2 ethyl 3  (Millipore)


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  • 99
    Name:
    R N4 Hydroxy N1 S 2 1H indol 3 yl 1 methylcarbamoyl ethyl 2 isobutyl succinamide
    Description:

    Catalog Number:
    m5939
    Price:
    None
    Applications:
    (R)-N4-Hydroxy-N1-[(S)-2-(1H-indol-3-yl)-1-methylcarbamoyl-ethyl]-2-isobutyl-succinamide has been used:. To study its effect on the profiling of active aggrecanases and their specific aggrecan degradation fragments. . To study the involvement of autocrine EGF (epidermal growth factor) receptor activation in the regulation of the morphogenetic process, using human umbilical vein endothelial cells.. To study the effect of GM6001 blockade on the expression of angiotensin II, the interstitial collagenases and soluble elastin fragments in explant culture supernatants.
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    Structured Review

    Millipore 2 ethyl 3
    R N4 Hydroxy N1 S 2 1H indol 3 yl 1 methylcarbamoyl ethyl 2 isobutyl succinamide

    https://www.bioz.com/result/2 ethyl 3/product/Millipore
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    2 ethyl 3 - by Bioz Stars, 2020-09
    99/100 stars

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    Concentration Assay:

    Article Title: The Effect of Protease Inhibitors on the Induction of Osteoarthritis-Related Biomarkers in Bovine Full-Depth Cartilage Explants
    Article Snippet: .. GM6001 (cat#, M5939, Sigma-Aldrich) stock solution was dissolved in DMSO and then 1000x diluted in culture medium to a final concentration of 10μM. .. Proprotein Convertase (PC) inhibitor (cat#, 537076, Millipore) stock solution was prepared in DMSO and 1000x diluted in culture medium to a final concentration of 10μM.

    Incubation:

    Article Title: Inhibition of Pseudomonas aeruginosa secreted virulence factors reduces lung inflammation in CF mice
    Article Snippet: .. Briefly, 350 µl reaction mixture containing 0.1 M Tris-HCl pH 8.0 and 1% azocasein (Sigma-Aldrich, cat. n. A2765) resuspended in 0.5% NaHCO3 was added to 150 µl supernatant with/without MMPIs Ilomastat, Marimastat, Batimastat (Sigma-Aldrich, cat. n. M5939, M2699, SML0041) and incubated at 37°C for 20 minutes shaking. ..

