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Editorial
. 2011 Jan;18(1):2-4.
doi: 10.1038/cdd.2010.132.

c-Abl tyrosine kinase in the DNA damage response: cell death and more

V Meltser, M Ben-Yehoyada, Y Shaul
Editorial

c-Abl tyrosine kinase in the DNA damage response: cell death and more

V Meltser et al. Cell Death Differ. 2011 Jan.
No abstract available

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Figures

Figure 1
Figure 1
The primary steps of the DNA damage response constitute immediate activation of DNA repair and induction of cell-cycle arrest. At later stages of the response DSB repair becomes significantly slower and is terminated while the cells recover and resume progression through the cell cycle. In response to DNA damage c-Abl is activated, potentially also by the ATM kinase. (a) Wang et al demonstrate that c-Abl may be necessary for the full activation of ATM and ATR and that of their respective signaling pathways. Accumulating evidence implicates c-Abl in interactions with many key DDR proteins involved in DNA repair (blue) and cell-cycle arrest (green). Some of the known c-Abl targets in this context are shown. (b) The outcome of many of these interactions suggests that c-Abl has an inhibitory role in the response. In addition, a recent study has demonstrated that c-Abl may functionally downregulate late-stage DSB repair concomitant with late activation of c-Abl by DNA damage. (c) c-Abl is best known in the DDR for its involvement in DNA-damage-induced p73-dependent cell death. A recent study reported a similar function for c-Abl in p63-dependent cell death in oocytes. Downregulation of late DSB repair by c-Abl could potentially constitute a prerequisite for later engagement of cells in DNA-damage-induced programmed cell death
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