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dynasore 14062 (Cayman Chemical)

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Cayman Chemical dynasore 14062

(A) After pre-treatment with 20 <t>µM</t> <t>pitstop</t> II, 0.5 mM methyl-β-cyclodextrin (MβC), 80 µM <t>dynasore,</t> 20 µM cytochalasin d (Cyto D) or 20 µM chlorpromazine (CPZ) for 1 h, HCC1937 cells were treated with 8 µM AG-08 for 24 h. Then cell viability was determined by using WST-1. Reported values were normalized on cells treated with only AG-08. Error bars are the standard deviations (n=3). p-values were calculated with respect to AG-08 treated cells by two-tailed equal variance Student’s t-test (*p<0.05, ***p<0.001, ****p<0.0001) (B) HCC1937 cells were treated with brefeldin A (Bref A) for 1 h and then treated with 8 µM AG-08 for 24 h. Error bars represent standard deviations (n=3). p-values were calculated with respect to AG-08-treated cells (*p<0.05, **p<0.005, ***p<0.001). (C) Following AG-08 treatment for 16 h, EEA1 proteins were stained using anti-EEA1 antibody in HCC1937 cells. (Scale bar=25 µm).

Dynasore 14062, supplied by Cayman Chemical, 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/dynasore+14062/bio_rxiv__2021__09__07__459231-235-12-13?v=Cayman+Chemical
Average 90 stars, based on 1 article reviews

dynasore 14062 - by Bioz Stars, 2026-07

90/100 stars

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1) Product Images from "Sapogenin based self-assembly structures activating a non-apoptotic cell death via multiple pathways"

Article Title: Sapogenin based self-assembly structures activating a non-apoptotic cell death via multiple pathways

Journal: bioRxiv

doi: 10.1101/2021.09.07.459231

(A) After pre-treatment with 20 µM pitstop II, 0.5 mM methyl-β-cyclodextrin (MβC), 80 µM dynasore, 20 µM cytochalasin d (Cyto D) or 20 µM chlorpromazine (CPZ) for 1 h, HCC1937 cells were treated with 8 µM AG-08 for 24 h. Then cell viability was determined by using WST-1. Reported values were normalized on cells treated with only AG-08. Error bars are the standard deviations (n=3). p-values were calculated with respect to AG-08 treated cells by two-tailed equal variance Student’s t-test (*p<0.05, ***p<0.001, ****p<0.0001) (B) HCC1937 cells were treated with brefeldin A (Bref A) for 1 h and then treated with 8 µM AG-08 for 24 h. Error bars represent standard deviations (n=3). p-values were calculated with respect to AG-08-treated cells (*p<0.05, **p<0.005, ***p<0.001). (C) Following AG-08 treatment for 16 h, EEA1 proteins were stained using anti-EEA1 antibody in HCC1937 cells. (Scale bar=25 µm).

Figure Legend Snippet: (A) After pre-treatment with 20 µM pitstop II, 0.5 mM methyl-β-cyclodextrin (MβC), 80 µM dynasore, 20 µM cytochalasin d (Cyto D) or 20 µM chlorpromazine (CPZ) for 1 h, HCC1937 cells were treated with 8 µM AG-08 for 24 h. Then cell viability was determined by using WST-1. Reported values were normalized on cells treated with only AG-08. Error bars are the standard deviations (n=3). p-values were calculated with respect to AG-08 treated cells by two-tailed equal variance Student’s t-test (*p<0.05, ***p<0.001, ****p<0.0001) (B) HCC1937 cells were treated with brefeldin A (Bref A) for 1 h and then treated with 8 µM AG-08 for 24 h. Error bars represent standard deviations (n=3). p-values were calculated with respect to AG-08-treated cells (*p<0.05, **p<0.005, ***p<0.001). (C) Following AG-08 treatment for 16 h, EEA1 proteins were stained using anti-EEA1 antibody in HCC1937 cells. (Scale bar=25 µm).

