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Image Search Results
Journal: Journal of the American Chemical Society
Article Title: Hijacking Methyl Reader Proteins for Nuclear-Specific Protein Degradation
doi: 10.1021/jacs.2c00874
Figure Lengend Snippet: A) Structure of the L3MBTL3 antagonist, UNC1215. B) Structure of biotin-UNC1215. C) UNC1215 does not disrupt the L3MBTL3-Cul4DCAF5 interaction. HEK293T (293T) cells were transiently transfected with L3MBTL3-HA and myc-DCAF5, lysed after 48 h and incubated in the presence or absence of 20 μM UNC1215 followed by biotin probe (200 nM) pulldown (n = 2). D) L3MBTL3 interacts with DCAF5 and DDB1 in HEK293T cells and E) HCT116 cells. HEK293T or HCT116 cells were co-transfected with L3MBTL3-HA and myc-DCAF5, lysed after 48 h and incubated in the presence or absence of 5 μM UNC1215 followed by immunoprecipitation of L3MBTL3-HA (n = 2).
Article Snippet: Cell lines HEK293T cells, THP1 and
Techniques: Transfection, Incubation, Immunoprecipitation
Journal: Journal of the American Chemical Society
Article Title: Hijacking Methyl Reader Proteins for Nuclear-Specific Protein Degradation
doi: 10.1021/jacs.2c00874
Figure Lengend Snippet: A) Schematic of BRD and L3MBTL3 proteins in complex with the JQ1-UNC1215 PROTAC. Figure was created with BioRender.com Structure of KL-7. B) KL-7 degrades BRD2 in a dose-dependent manner in HCT116 cells. HCT116 cells were treated with increasing concentrations of KL-7 for 12 h. Quantitation is on the right and the quantified data represent mean ± SEM (n = 3, ****P<0.0001). C) BRD2 forms a ternary complex with L3MBTL3 in a KL-7 dependent manner. HEK293T cells were co-transfected with L3MBTL3-HA and GFP-BRD2-V5 for 48 h and lysates were incubated with 5 μM KL-7 for 2 h, followed by V5 immunoprecipitation (n = 2). D) Excess JQ1 ligand blocks KL-7 induced BRD2 degradation. HCT116 cells were pre-treated 100 μM JQ1 for 1.5 h, and then co-treated with 5 μM KL-7 for 12 h. Quantitation is below and the quantified data represent mean ± SEM (n = 2, **P<0.005). E) KL-7 induced BRD2 degradation is L3MBTL3-dependent. L3MBTL3 wildtype (WT) and Knockout (KO) 293T cells were treated with 5 μM KL-7 for 8 h. Quantitation is below and the quantified data represent mean ± SEM (n = 2, ****P<0.0001). F) KL-7 induced BRD2 degradation is neddylation and proteasome-dependent. HCT116 cells were pre-treated with 1 μM MLN4924 and 0.5 μM epoxomicin for 1.5 h, and then co-treated with 5 μM KL-7 for 12 h. Quantitation is on the right and the quantified data represent mean ± SEM (n = 2, **P<0.005).
Article Snippet: Cell lines HEK293T cells, THP1 and
Techniques: Quantitation Assay, Transfection, Incubation, Immunoprecipitation, Knock-Out
Journal: Journal of oncology
Article Title: Characterization of the Newly Established Homoharringtonine- (HHT-) Resistant Cell Lines and Mechanisms of Resistance.
doi: 10.1155/2022/2813938
Figure Lengend Snippet: Figure 1: )e inhibitory effect of HHTon nine AML cell lines. (a) )e IC50 values of HHTon nine AML cell lines. (b) )e inhibitory effect of HHT on FLT3-ITD mutant cell lines was significantly higher than that in nonmutant ones. ∗P < 0.05.
Article Snippet:
Techniques: Mutagenesis
Journal: Journal of oncology
Article Title: Characterization of the Newly Established Homoharringtonine- (HHT-) Resistant Cell Lines and Mechanisms of Resistance.
doi: 10.1155/2022/2813938
Figure Lengend Snippet: Figure 6: Verification of the hub genes (CALCRL and GNAI1) and the prognostic significance of CALCRL and GNAI1 for AML. (a) )e mRNA level of GPR183, CNR2, CALCRL, and GNAI1 in four AML cell lines by RT-qPCR. (b) )e protein level of CALCRL and GNAI1 in four AML cell lines and the mice tumor mass from HHT-sensitive and HHT-resistant mice groups. (c) )e expression level and OS of GNAI1 and CALCRL in online database GEPIA in AML. (d) )e OS and EFS of CALCRL in our cohorts. (e) )e correlation of GNAI1 and CALCRL through correlation analysis. P < 0.01∗∗and P < 0.001∗∗∗.
Article Snippet:
Techniques: Quantitative RT-PCR, Expressing