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nocodazol  (MedChemExpress)
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MedChemExpress nocodazol
a , Typical mitotic EKAREV-FRET profile in HEK293 cells, including rising phase, steep increase at nuclear envelope breakdown (NEB) and sharp decline at anaphase ( .) Corresponding snapshots of above cells with H2B-mScarlet support cell-cycle phases (20 cells; 1 experiment). 1, G 2 ; 2, NEB; 3, metaphase; 4, anaphase; 5, cytokinesis (c.k.); 6, G 1 . FRET-signal relative to PMA saturation (150nM). Black, FRET-ratio of YPet(yellow)/Turq2(blue) intensities. b , As a , with cell-cycle stages recognized by EKAREV(Tq) biosensor exclusion from condensed chromosomes; consistently observed (53 cells, 4 experiments). c , As a , but EKAREV(Tq) biosensor lacking nuclear localization. Observed in 28 cells, 2 experiments. d , As a , but EKAREV(TA) control biosensor that cannot be phosphorylated. Observed in 5 cells, 1 experiment. e , EKAREV(Tq) FRET signal in mitotic arrested HEK293 cells <t>(nocodazol,</t> 0.83μM; 2hrs) is sensitive to CDK1 inhibitor RO-3306. In mitotic cells, recognized by absence of nuclear localization (NEB) of NLS-tagged biosensor (insert images), FRET decreased upon 10μM RO-3306 (9 cells; 2 experiments with similar results), or 3x 1μM (1 cell). e’ , Loss of normalized FRET signal (ΔR, %) upon RO-3306 (10μM) or MAPK pathway inhibitors (sel+SCH, 5μM each). Box-and-whisker plots: boxes represent quartile 2 and 3, horizontal line represents median, whiskers represent minimum and maximum within 1,5x interquartile range. RO-3306: n=23 cells, sel+SCH n=16 cells. f , EKAREV(Tq) FRET signal is sensitive to CDK1-inhibition in G 2 -phase. Synchronized cells were imaged before, during and after incubation with RO-3306 (10μM) and retrospectively analyzed if mitotic entry was observed <15 minutes after drug washout (n=23 cells). Right, similar experiment, here inhibiting MEK and ERK (n=20 cells). Graph shows mean±s.d. of baseline-normalized traces. g , As f , monitoring G 2 -phase in HeLa cells (n=19) co-expressing ERK-KTR-mCherry and EKAREV(Tq). ERK-KTR biosensor suffers from same undesired CDK1-sensitivity. ***, two-sided student’s T-test, p<0.0005. Scale bar, 10μm.
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Image Search Results


a , Typical mitotic EKAREV-FRET profile in HEK293 cells, including rising phase, steep increase at nuclear envelope breakdown (NEB) and sharp decline at anaphase ( .) Corresponding snapshots of above cells with H2B-mScarlet support cell-cycle phases (20 cells; 1 experiment). 1, G 2 ; 2, NEB; 3, metaphase; 4, anaphase; 5, cytokinesis (c.k.); 6, G 1 . FRET-signal relative to PMA saturation (150nM). Black, FRET-ratio of YPet(yellow)/Turq2(blue) intensities. b , As a , with cell-cycle stages recognized by EKAREV(Tq) biosensor exclusion from condensed chromosomes; consistently observed (53 cells, 4 experiments). c , As a , but EKAREV(Tq) biosensor lacking nuclear localization. Observed in 28 cells, 2 experiments. d , As a , but EKAREV(TA) control biosensor that cannot be phosphorylated. Observed in 5 cells, 1 experiment. e , EKAREV(Tq) FRET signal in mitotic arrested HEK293 cells (nocodazol, 0.83μM; 2hrs) is sensitive to CDK1 inhibitor RO-3306. In mitotic cells, recognized by absence of nuclear localization (NEB) of NLS-tagged biosensor (insert images), FRET decreased upon 10μM RO-3306 (9 cells; 2 experiments with similar results), or 3x 1μM (1 cell). e’ , Loss of normalized FRET signal (ΔR, %) upon RO-3306 (10μM) or MAPK pathway inhibitors (sel+SCH, 5μM each). Box-and-whisker plots: boxes represent quartile 2 and 3, horizontal line represents median, whiskers represent minimum and maximum within 1,5x interquartile range. RO-3306: n=23 cells, sel+SCH n=16 cells. f , EKAREV(Tq) FRET signal is sensitive to CDK1-inhibition in G 2 -phase. Synchronized cells were imaged before, during and after incubation with RO-3306 (10μM) and retrospectively analyzed if mitotic entry was observed <15 minutes after drug washout (n=23 cells). Right, similar experiment, here inhibiting MEK and ERK (n=20 cells). Graph shows mean±s.d. of baseline-normalized traces. g , As f , monitoring G 2 -phase in HeLa cells (n=19) co-expressing ERK-KTR-mCherry and EKAREV(Tq). ERK-KTR biosensor suffers from same undesired CDK1-sensitivity. ***, two-sided student’s T-test, p<0.0005. Scale bar, 10μm.