Techniques Used: Two Tailed Test, Staining

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Journal: bioRxiv

Article Title: Sapogenin based self-assembly structures activating a non-apoptotic cell death via multiple pathways

doi: 10.1101/2021.09.07.459231

Figure Lengend Snippet: (A) After pre-treatment with 20 µM pitstop II, 0.5 mM methyl-β-cyclodextrin (MβC), 80 µM dynasore, 20 µM cytochalasin d (Cyto D) or 20 µM chlorpromazine (CPZ) for 1 h, HCC1937 cells were treated with 8 µM AG-08 for 24 h. Then cell viability was determined by using WST-1. Reported values were normalized on cells treated with only AG-08. Error bars are the standard deviations (n=3). p-values were calculated with respect to AG-08 treated cells by two-tailed equal variance Student’s t-test (*p<0.05, ***p<0.001, ****p<0.0001) (B) HCC1937 cells were treated with brefeldin A (Bref A) for 1 h and then treated with 8 µM AG-08 for 24 h. Error bars represent standard deviations (n=3). p-values were calculated with respect to AG-08-treated cells (*p<0.05, **p<0.005, ***p<0.001). (C) Following AG-08 treatment for 16 h, EEA1 proteins were stained using anti-EEA1 antibody in HCC1937 cells. (Scale bar=25 µm).

Article Snippet: Pitstop II (Sigma; SML1169), methyl β cyclodextrin (Cayman; 21633), chlorpromazine (Cayman; 16129), dynasore (Cayman,14062) and cytochalasin D (Cayman; 11330) were used as endocytosis inhibitors.

Techniques: Two Tailed Test, Staining

Inhibition of dynamins led to embryonic lethality in Japanese quail. (A) Appearance of the Japanese quail embryos at incubation d 10 from the eggs of control, (B) sham, (C) vehicle (DMSO), and (D) dynasore groups. (D-1 to D-3) Magnified pictures of embryos from D. After injection on incubation d 3, Japanese quail were incubated at 37°C until d 10. Thirty five µL DMSO (dimethyl sulfoxide) was injected into the DMSO group whereas the same amount of PBS was injected into the sham group. The dynasore group received dynasore (225 mM) in 35 µL DMSO. (E) The ratios of the embryonic lethality in control, sham, vehicle, and dynasore groups; the values were shown as mean ± SEM. Control group, n = 11; sham group, n = 12; DMSO group, n = 15, Dynasore group, n = 15. The statistical analysis used a nonparametric method, Kruskal-Wallis one-way ANOVA followed by Dunn's multiple comparison test. A P -value ≤ 0.05 was considered statistically different. The groups that share the same letters indicated no significant differences.

Journal: Poultry Science

Article Title: The role of dynamin in absorbing lipids into endodermal epithelial cells of yolk sac membranes during embryonic development in Japanese quail

doi: 10.1016/j.psj.2021.101470

Figure Lengend Snippet: Inhibition of dynamins led to embryonic lethality in Japanese quail. (A) Appearance of the Japanese quail embryos at incubation d 10 from the eggs of control, (B) sham, (C) vehicle (DMSO), and (D) dynasore groups. (D-1 to D-3) Magnified pictures of embryos from D. After injection on incubation d 3, Japanese quail were incubated at 37°C until d 10. Thirty five µL DMSO (dimethyl sulfoxide) was injected into the DMSO group whereas the same amount of PBS was injected into the sham group. The dynasore group received dynasore (225 mM) in 35 µL DMSO. (E) The ratios of the embryonic lethality in control, sham, vehicle, and dynasore groups; the values were shown as mean ± SEM. Control group, n = 11; sham group, n = 12; DMSO group, n = 15, Dynasore group, n = 15. The statistical analysis used a nonparametric method, Kruskal-Wallis one-way ANOVA followed by Dunn's multiple comparison test. A P -value ≤ 0.05 was considered statistically different. The groups that share the same letters indicated no significant differences.

Article Snippet: The eggs at incubation d 3 were randomly divided into 4 groups as follows: 1) a control group with no treatment (n = 11); 2) a sham group with a drilled hole and puncture by a 30 G needle into the egg yolk to simulate the dynasore (#14062, Cayman Chemical, MI) injection (n = 12); 3) a vehicle group injected with the same volume of dimethyl sulfoxide ( DMSO ) as the volume of injected dynasore (n = 15), and 4) a dynasore group injected with 35 μL of 225 mM dynasore, dissolved in DMSO, into the egg's yolk (final dosage = 2.538 mg / egg) (n = 15).

