High impact information on HIPK1

• Phosphorylation of p300 and AML1 is impaired in Hipk1/2 double-deficient mouse embryos [1].
• We have previously observed that metabolic oxidative stress-induced death domain-associated protein (Daxx) trafficking is mediated by the ASK1-SEK1-JNK1-HIPK1 signal transduction pathway [2].
• The occurrence of HIPK domains in PML-/- fibroblasts reveals their independence from the PML protein [3].
• Tumor necrosis factor alpha-induced desumoylation and cytoplasmic translocation of homeodomain-interacting protein kinase 1 are critical for apoptosis signal-regulating kinase 1-JNK/p38 activation [4].
• Taken together, these results show that glucose deprivation activates the ASK1-SEK1-JNK1-HIPK1 pathway, and the activated HIPK1 is probably involved in the relocalization of Daxx from the nucleus to the cytoplasm [5].

Biological context of HIPK1

• Studies from in vivo labeling and immune complex kinase assay demonstrated that phosphorylation of Daxx occurred during glucose deprivation, and its phosphorylation was mediated through the ASK1-SEK1-JNK1-HIPK1 signal transduction pathway [5].
• DJ-1 interacts with HIPK1 and affects H2O2-induced cell death [6].

Other interactions of HIPK1

• HIPK2 was first described as a homeodomain-interacting protein kinase acting as a corepressor for homeodomain transcription factors [7].
• The N-terminal SUMO-1 modification site is conserved between all vertebrate HIPK2 proteins and is found in all members of the HIPK family of protein kinases [8].

References