), CI-1033 (1.5 μM, ∎), SU11274 (2.5 μM, ▴), 17-AAG (0.5 μM, *), SU11274 and CI-1033 (◻), or SU11274 and rottlerin (1 μM, ▵). Cell density was monitored for 6 consecutive days by MTS assay. Each point represents the mean of 4 determinations; error bars, SD.

    Journal: Cell cycle (Georgetown, Tex.)

    Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

    doi: 10.4161/cc.8.13.8861

    Figure Lengend Snippet: Involvement of PKC δ in the reactivation of EGFR family members and downstream Akt and Erk signaling following prolonged c-Met TKI treatment. (A) H1993 cells were treated with SU11274 or 17-AAG for the indicated times and analyzed by immunoblotting using anti-PKC δ or anti-PKC δ (pS664) antibodies. Tubulin was used as a loading control. (B) H1993 cells were treated with SU1274 for 4 h (lane 2) or 48 h (lane 3–6). CI-1033 (1.5 μM, lane 4), rottlerin (10 μM, lane 5), or GO6976 (10 μM, lane 6) were added 4 hours before the cells were harvested. Untreated (lane 1) or treated cells were analyzed by immunobloting with the indicated antibodies. (C) H1993 cells were incubated continuously with DMSO (◆), CI-1033 (1.5 μM, ∎), SU11274 (2.5 μM, ▴), 17-AAG (0.5 μM, *), SU11274 and CI-1033 (◻), or SU11274 and rottlerin (1 μM, ▵). Cell density was monitored for 6 consecutive days by MTS assay. Each point represents the mean of 4 determinations; error bars, SD.

    Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

    Techniques: Western Blot, Incubation, MTS Assay

    Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5). Rottlerin (10 μM) was added for 4 h (lane 4) or 96 h (lane 5). Cell lysates were analyzed by immunobloting with the indicated antibodies. (C) MKN45 cells were incubated continuously with DMSO (◆), SU11274 (▴), 17-AAG (◻) or SU11274 and rottlerin (*), and cell proliferation was monitored by MTS assay. Each point represents the mean of 4 determinations; error bars, SD.

    Journal: Cell cycle (Georgetown, Tex.)

    Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors

    doi: 10.4161/cc.8.13.8861

    Figure Lengend Snippet: Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5). Rottlerin (10 μM) was added for 4 h (lane 4) or 96 h (lane 5). Cell lysates were analyzed by immunobloting with the indicated antibodies. (C) MKN45 cells were incubated continuously with DMSO (◆), SU11274 (▴), 17-AAG (◻) or SU11274 and rottlerin (*), and cell proliferation was monitored by MTS assay. Each point represents the mean of 4 determinations; error bars, SD.

    Article Snippet: As in H1993 cells, 17-AAG treatment resulted in robust and durable inhibition of each of these parameters. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window Figure 5. caption a7 Effects of c-Met TKI and Hsp90 inhibitor on cell signaling and proliferation of MKN45 cells. (A) MKN45 cells were treated with SU11274 (2.5 μM) or 17-AAG (0.5 μM) for the indicated times, and analyzed by immunoblotting using specific antibodies. (B) MKN45 cells were treated with SU11274 for 4 h (lane 2) or 96 h (lane 3–5).

    Techniques: Western Blot, Incubation, MTS Assay