Techniques: Inhibition, Incubation, Control, Injection, Comparison

(A) Co-staining of IRAK1 clusters and proteasome in iBMDMs. Kdo-2 Lipid A and P3C co-treatment (50 nM). Scale Bar: 10 μ . (B) Dose response of IRAK1 clustering in iBMDMs with Kdo-2 Lipid A and P3C ± 2h pre-treatment with 4uL of monensin, BD GolgiStop™ for every 3 mL of cell culture. (C-K) Kdo-2 Lipid A and P3C co-treatment (50 nM) in iBMDMs. Co-staining of IRAK1 clusters and (C) MyD88, (D) TICAM2, (E) IRAK4, (F) IRAK2, (G) TRAF6 and (H) pTBK1. Scale Bar: 10 μ . (I) Summary of IRAK1 clustering with TLR signaling components. ND: Not Determined. (J-L) IRAK1 clustering in iBMDMs 0, 2 and 3h post-treatment with 50 nM Kdo-2 Lipid A and P3C ± 30 min pre-treatment with (J) dynasore, an internalization inhibitor (20 μ M); (K) ST2825, a MyD88 dimerization inhibitor (20 μ M); and (L) thymoquinone, an IRAK1 kinase inhibitor (25 μ M). (Panels B, J-L) Data are represented as median ± MAD. (Panels J-L) Unpaired t test with Holm-Šídák’s correction. p = 0.1234 (ns), 0.0332(*); 0.0021 (**); 0.0002 (***); < 0.0001 (****). Data shown are representative of at least two independent experiments. See also supporting .

Journal: bioRxiv

Article Title: IRAK1-mediated coincidence detection of microbial signals licenses inflammasome activation

doi: 10.1101/2019.12.26.888776

Figure Lengend Snippet: (A) Co-staining of IRAK1 clusters and proteasome in iBMDMs. Kdo-2 Lipid A and P3C co-treatment (50 nM). Scale Bar: 10 μ . (B) Dose response of IRAK1 clustering in iBMDMs with Kdo-2 Lipid A and P3C ± 2h pre-treatment with 4uL of monensin, BD GolgiStop™ for every 3 mL of cell culture. (C-K) Kdo-2 Lipid A and P3C co-treatment (50 nM) in iBMDMs. Co-staining of IRAK1 clusters and (C) MyD88, (D) TICAM2, (E) IRAK4, (F) IRAK2, (G) TRAF6 and (H) pTBK1. Scale Bar: 10 μ . (I) Summary of IRAK1 clustering with TLR signaling components. ND: Not Determined. (J-L) IRAK1 clustering in iBMDMs 0, 2 and 3h post-treatment with 50 nM Kdo-2 Lipid A and P3C ± 30 min pre-treatment with (J) dynasore, an internalization inhibitor (20 μ M); (K) ST2825, a MyD88 dimerization inhibitor (20 μ M); and (L) thymoquinone, an IRAK1 kinase inhibitor (25 μ M). (Panels B, J-L) Data are represented as median ± MAD. (Panels J-L) Unpaired t test with Holm-Šídák’s correction. p = 0.1234 (ns), 0.0332(*); 0.0021 (**); 0.0002 (***); < 0.0001 (****). Data shown are representative of at least two independent experiments. See also supporting .

Article Snippet: Monensin (BD GolgiStop 554724), Dynasore (Cayman Chemical 14062), Thymoquinone (Sigma-Aldrich 274666), ST2825 (ApexBio A3840), JNK Inhibitor VIII (Cayman Chemical 15946), U0126 (MEK1/2 inhibitor to inhibit ERK1, Cayman Chemical 70970), XMD8-92 (ER5i, ApexBio A3943)

