Fig. 4
- ID
- ZDB-FIG-211101-34
- Publication
- Zhang et al., 2021 - Selective and competitive functions of the AAR and UPR pathways in stress-induced angiogenesis
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Genetic and pharmacological inhibition of AAR, but not UPR, suppresses the tars-deficiency-induced angiogenesis.
a, b Quantification and statistical analysis of the ectopic branch points per ISV of the tars−/− and sibling embryos that were treated with gcn2 MO or perk MO. c Knockout of gcn2, but not perk, suppressed the tars-deficiency-induced angiogenesis. The embryos were produced by self-cross of gcn2−/−tars+/− or perk−/−tars+/− lines, and the tars−/− ones were compared with their siblings in the same litter. d Pharmacological inhibition of Gcn2 by GCN2-IN-1 and GCN2iB significantly suppressed the angiogenic phenotypes of the tars−/− embryos. e Inhibition of Perk by Perk-specific inhibitor GSK2656157 showed no significant rescue effect on the angiogenetic phenotypes. f Attenuation of UPR by 4-phenylbutyrate (4-PBA) could not rescue the angiogenetic phenotypes. In panels d–f, the solvents DMSO and H2O were applied as negative controls, respectively. In the statistical analyses, data are presented as means ± SD; two-tailed t-test; ***P < 0.001; n.s., not significant. |