Journal: Nature cell biology

Article Title: Quantifying single-cell ERK dynamics in colorectal cancer organoids reveals EGFR as an amplifier of oncogenic MAPK pathway signaling

doi: 10.1038/s41556-021-00654-5

Figure Lengend Snippet: a , Typical mitotic EKAREV-FRET profile in HEK293 cells, including rising phase, steep increase at nuclear envelope breakdown (NEB) and sharp decline at anaphase ( .) Corresponding snapshots of above cells with H2B-mScarlet support cell-cycle phases (20 cells; 1 experiment). 1, G 2 ; 2, NEB; 3, metaphase; 4, anaphase; 5, cytokinesis (c.k.); 6, G 1 . FRET-signal relative to PMA saturation (150nM). Black, FRET-ratio of YPet(yellow)/Turq2(blue) intensities. b , As a , with cell-cycle stages recognized by EKAREV(Tq) biosensor exclusion from condensed chromosomes; consistently observed (53 cells, 4 experiments). c , As a , but EKAREV(Tq) biosensor lacking nuclear localization. Observed in 28 cells, 2 experiments. d , As a , but EKAREV(TA) control biosensor that cannot be phosphorylated. Observed in 5 cells, 1 experiment. e , EKAREV(Tq) FRET signal in mitotic arrested HEK293 cells (nocodazol, 0.83μM; 2hrs) is sensitive to CDK1 inhibitor RO-3306. In mitotic cells, recognized by absence of nuclear localization (NEB) of NLS-tagged biosensor (insert images), FRET decreased upon 10μM RO-3306 (9 cells; 2 experiments with similar results), or 3x 1μM (1 cell). e’ , Loss of normalized FRET signal (ΔR, %) upon RO-3306 (10μM) or MAPK pathway inhibitors (sel+SCH, 5μM each). Box-and-whisker plots: boxes represent quartile 2 and 3, horizontal line represents median, whiskers represent minimum and maximum within 1,5x interquartile range. RO-3306: n=23 cells, sel+SCH n=16 cells. f , EKAREV(Tq) FRET signal is sensitive to CDK1-inhibition in G 2 -phase. Synchronized cells were imaged before, during and after incubation with RO-3306 (10μM) and retrospectively analyzed if mitotic entry was observed <15 minutes after drug washout (n=23 cells). Right, similar experiment, here inhibiting MEK and ERK (n=20 cells). Graph shows mean±s.d. of baseline-normalized traces. g , As f , monitoring G 2 -phase in HeLa cells (n=19) co-expressing ERK-KTR-mCherry and EKAREV(Tq). ERK-KTR biosensor suffers from same undesired CDK1-sensitivity. ***, two-sided student’s T-test, p<0.0005. Scale bar, 10μm.

Article Snippet: EGF was from Invitrogen; selumetinib, afatinib, lapatinib, lapatinib, gefitinib, erlotinib, SHP099 and LY3009120 were from SelleckChem; SCH772984 was from MedChem Express; PMA, nocodazol and CP-724714 were from Sigma-Aldrich; RO-3306 was from Tocris Bioscience; AMG-510 was from MedChemExpress.

Techniques: Control, Whisker Assay, Inhibition, Incubation, Expressing