The Tumor Suppressor Kinase LKB1 Activates the Downstream Kinases SIK2 and SIK3 to Stimulate Nuclear Export of Class IIa Histone Deacetylases
作者： Donald R. Walkinshaw , Ryan Weist , Go-Woon Kim , Linya You , Lin Xiao
关键词: Mef2 、 HDAC4 、 Kinase activity 、 Nuclear receptor co-repressor 2 、 Biology 、 Nuclear receptor co-repressor 1 、 Nuclear export signal 、 Transcription factor 、 Cell biology 、 Histone deacetylase 、 Biochemistry
摘要: Histone deacetylases 4 (HDAC4), -5, -7, and -9 form class IIa within the HDAC superfamily regulate diverse physiological pathological cellular programs. With conserved motifs for phosphorylation-dependent 14-3-3 binding, these serve as novel signal transducers that are able to modulate histone acetylation gene expression in response extracellular cues. Here, we report a PKA-sensitive manner tumor suppressor kinase LKB1 acts through salt-inducible 2 (SIK2) SIK3 promote nucleocytoplasmic trafficking of HDACs. Both SIK2 phosphorylate at stimulate binding. activates MEF2-dependent transcription relieves repression myogenesis by deacetylases. Distinct from SIK2, induces nuclear export independent activity These findings highlight difference among members SIK family indicate LKB1-dependent activation constitutes an important signaling module upstream regulating programs controlled MEF2 other factors.
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