Techniques: Staining, Cell Culture

(A-K) Kdo-2 Lipid A and P3C co-treatment (50 nM each) in iBMDMs. Co-staining of IRAK1 clusters and (A) ßTrCp, (B) pellino, and (C) IRAK3. Scale Bar: 10 μ . (D) Quantification of the Pearson’s correlation coefficient (PCC) for the correlation of TRAF6 antibody staining in IRAK1 clusters. (E) Quantification of the Mander’s colocalization coefficient (MCC) for the co-occurrence of TRAF6 antibody staining in IRAK1 clusters in iBMDMs. (F) PCC and (G) MCC for pTBK1 antibody staining in IRAK1 clusters. (H-K) Proximity ligation assay in iBMDMs. (H) IRAK1-TRAF6 PLA, (I) IRAK1-pTBK1 PLA, (J) IRAK2-TRAF6 PLA, (K) IRAK1-pTBK1 PLA. (L, M) Single or co-TLR stimulation of TLR4 and TLR1/2 with Kdo-2 Lipid A and P3C (50 nM each). Quantification of (L) pp65 nuclear translocation (M) pATF2 nuclear translocation. (N) Quantification of pATF2 nuclear translocation on co-TLR stimulation of TLR4 and TLR1/2 with Kdo-2 Lipid A and P3C ± 30 min pre-treatment with dynasore, an internalization inhibitor, 20 μ M, ST2825, a MyD88 dimerization inhibitor, 20 μ M, and thymoquinone, an IRAK1 kinase inhibitor, 25 μ M. (D-G) Data are represented as mean ± SD. (H-N) Data are represented as median ± MAD. (Panels D-G) Each data point represents value from a randomly selected non-over lapping field of cells. Paired t test. (Panels H-M) Tukey’s multiple comparisons test. (Panel N) Dunnett’s multiple comparisons test. p = 0.1234 (ns), 0.0332(*); 0.0021 (**); 0.0002 (***); < 0.0001 (****). Data shown are representative of at least two independent experiments.

Journal: bioRxiv

Article Title: IRAK1-mediated coincidence detection of microbial signals licenses inflammasome activation

doi: 10.1101/2019.12.26.888776

Figure Lengend Snippet: (A-K) Kdo-2 Lipid A and P3C co-treatment (50 nM each) in iBMDMs. Co-staining of IRAK1 clusters and (A) ßTrCp, (B) pellino, and (C) IRAK3. Scale Bar: 10 μ . (D) Quantification of the Pearson’s correlation coefficient (PCC) for the correlation of TRAF6 antibody staining in IRAK1 clusters. (E) Quantification of the Mander’s colocalization coefficient (MCC) for the co-occurrence of TRAF6 antibody staining in IRAK1 clusters in iBMDMs. (F) PCC and (G) MCC for pTBK1 antibody staining in IRAK1 clusters. (H-K) Proximity ligation assay in iBMDMs. (H) IRAK1-TRAF6 PLA, (I) IRAK1-pTBK1 PLA, (J) IRAK2-TRAF6 PLA, (K) IRAK1-pTBK1 PLA. (L, M) Single or co-TLR stimulation of TLR4 and TLR1/2 with Kdo-2 Lipid A and P3C (50 nM each). Quantification of (L) pp65 nuclear translocation (M) pATF2 nuclear translocation. (N) Quantification of pATF2 nuclear translocation on co-TLR stimulation of TLR4 and TLR1/2 with Kdo-2 Lipid A and P3C ± 30 min pre-treatment with dynasore, an internalization inhibitor, 20 μ M, ST2825, a MyD88 dimerization inhibitor, 20 μ M, and thymoquinone, an IRAK1 kinase inhibitor, 25 μ M. (D-G) Data are represented as mean ± SD. (H-N) Data are represented as median ± MAD. (Panels D-G) Each data point represents value from a randomly selected non-over lapping field of cells. Paired t test. (Panels H-M) Tukey’s multiple comparisons test. (Panel N) Dunnett’s multiple comparisons test. p = 0.1234 (ns), 0.0332(*); 0.0021 (**); 0.0002 (***); < 0.0001 (****). Data shown are representative of at least two independent experiments.

Techniques: Staining, Proximity Ligation Assay, Translocation Assay

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1) Product Images from "Sapogenin based self-assembly structures activating a non-apoptotic cell death via multiple pathways"

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