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  • 94
    Millipore 2 arachidonyl glycerol
    Treatment with Secoisolariciresinol diglycoside (SDG) and <t>2-Arachidonyl</t> glycerol (2-AG) has an effect on cytokine production. Groups of 80 organoids each were pooled treated for 48 hours prior to culturing under hypoxic condition (*), treated during hypoxic condition only ( # ), or were non-treated, cultured under hypoxic conditions and then re-oxygenated under normoxic conditions for 24 hours ( HR) . Total protein extract from 80 organoids was then added to 6 well for the ELISA. Expression of VEGF was significantly increased under hypoxic condition compared to normoxic condition ( A ). Preliminary experiments to assess effects of SDG and 2-AG on the expression of VEGF shows a significant decrease when treated with 2-AG while SDG elicited not significant decrease in VEGF expression when compared to hypoxic condition ( A ). There was a slight increase in the secretion on IL-6 under hypoxic condition compared to normoxic condition. Treatment with SDG lowered the secretion of the cytokine and 2-AG treatment resulted in a significant decrease compared to hypoxic condition ( B ). Re-oxygenated organoids secreted higher amounts of IL-6 compared to hypoxic condition ( B ). There was no significant difference in IL-2 secretion in organoids under hypoxia compared to those under normoxia. Furthermore, the treatments did not have a significantly different profile compared to organoids under hypoxic conditions ( C ). IL-8 secretion under hypoxia was significantly increased compared to normoxia. Pretreatment with both SDG and 2-AG resulted in reduction in IL-8 secretion while reoxygenation did not have an effect ( D ). One-way ANOVA multiple comparison to hypoxia was used to analyze the data. n = 6 wells, ***P
    2 Arachidonyl Glycerol, supplied by Millipore, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Millipore fl118
    Inhibitory effects of AMR-MeOAc and <t>FL118</t> on NF-κB activation. A. Nuclear extracts from HPAF-II and BxPC-3 cells were analyzed for NF-κB DNA binding activity by EMSA using biotin-labeled NF-κB oligonucleotide. B-D. BxPC-3 cells
    Fl118, supplied by Millipore, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Millipore rabbit anti histone h3 ps10
    The Ska complex is required for Aurora B activity in cells. Immunofluorescence images (A, C, E, and G) and quantification (B, D, F, and H) of relative Hec1-pS44, KNL1-pS24, MCAK, and histone <t>H3-pS10</t> intensities, respectively, in HeLa S3 cells treated for 48 h with control or Ska1 and Ska3 siRNAs. The Aurora B inhibitor ZM was added to siControl cells 1 h before fixation ( n = 10–20, n = 15–20, n = 10–77, and n = 47–61 cells per condition, respectively, from one to three experiments). (I) HeLa S3 cells were depleted of endogenous Ska1 and Ska3 or treated with control siRNAs, synchronized by a double thymidine arrest/release, and rescued (Res.) by transfection with siRNA-resistant mCherry (mCh.)-Ska1 and Myc-Ska3 or empty mCherry- and Myc-Vectors (Vector), as control, and stained with the indicated antibodies. (J) Relative H3-pS10 intensities in cells treated as in I ( n = 44–59 cells from two experiments). Res., rescue with mCh.-Ska1 and Myc-Ska3. Live-cell images of HeLa K cells stably expressing a CENP-B–fused (K and L) or H2B-fused (M and N) Aurora B FRET sensor treated as in A. The FRET sensors were completely dephosphorylated in siControl cells treated with ZM 30 min before imaging. Shown are emission ratio images (TFP/YFP or CFP/YFP) and images for sensor localization (TFP or CFP emission). (L) Scatter plot showing TFP/YFP emission ratios calculated for individual aligned KTs in siControl and siSka1+3 cells ( n = 500 KTs from 50 cells each from two experiments) or mostly unaligned KTs in ZM-treated cells ( n = 100 KTs from 10 cells from one experiment). (N) CFP/YFP emission ratios calculated for individual siControl and siSka1+3 cells with aligned chromosomes ( n = 33–55 cells from three experiments) or ZM-treated cells with mostly unaligned chromosomes ( n = 33 cells from one experiment). Horizontal lines depict mean. Asterisks show statistical significance (Student’s t test, unpaired). ****, P ≤ 0.0001; ns, nonsignificant. Bars, 5 µm.
    Rabbit Anti Histone H3 Ps10, supplied by Millipore, 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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    Image Search Results


    Treatment with Secoisolariciresinol diglycoside (SDG) and 2-Arachidonyl glycerol (2-AG) has an effect on cytokine production. Groups of 80 organoids each were pooled treated for 48 hours prior to culturing under hypoxic condition (*), treated during hypoxic condition only ( # ), or were non-treated, cultured under hypoxic conditions and then re-oxygenated under normoxic conditions for 24 hours ( HR) . Total protein extract from 80 organoids was then added to 6 well for the ELISA. Expression of VEGF was significantly increased under hypoxic condition compared to normoxic condition ( A ). Preliminary experiments to assess effects of SDG and 2-AG on the expression of VEGF shows a significant decrease when treated with 2-AG while SDG elicited not significant decrease in VEGF expression when compared to hypoxic condition ( A ). There was a slight increase in the secretion on IL-6 under hypoxic condition compared to normoxic condition. Treatment with SDG lowered the secretion of the cytokine and 2-AG treatment resulted in a significant decrease compared to hypoxic condition ( B ). Re-oxygenated organoids secreted higher amounts of IL-6 compared to hypoxic condition ( B ). There was no significant difference in IL-2 secretion in organoids under hypoxia compared to those under normoxia. Furthermore, the treatments did not have a significantly different profile compared to organoids under hypoxic conditions ( C ). IL-8 secretion under hypoxia was significantly increased compared to normoxia. Pretreatment with both SDG and 2-AG resulted in reduction in IL-8 secretion while reoxygenation did not have an effect ( D ). One-way ANOVA multiple comparison to hypoxia was used to analyze the data. n = 6 wells, ***P

