ReviewAging2010
Unfolded p53 in the pathogenesis of Alzheimer's disease: is HIPK2 the link?
Review in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Cell-type-aware transcriptome-wide association studies identify 91 independent risk genes for Alzheimer's disease dementia.Communications biology · 2026Article
- Recent Advances on Mutant p53: Unveiling Novel Oncogenic Roles, Degradation Pathways, and Therapeutic Interventions.Biomolecules · 2024Review
- HIPK2 in the physiology of nervous system and its implications in neurological disorders.Biochimica et biophysica acta. Molecular cell research · 2023Review
- Sting and p53 DNA repair pathways are compromised in Alzheimer's disease.Scientific reports · 2023Article
- The Sweet Side of HIPK2.Cancers · 2023Review
- Post-translational Modifications of the p53 Protein and the Impact in Alzheimer's Disease: A Review of the Literature.Frontiers in aging neuroscience · 2022Review
- Anti-Oxidative, Anti-Inflammatory and Anti-Apoptotic Effects of Flavonols: Targeting Nrf2, NF-κB and p53 Pathways in Neurodegeneration.Antioxidants (Basel, Switzerland) · 2021Review
- EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2020Review
- How to Build and to Protect the Neuromuscular Junction: The Role of the Glial Cell Line-Derived Neurotrophic Factor.International journal of molecular sciences · 2020Review
- Mitochondria: A Galaxy in the Hematopoietic and Leukemic Stem Cell Universe.International journal of molecular sciences · 2020Review
- Role of p53 in the Regulation of Cellular Senescence.Biomolecules · 2020Review
- HIPK2 role in the tumor-host interaction: Impact on fibroblasts transdifferentiation CAF-like.IUBMB life · 2019Article
- Gut Microbiota Disorder, Gut Epithelial and Blood-Brain Barrier Dysfunctions in Etiopathogenesis of Dementia: Molecular Mechanisms and Signaling Pathways.Neuromolecular medicine · 2019Review
- Variants regulating ZBTB4 are associated with age-at-onset of Alzheimer's disease.Genes, brain, and behavior · 2018Article
- Molecular Mechanisms for Herpes Simplex Virus Type 1 Pathogenesis in Alzheimer's Disease.Frontiers in aging neuroscience · 2018Review
- Inflammatory Response in the CNS: Friend or Foe?Molecular neurobiology · 2017Review
- Biomarkers for Alzheimer's Disease Diagnosis.Current Alzheimer research · 2017Review
- Plasma microRNA biomarker detection for mild cognitive impairment using differential correlation analysis.Biomarker research · 2016Article
- Amyloid accumulation is a late event in sporadic Alzheimer's disease-like pathology in nontransgenic rats.Oncotarget · 2015Article
- HIPK2 is a new drug target for anti-fibrosis therapy in kidney disease.Frontiers in physiology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p53 transcriptional activity depends mainly on posttranslational modifications and protein/protein interaction. Another important mechanism that controls p53 function is its conformational stability since p53 is an intrinsically unstable protein. An altered conformational state of p53, independent from point mutations, has been reported in tissues from patients with Alzheimer's disease (AD), leading to an impaired and dysfunctional response to stressors. Recent evidence shows that one of the activators that induces p53 posttranslational modification and wild-type conformational stability is homeodomain interacting protein kinase 2 (HIPK2). Hence, conditions that induce HIPK2 deregulation would result in a dysfunctional response to stressors by affecting p53 activity. Discovering the mechanisms of HIPK2 activation/inhibition and the ways to manipulate HIPK2 activity are an interesting option to affect several biological pathways, including those underlying AD. Soluble beta-amyloid peptides have recently been involved in HIPK2 degradation, in turn regulating the p53 conformational state and vulnerability to a noxious stimulus, before triggering the amyloidogenic cascade. Here we discuss about these findings and the potential relevance of HIPK2 as a target for AD and highlight the existence of a novel amyloid-based mechanism in AD potentially leading to the survival of injured dysfunctional cells.
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What OpenQuestion holds
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.