@article{fdi:010068119,
  title = {{MSK}1 triggers the expression of the {INK}4{AB}/{ARF} locus in oncogene-induced senescence},
  author = {{C}ulerrier, {R}. and {C}arraz, {M}a{\¨e}lle and {M}ann, {C}. and {D}jabali, {M}.},
  editor = {},
  language = {{ENG}},
  abstract = {{T}he tumor suppressor proteins p15({INK}4{B}), p16({INK}4{A}), and p14({ARF}), encoded by the {INK}4{AB}/{ARF} locus, are crucial regulators of cellular senescence. {T}he locus is epigenetically silenced by the repressive {P}olycomb complexes in growing cells but is activated in response to oncogenic stress. {H}ere we show that the mitogen-and stress-activated kinase ({MSK}1) is up-regulated after {RAF}1 oncogenic stress and that the phosphorylated (activated) form of {MSK}1 is significantly increased in the nucleus and recruited to the {INK}4{AB}/{ARF} locus. {W}e show that {MSK}1 mediates histone {H}3{S}28 phosphorylation at the {INK}4{AB}/{ARF} locus and contributes to the rapid transcriptional activation of p15({INK}4{B}) and p16({INK}4{A}) in human cells despite the presence of the repressive {H}3{K}27me3 mark. {F}urthermore, we show that upon {MSK}1 depletion in oncogenic {RAF}1-expressing cells, {H}3{S}28ph presence at the {INK}4 locus and p15({INK}4{B}) and p16({INK}4{A}) expression are reduced. {F}inally, we show that {H}3{S}28-{MSK}-dependent phosphorylation functions in response to {RAF}1 signaling and that {ERK} and p38a contribute to {MSK}1 activation in oncogene-induced senescence.},
  keywords = {},
  booktitle = {},
  journal = {{M}olecular {B}iology of the {C}ell},
  volume = {27},
  numero = {17},
  pages = {2726--2734},
  ISSN = {1059-1524},
  year = {2016},
  DOI = {10.1091/mbc.{E}15-11-0772},
  URL = {https://www.documentation.ird.fr/hor/fdi:010068119},
}