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CASP8 — MST1

Text-mined interactions from Literome

Glantschnig et al., J Biol Chem 2002 : Further activation of MST1 by caspase cleavage is best promoted by caspase-3 , although this appears to be unnecessary for signaling and morphological responses
Ura et al., Mol Cell Biol 2007 : Taken together, our results indicate that caspase mediated cleavage of MST1 , followed by MST1 mediated activation of the JNK pathway, is the mechanism responsible for inducing chromatin condensation during apoptosis
Hu et al., Cell Death Differ 2007 : Surprisingly, depletion of Mst1 triggers caspase-3 activation, provoking H2B phosphorylation through activating PKC-delta
Wong et al., Nat Cell Biol 2009 : Furthermore, the expression of phosphomimetic histone H2B or caspase activated Mst1 immobilizes RCC1 and causes reduction of nuclear RanGTP levels, which leads to inactivation of the nuclear transport machinery ... Therefore, we propose that RCC1 reads the histone code created by caspase activated Mst1 to initiate apoptosis by reducing the level of RanGTP in the nucleus
Lu et al., Sci China Life Sci 2010 : Full inhibition of caspase-3 activity reduced Mst1 activation and partially inhibited H2B phosphorylation ( Ser14 ), but ERK1/2, JNK1/2 and p38 activities were not affected
Graves et al., EMBO J 1998 : Caspase mediated cleavage of Mst1 removes the C-terminal regulatory domain and correlates with an increase in Mst1 activity in vivo, consistent with caspase mediated cleavage activating Mst1