ArticleCell proliferation2009
HIPK2 is involved in cell proliferation and its suppression promotes growth arrest independently of DNA damage.
Article in Cell proliferation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Cardiomyocytes HIPK2 regulates myocardial inflammation and heart function through purinergic signaling.Cell communication and signaling : CCS · 2026Article
- The Sweet Side of HIPK2.Cancers · 2023Review
- High glucose macrophage exosomes enhance atherosclerosis by driving cellular proliferation & hematopoiesis.iScience · 2021Article
- Phenotypic Effects of Homeodomain-Interacting Protein Kinase 2 Deletion in Mice.International journal of molecular sciences · 2021Article
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- Homeodomain-interacting protein kinase 2 suppresses proliferation and aerobic glycolysis via ERK/cMyc axis in pancreatic cancer.Cell proliferation · 2019Article
- Midface and upper airway dysgenesis in FGFR2-related craniosynostosis involves multiple tissue-specific and cell cycle effects.Development (Cambridge, England) · 2018Article
- Homeodomain-interacting protein kinase promotes tumorigenesis and metastatic cell behavior.Disease models & mechanisms · 2018Article
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- Homeodomain-interacting protein kinase 2 (HIPK2): a promising target for anti-cancer therapies.Oncotarget · 2017Review
- HIPK2 Overexpression and Its Prognostic Role in Human Papillomavirus-Positive Tonsillar Squamous Cell Carcinoma.BioMed research international · 2017Article
- Article
- Genetic ablation of homeodomain-interacting protein kinase 2 selectively induces apoptosis of cerebellar Purkinje cells during adulthood and generates an ataxic-like phenotype.Cell death & disease · 2015Article
- HIPK2 deficiency causes chromosomal instability by cytokinesis failure and increases tumorigenicity.Oncotarget · 2015Article
- HIPK2 sustains apoptotic response by phosphorylating Che-1/AATF and promoting its degradation.Cell death & disease · 2014Article
- Homeodomain-interacting protein kinase 2-dependent repression of myogenic differentiation is relieved by its caspase-mediated cleavage.Nucleic acids research · 2013Article
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- Homeodomain-interacting protein kinase-2 stabilizes p27(kip1) by its phosphorylation at serine 10 and contributes to cell motility.The Journal of biological chemistry · 2011Article
- High-throughput kinase profiling: a more efficient approach toward the discovery of new kinase inhibitors.Chemistry & biology · 2011Article
- The loss of the p53 activator HIPK2 is responsible for galectin-3 overexpression in well differentiated thyroid carcinomas.PloS one · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
INTRODUCTION/
objectivesThe serine/threonine kinase homeodomain-interacting protein kinase 2 (HIPK2) is a co-regulator of an increasing number of transcription factors and cofactors involved in DNA damage response and development. We and others have cloned HIPK2 as an interactor of the p53 oncosuppressor, and have studied the role of this interaction in cell response to stress. Nevertheless, our original cloning of HIPK2 as a p53-binding protein, was aimed at discovering partners of p53 involved in cell differentiation and development, still controversial p53 functions. To this aim, we used p53 as bait in yeast two-hybrid screening of a cDNA library from mouse embryo (day 11 postcoitus) when p53 is highly expressed. METHODS AND
resultsIn this study, we directly explored whether HIPK2 and p53 cooperate in cell differentiation. By measuring HIPK2 expression and activity in skeletal muscle and haemopoietic differentiation, we observed inverse behaviour of HIPK2 and p53--excluding cooperation activity of these two factors in this event. However, by HIPK2 depletion experiments, we showed that drastic HIPK2 suppression promotes cell-cycle arrest by induction of the cyclin-dependent kinase inhibitor p21(Waf-1/Cip-1). HIPK2 activity is independent of DNA damage and takes place in cell-cycle-arresting conditions, such as terminal differentiation, growth factor deprivation, and G(0) resting.
conclusionsHIPK2 was found to be involved in cell-cycle regulation dependent on p21(Waf-1/Cip-1) and independent of DNA damage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.