ArticleCell death & disease2015
Genetic ablation of homeodomain-interacting protein kinase 2 selectively induces apoptosis of cerebellar Purkinje cells during adulthood and generates an ataxic-like phenotype.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- PIWIL2 drives stroke progression via modulation of NF-κB signaling.Molecular therapy. Nucleic acids · 2026Article
- Loss of YY1 in Purkinje cells triggers cerebellar ataxia via Wnt10b-mediated impairment of dendrite development.iScience · 2026Article
- MiR-140-3p regulates axonal motor protein KIF5A and contributes to axonal transport degeneration in SMA.Cell death discovery · 2025Article
- Heparan sulfate binding protein treatment ameliorates neuropathology and behavioral abnormalities in mucopolysaccharidosis IIIB mice.Cell death discovery · 2025Article
- Phenotypical, genotypical and pathological characterization of the moonwalker mouse, a model of ataxia.Neurobiology of disease · 2024Article
- Metabolic rewiring and autophagy inhibition correct lysosomal storage disease in mucopolysaccharidosis IIIB.iScience · 2024Article
- miR135a administration ameliorates brain ischemic damage by preventing TRPM7 activation during brain ischemia.CNS neuroscience & therapeutics · 2024Article
- HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Preconditioning in hypoxic-ischemic neonate mice triggers NaCell death discovery · 2022Article
- Phenotypic Effects of Homeodomain-Interacting Protein Kinase 2 Deletion in Mice.International journal of molecular sciences · 2021Article
- HIPK2 phosphorylates HDAC3 for NF-κB acetylation to ameliorate colitis-associated colorectal carcinoma and sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Genetic Up-Regulation or Pharmacological Activation of the NaMolecular neurobiology · 2020Article
- miR-206 Reduces the Severity of Motor Neuron Degeneration in the Facial Nuclei of the Brainstem in a Mouse Model of SMA.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- Anti-miR-223-5p Ameliorates Ischemic Damage and Improves Neurological Function by Preventing NCKX2 Downregulation after Ischemia in Rats.Molecular therapy. Nucleic acids · 2019Article
- Double knock-out of Hmga1 and Hipk2 genes causes perinatal death associated to respiratory distress and thyroid abnormalities in mice.Cell death & disease · 2019Article
- HIPK2 is necessary for type I interferon-mediated antiviral immunity.Science signaling · 2019Article
- Midface and upper airway dysgenesis in FGFR2-related craniosynostosis involves multiple tissue-specific and cell cycle effects.Development (Cambridge, England) · 2018Article
- Preconditioning, induced by sub-toxic dose of the neurotoxin L-BMAA, delays ALS progression in mice and prevents NaCell death & disease · 2018Article
- High mobility group A1 protein modulates autophagy in cancer cells.Cell death and differentiation · 2017Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homeodomain-interacting protein kinase 2 (HIPK2) is a multitalented coregulator of an increasing number of transcription factors and cofactors involved in cell death and proliferation in several organs and systems. As Hipk2(-/-) mice show behavioral abnormalities consistent with cerebellar dysfunction, we investigated whether Hipk2 is involved in these neurological symptoms. To this aim, we characterized the postnatal developmental expression profile of Hipk2 in the brain cortex, hippocampus, striatum, and cerebellum of mice by real-time PCR, western blot analysis, and immunohistochemistry. Notably, we found that whereas in the brain cortex, hippocampus, and striatum, HIPK2 expression progressively decreased with age, that is, from postnatal day 1 to adulthood, it increased in the cerebellum. Interestingly, mice lacking Hipk2 displayed atrophic lobules and a visibly smaller cerebellum than did wild-type mice. More important, the cerebellum of Hipk2(-/-) mice showed a strong reduction in cerebellar Purkinje neurons during adulthood. Such reduction is due to the activation of an apoptotic process associated with a compromised proteasomal function followed by an unpredicted accumulation of ubiquitinated proteins. In particular, Purkinje cell dysfunction was characterized by a strong accumulation of ubiquitinated β-catenin. Moreover, our behavioral tests showed that Hipk2(-/-) mice displayed muscle and balance impairment, indicative of Hipk2 involvement in cerebellar function. Taken together, these 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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