Genotoxic stress induces nuclear accumulation and phosphorylation of SRPK2.
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Abstract
<p>A. PQ induces DNA damage. Representative confocal micrographs of SH-SY5Y cells treated with PQ and fixed at the indicated time-points. Cells were stained with an anti-γH2AX antibody (<i>upper row</i>) or with an antibody specific for SRPK2 (<i>lower row</i>). B. Inhibition of PQ-induced H2AX phosphorylation by roscovitine. Representative confocal micrographs of SH-SY5Y cells incubated with 10 µM roscovitine and PQ treatment. ãH2AX was detected by immunocytochemistry; nuclei were stained with DAPI. C. Inhibition of the DDR blocks nuclear localization of SRPK2. Representative confocal micrographs of control SH-SY5Y cells (<i>first row</i>), or SH-SY5Y cells incubated with PQ alone (<i>second row</i>), or with PQ and with 10 µM roscovitine (<i>third row</i>), or with PQ and 10 mM caffeine (<i>forth row</i>). SRPK2 was detected by immunocytochemistry; nuclei were stained with DAPI. D. Genotoxic treatments induce nuclear localization of SRPK2. Representative confocal micrographs of untreated SH-SY5Y cells (<i>upper row</i>) or cells treated with 20 µM cisplatin for 18 h (<i>middle row</i>) or irradiated with 10 Gy (<i>lower row</i>) were stained with DAPI and with an anti-SRPK2 antibody. E. Genotoxic treatments induce hyperphosphorylation of SRPK2. Western blots of total cell extract prepared from untreated SH-SY5Y cells or from cells treated with PQ, or with cisplatin for the indicated times. The blot was probed with an anti-SRPK2 antibody. Actin was used as loading control. The slower migrating band is indicated by an arrow.</p