pgen.1009512.s010.tif (2.03 MB)
Download fileJMY is not required for p53 stabilization, nuclear accumulation, phosphorylation, or acetylation.
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posted on 2021-04-19, 17:34 authored by Virginia L. King, Nathan K. Leclair, Alyssa M. Coulter, Kenneth G. Campellone(A) HAP1 and JMYKO cells were treated with DMSO or 5μM etoposide for 6h before immunoblotting with antibodies to p53, p53phospho-S15, p53acetyl-K382, p53phospho-S46, GAPDH, and tubulin. (B) HAP1 and JMYKO cells were treated with DMSO or etoposide for 6h before being fixed and stained with a p53 antibody (green) and DAPI (DNA; blue). Scale bar, 30μm. (C) Cellular p53 fluorescence intensities were measured in ImageJ and the total p53 intensity was normalized to the HAP1 DMSO sample. Each bar represents the mean ±SD from 3 experiments (n = 196–343 cells per timepoint). AU = Arbitrary Units.
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actin nucleationDNA damage-induced apoptosisJMY-mediated apoptosiscaspase -3.actin assembly machinery impactsactin filamentscell death responsesmitochondrial permeabilizationinitiator caspase cleavageactin nucleation factors JMYactin nucleation factorsWASP-family genep 53-dependent cell death pathwaygene expressioncytoplasmic territoriesWHAMM-interacting G-protein RhoDcell death pathwaysapoptotic responsesRHOD increases cell deathactin cytoskeletonWiskott-Aldrich Syndrome Proteincytochrome ccell survivalexecutioner caspase activation