    Journal: Scientific Reports

    Article Title: Multicellular 3D Neurovascular Unit Model for Assessing Hypoxia and Neuroinflammation Induced Blood-Brain Barrier Dysfunction

    doi: 10.1038/s41598-020-66487-8

    Figure Lengend Snippet: Treatment with Secoisolariciresinol diglycoside (SDG) and 2-Arachidonyl glycerol (2-AG) has an effect on cytokine production. Groups of 80 organoids each were pooled treated for 48 hours prior to culturing under hypoxic condition (*), treated during hypoxic condition only ( # ), or were non-treated, cultured under hypoxic conditions and then re-oxygenated under normoxic conditions for 24 hours ( HR) . Total protein extract from 80 organoids was then added to 6 well for the ELISA. Expression of VEGF was significantly increased under hypoxic condition compared to normoxic condition ( A ). Preliminary experiments to assess effects of SDG and 2-AG on the expression of VEGF shows a significant decrease when treated with 2-AG while SDG elicited not significant decrease in VEGF expression when compared to hypoxic condition ( A ). There was a slight increase in the secretion on IL-6 under hypoxic condition compared to normoxic condition. Treatment with SDG lowered the secretion of the cytokine and 2-AG treatment resulted in a significant decrease compared to hypoxic condition ( B ). Re-oxygenated organoids secreted higher amounts of IL-6 compared to hypoxic condition ( B ). There was no significant difference in IL-2 secretion in organoids under hypoxia compared to those under normoxia. Furthermore, the treatments did not have a significantly different profile compared to organoids under hypoxic conditions ( C ). IL-8 secretion under hypoxia was significantly increased compared to normoxia. Pretreatment with both SDG and 2-AG resulted in reduction in IL-8 secretion while reoxygenation did not have an effect ( D ). One-way ANOVA multiple comparison to hypoxia was used to analyze the data. n = 6 wells, ***P

    Article Snippet: Organoid Media was then replaced with a fresh full media change containing secoisolariciresinol diglycoside or 2-arachidonyl glycerol before incubating in hypoxic chamber for 24 hours.

    Techniques: Cell Culture, Enzyme-linked Immunosorbent Assay, Expressing

    Inhibitory effects of AMR-MeOAc and FL118 on NF-κB activation. A. Nuclear extracts from HPAF-II and BxPC-3 cells were analyzed for NF-κB DNA binding activity by EMSA using biotin-labeled NF-κB oligonucleotide. B-D. BxPC-3 cells

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: Inhibitory effects of AMR-MeOAc and FL118 on NF-κB activation. A. Nuclear extracts from HPAF-II and BxPC-3 cells were analyzed for NF-κB DNA binding activity by EMSA using biotin-labeled NF-κB oligonucleotide. B-D. BxPC-3 cells

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques: Activation Assay, Binding Assay, Activity Assay, Labeling

    Synergistic antineoplastic effects induced by AMR-MeOAc in combination with a low nM FL118 in pancreatic cancer cells

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: Synergistic antineoplastic effects induced by AMR-MeOAc in combination with a low nM FL118 in pancreatic cancer cells

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques:

    Chemical structure of AMR-MeOAc (A) and FL118 (B).

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: Chemical structure of AMR-MeOAc (A) and FL118 (B).

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques:

    ROS production in HPAF-II cells after treatment with AMR-MeOAc and FL118. A. HPAF-II cells were treated with AMR-MeOAc and FL118 individually or in combination for 12 h. Cells were then stained with Dichloro-dihydro-fluorescein diacetate (H 2 DCF-DA), followed

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: ROS production in HPAF-II cells after treatment with AMR-MeOAc and FL118. A. HPAF-II cells were treated with AMR-MeOAc and FL118 individually or in combination for 12 h. Cells were then stained with Dichloro-dihydro-fluorescein diacetate (H 2 DCF-DA), followed

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques: Staining

    AMR-MeOAc and FL118 induce apoptosis. A. HPAF-II cells were treated with AMR-MeOAc (8 µM) and FL118 (20 nM) alone or in combination for 48 h. Cell apoptosis was measured using Annexin V-FITC/PI staining and flow cytometry. B. BxPC-3 cells were

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: AMR-MeOAc and FL118 induce apoptosis. A. HPAF-II cells were treated with AMR-MeOAc (8 µM) and FL118 (20 nM) alone or in combination for 48 h. Cell apoptosis was measured using Annexin V-FITC/PI staining and flow cytometry. B. BxPC-3 cells were

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques: Staining, Flow Cytometry, Cytometry

    Effects of AMR-MeOAc and FL118 alone and in combination on mutant KRAS G12D activity and downstream signaling. A. HPAF-II cells were treated with 8 µM AMR-MeOAc or 20 nM FL118 alone and in combination for 6, 12, 24, and 48 h. RAS Pull-Down assays

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: Effects of AMR-MeOAc and FL118 alone and in combination on mutant KRAS G12D activity and downstream signaling. A. HPAF-II cells were treated with 8 µM AMR-MeOAc or 20 nM FL118 alone and in combination for 6, 12, 24, and 48 h. RAS Pull-Down assays

