Fig 1: Compound 11 promoted TyrRS nuclear localization in HeLa cells. Hela cells were treated with compound 11 (1.1, 3.3, 10, or 30 μM) or DMSO for 8 h. Cells cultured in serum-free media for 8 h were under serum starvation. The cytoplasmic and nuclear fractions from cells were subjected to immunoblot assays. Quantification of immunoblots is shown below.
Fig 2: Nuclear TyrRS promoted by compound 11 protected cells from DNA damage in HeLa cells. HeLa cells were pre-treated with compound 11 (30, 10, 3.3, 1.1, or 0.37 μM), RSV (1 μM), or DMSO for 24 h. To induce DNA damage, cells were treated with cisplatin (30 μM) or DMSO in the presence of the test compounds or DMSO for 24 h. Then, whole cell lysates were subjected to immunoblot assays.
Fig 3: Binding modes of compound 11 and RSV with TyrRS (PDB code 4Q93). Compound 11 is shown as green sticks, and RSV is displayed as marine sticks.
Fig 4: DSF and DSC were used to test the stabilization of TyrRS by RSV and compound 11. (A) The Tm value of compound 11. (B) The Tm value of RSV. Also shown are graphs of the unfolding transition of 2 μM TyrRS in the presence of 50 μM RSV or compound 11, respectively. (C and D) Representative DSC melting profiles for TyrRS with RSV or compound 11; ΔTm of RSV and compound 11 obtained from DSC.
Fig 5: YARS augmented proliferation, invasiveness, and homologous recombination in gastric cancer through activating PI3K-Akt signaling. For YARS-overexpressed HGC-27/AGS cells, a changes of the PI3K-Akt pathway representative members (p-S6, S6, p-Akt, Akt), the homologous recombination pathway representative components (BRCA1, 53BP1, RAD51) and YARS; b changes of cell proliferation, as well as c, d changes of migration/invasion after BEZ235 administration were assessed, while e the 48 h responses to Olaparib combining BEZ235 were assessed with CCK-8 assay. v vector, Y YARS. *p < 0.05. ns not significant
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