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The data confirm a key role for HIPK2 and H2B in cytokinesis and offer the possibility of testing HIPK2 and extrachromosomal histone H2B as therapeutic targets for inhibition of cell division.
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HIPK1, HIPK2 and HIPK3 interact with the components of the carbon catabolite repressor 4 (CCR4)-negative on TATA (NOT) complex, an important regulator of all the major steps in the mRNA metabolism. it has emerged that HIPKs and their related miRNAs are involved in diabetic nephropathy, gastric cancer chemoresistance, cervical cancer progression, and recombinant protein expression in cultured cells. [Review]
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The downregulation of miR-197 suppresses the EMT and migration ability. HIPK2 is a direct functional target of miR-197 in LAD metastasis. In summary, miR-197 controls EMT and metastasis by directly silencing HIPK2.
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Immunoprecipitation and pulldown experiments identified DCAF7 as an adaptor for the association of the adenovirus E1A protein with DYRK1A and HIPK2
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HIPK2 polymorphisms rs2058265, rs6464214, and rs7456421 may have a role in kidney stone disease in Chinese males
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HIPK2 overexpression may be a potential prognostic marker for predicting prognoses and a high risk of recurrence, particularly in patients with HPV-positive Tonsillar squamous cell carcinomas.
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Furthermore, our results suggest that modulation of either HIPK2 levels or activity could be exploited to impair NRF2-mediated signalling in cancer cells, and thus sensitise them to chemotherapeutic drugs.
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PARP1 can modulate the tumor-suppressing function of HIPK2 by regulating the protein stability of HIPK2.
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Data show that HIPK2-T566 phosphorylation contributes to UV-induced HIPK2 activity but it is dispensable for doxorubicin response.
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In this study, we report that the kinase HIPK2 is responsible for facilitating the Fbw7-dependent proteasomal degradation of Notch1 by phosphorylating its intracellular domain (Notch1-IC) within the Cdc4 phosphodegron motif.
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the migration and invasion of hepatocellular carcinoma cells were impaired by knockdown of histone deacetylase 5 or hypoxia-inducible factor-1alpha but rescued when eliminating homeodomain-interacting protein kinase-2 in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2-hypoxia-inducible factor-1alpha pathway in hypoxia-induced metastasis.
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These results suggest that the HIPK2-phospho-Ser271 CREB axis is a new arsenic-responsive CREB activation mechanism in parallel with the PKA-phospho-Ser133 CREB axis.
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Results demonstrated that HIPK2 may function as a novel regulator to modulate hepatic stellate cells activation, potentially by inhibiting the TGF-beta1/Smad3 signaling pathway.
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Data show strong reduction of cell viability was induced in vitro and in vivo by the homeodomain interacting protein kinase 2 exon 8 spliced isoform (Hipk2-Deltae8)-specific siRNA, supporting a potential therapeutic application.
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Results indicate that Hipk2 exerts a relevant role in the survival of cerebellar Purkinje cells and that Hipk2 genetic ablation generates cerebellar dysfunction compatible with an ataxic-like phenotype.
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Our findings indicate that phosphorylation-dependent restriction of SIRT1 activity by HIPK2 shapes the p53 response
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The findings highlight a complex regulation of CREB-binding protein activity by HIPK2, which might be relevant for the control of specific sets of target genes involved in cellular proliferation, differentiation and apoptosis.
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MDM4/HIPK2/p53 cytoplasmic assembly uncovers coordinated repression of molecules with anti-apoptotic activity during early DNA damage response.
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Results indicate that HIPK2 acts as a caretaker gene, whose inactivation increases tumorigenicity and causes chromosomal instability by cytokinesis failure.
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HIPK2 expression tends to be decreased along tumor progression and may be involved with the invasive potential, suggesting a possible tumor suppressor role for HIPK2.