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques: Mutagenesis, Activity Assay

    Antiproliferative activity of AMR-MeOAc and FL118 in pancreatic cancer cells. A and B are HPAF-II cell viability curves upon treatment with AMR-MeOAc and FL118, respecitvely. C and D are BxPC-3 cell viability curves upon treatment with AMR-MeOAc and FL118,

    Journal: American Journal of Cancer Research

    Article Title: Multiple mechanisms involved in a low concentration of FL118 enhancement of AMR-MeOAc to induce pancreatic cancer cell apoptosis and growth inhibition

    doi:

    Figure Lengend Snippet: Antiproliferative activity of AMR-MeOAc and FL118 in pancreatic cancer cells. A and B are HPAF-II cell viability curves upon treatment with AMR-MeOAc and FL118, respecitvely. C and D are BxPC-3 cell viability curves upon treatment with AMR-MeOAc and FL118,

    Article Snippet: HPAF-II cells were treated with AMR-MeOAc and FL118 alone or in combination for 0, 6, 12, 24, or 48 h. RAS GTP levels were determined using a RAS activation assay kit (Millipore) according to the manufacturer’s instructions.

    Techniques: Activity Assay

    The Ska complex is required for Aurora B activity in cells. Immunofluorescence images (A, C, E, and G) and quantification (B, D, F, and H) of relative Hec1-pS44, KNL1-pS24, MCAK, and histone H3-pS10 intensities, respectively, in HeLa S3 cells treated for 48 h with control or Ska1 and Ska3 siRNAs. The Aurora B inhibitor ZM was added to siControl cells 1 h before fixation ( n = 10–20, n = 15–20, n = 10–77, and n = 47–61 cells per condition, respectively, from one to three experiments). (I) HeLa S3 cells were depleted of endogenous Ska1 and Ska3 or treated with control siRNAs, synchronized by a double thymidine arrest/release, and rescued (Res.) by transfection with siRNA-resistant mCherry (mCh.)-Ska1 and Myc-Ska3 or empty mCherry- and Myc-Vectors (Vector), as control, and stained with the indicated antibodies. (J) Relative H3-pS10 intensities in cells treated as in I ( n = 44–59 cells from two experiments). Res., rescue with mCh.-Ska1 and Myc-Ska3. Live-cell images of HeLa K cells stably expressing a CENP-B–fused (K and L) or H2B-fused (M and N) Aurora B FRET sensor treated as in A. The FRET sensors were completely dephosphorylated in siControl cells treated with ZM 30 min before imaging. Shown are emission ratio images (TFP/YFP or CFP/YFP) and images for sensor localization (TFP or CFP emission). (L) Scatter plot showing TFP/YFP emission ratios calculated for individual aligned KTs in siControl and siSka1+3 cells ( n = 500 KTs from 50 cells each from two experiments) or mostly unaligned KTs in ZM-treated cells ( n = 100 KTs from 10 cells from one experiment). (N) CFP/YFP emission ratios calculated for individual siControl and siSka1+3 cells with aligned chromosomes ( n = 33–55 cells from three experiments) or ZM-treated cells with mostly unaligned chromosomes ( n = 33 cells from one experiment). Horizontal lines depict mean. Asterisks show statistical significance (Student’s t test, unpaired). ****, P ≤ 0.0001; ns, nonsignificant. Bars, 5 µm.

    Journal: The Journal of Cell Biology

    Article Title: The Ska complex promotes Aurora B activity to ensure chromosome biorientation

    doi: 10.1083/jcb.201603019

    Figure Lengend Snippet: The Ska complex is required for Aurora B activity in cells. Immunofluorescence images (A, C, E, and G) and quantification (B, D, F, and H) of relative Hec1-pS44, KNL1-pS24, MCAK, and histone H3-pS10 intensities, respectively, in HeLa S3 cells treated for 48 h with control or Ska1 and Ska3 siRNAs. The Aurora B inhibitor ZM was added to siControl cells 1 h before fixation ( n = 10–20, n = 15–20, n = 10–77, and n = 47–61 cells per condition, respectively, from one to three experiments). (I) HeLa S3 cells were depleted of endogenous Ska1 and Ska3 or treated with control siRNAs, synchronized by a double thymidine arrest/release, and rescued (Res.) by transfection with siRNA-resistant mCherry (mCh.)-Ska1 and Myc-Ska3 or empty mCherry- and Myc-Vectors (Vector), as control, and stained with the indicated antibodies. (J) Relative H3-pS10 intensities in cells treated as in I ( n = 44–59 cells from two experiments). Res., rescue with mCh.-Ska1 and Myc-Ska3. Live-cell images of HeLa K cells stably expressing a CENP-B–fused (K and L) or H2B-fused (M and N) Aurora B FRET sensor treated as in A. The FRET sensors were completely dephosphorylated in siControl cells treated with ZM 30 min before imaging. Shown are emission ratio images (TFP/YFP or CFP/YFP) and images for sensor localization (TFP or CFP emission). (L) Scatter plot showing TFP/YFP emission ratios calculated for individual aligned KTs in siControl and siSka1+3 cells ( n = 500 KTs from 50 cells each from two experiments) or mostly unaligned KTs in ZM-treated cells ( n = 100 KTs from 10 cells from one experiment). (N) CFP/YFP emission ratios calculated for individual siControl and siSka1+3 cells with aligned chromosomes ( n = 33–55 cells from three experiments) or ZM-treated cells with mostly unaligned chromosomes ( n = 33 cells from one experiment). Horizontal lines depict mean. Asterisks show statistical significance (Student’s t test, unpaired). ****, P ≤ 0.0001; ns, nonsignificant. Bars, 5 µm.

    Article Snippet: DeLuca, Colorado State University, Fort Collins, CO), rabbit anti–histone H3-pS10 (1:1,000; 06-570; EMD Millipore), rabbit anti–histone H3-pS28 (1:500; 9713P; Cell Signaling Technology), rabbit anti–histone H3-pT3 (1:200; 9714S; Cell Signaling Technology), rabbit anti–KNL1-pS24 (1:2,000; gift of I.M.

    Techniques: Activity Assay, Immunofluorescence, Transfection, Plasmid Preparation, Staining, Stable Transfection, Expressing, Imaging

    The MT-binding capability of the Ska complex is required for Aurora B activity. Immunofluorescence images (A, C, E, G, and I) and quantification (B, D, F, H, and J) of relative Hec1-pS44, KNL1-pS24, MCAK, histone H3-pS10, and AurB-pT232 intensities, respectively, in HeLa cells stably expressing GFP-tagged and siRNA-resistant wild-type Ska1 (WT) or the MT-binding deficient mutants Ska1 R155A, R236A, R245A (ARG) and Ska1 1-131 (ΔMTBD), respectively, treated for 48 h with control or Ska1 siRNAs ( n = 25, n = 40–55, n = 17–26, n = 35–40, and n = 81–105 cells per condition, respectively, from one to four experiments). Note that spindle association of GFP-Ska1 WT is not visible in all cells because of the simultaneous cell permeabilization and fixation. Horizontal lines depict mean. Asterisks show statistical significance (Student’s t test, unpaired). ****, P ≤ 0.0001; ***, P ≤ 0.001. Bars, 5 µm.

    Journal: The Journal of Cell Biology

    Article Title: The Ska complex promotes Aurora B activity to ensure chromosome biorientation

    doi: 10.1083/jcb.201603019

    Figure Lengend Snippet: The MT-binding capability of the Ska complex is required for Aurora B activity. Immunofluorescence images (A, C, E, G, and I) and quantification (B, D, F, H, and J) of relative Hec1-pS44, KNL1-pS24, MCAK, histone H3-pS10, and AurB-pT232 intensities, respectively, in HeLa cells stably expressing GFP-tagged and siRNA-resistant wild-type Ska1 (WT) or the MT-binding deficient mutants Ska1 R155A, R236A, R245A (ARG) and Ska1 1-131 (ΔMTBD), respectively, treated for 48 h with control or Ska1 siRNAs ( n = 25, n = 40–55, n = 17–26, n = 35–40, and n = 81–105 cells per condition, respectively, from one to four experiments). Note that spindle association of GFP-Ska1 WT is not visible in all cells because of the simultaneous cell permeabilization and fixation. Horizontal lines depict mean. Asterisks show statistical significance (Student’s t test, unpaired). ****, P ≤ 0.0001; ***, P ≤ 0.001. Bars, 5 µm.

    Article Snippet: DeLuca, Colorado State University, Fort Collins, CO), rabbit anti–histone H3-pS10 (1:1,000; 06-570; EMD Millipore), rabbit anti–histone H3-pS28 (1:500; 9713P; Cell Signaling Technology), rabbit anti–histone H3-pT3 (1:200; 9714S; Cell Signaling Technology), rabbit anti–KNL1-pS24 (1:2,000; gift of I.M.

    Techniques: Binding Assay, Activity Assay, Immunofluorescence, Stable Transfection, Expressing