ArticleScientific reports2016
A PARP1-ERK2 synergism is required for the induction of LTP.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- The TyrRS cascade: circadian gating of neuronal DNA repair and its collapse in aging.GeroScience · 2026Review
- Synaptic potentiation requires PARP1 activation: prevailing concepts are revisited.Molecular psychiatry · 2026Review
- Exploring the role of parthanatos in CNS injury: Molecular insights and therapeutic approaches.Journal of advanced research · 2025Review
- Poly ADP-ribosylation regulates Arc expression and promotes adaptive stress-coping.Psychopharmacology · 2025Article
- Adenosine diphosphate-ribosylation greatly affects proteins function: a focus on neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Transcriptional regulation mechanism of PARP1 and its application in disease treatment.Epigenetics & chromatin · 2024Review
- 1,25-Dihydroxyvitamin DInternational journal of molecular sciences · 2024Article
- Role of NADCellular and molecular neurobiology · 2023Review
- Poly(ADP-ribosyl)ation of acetyltransferase NAT10 by PARP1 is required for its nucleoplasmic translocation and function in response to DNA damage.Cell communication and signaling : CCS · 2022Article
- Review
- The key players of parthanatos: opportunities for targeting multiple levels in the therapy of parthanatos-based pathogenesis.Cellular and molecular life sciences : CMLS · 2022Review
- The Modified Phenanthridine PJ34 Unveils an Exclusive Cell-Death Mechanism in Human Cancer Cells.Cancers · 2020Review
- Evidence for Decreased Nucleolar PARP-1 as an Early Marker of Cognitive Impairment.Neural plasticity · 2019Article
- Psoralidin Stimulates Expression of Immediate-Early Genes and Synapse Development in Primary Cortical Neurons.Neurochemical research · 2018Article
- PARP1-Erk synergism in proliferating cells.Oncotarget · 2018Article
- Antidepressant-Like Actions of Inhibitors of Poly(ADP-Ribose) Polymerase in Rodent Models.The international journal of neuropsychopharmacology · 2017Article
- A PARP1-Erk2 synergism is required for stimulation-induced expression of immediate early genes.Gene & translational bioinformatics · 2016Article
- Signal-induced PARP1-Erk synergism mediates IEG expression.Signal transduction and targeted therapyReview
- Presynaptic long-term potentiation requires extracellular signal-regulated kinases in the anterior cingulate cortex.Molecular painReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
Unexpectedly, a post-translational modification of DNA-binding proteins, initiating the cell response to single-strand DNA damage, was also required for long-term memory acquisition in a variety of learning paradigms. Our findings disclose a molecular mechanism based on PARP1-Erk synergism, which may underlie this phenomenon. A stimulation induced PARP1 binding to phosphorylated Erk2 in the chromatin of cerebral neurons caused Erk-induced PARP1 activation, rendering transcription factors and promoters of immediate early genes (IEG) accessible to PARP1-bound phosphorylated Erk2. Thus, Erk-induced PARP1 activation mediated IEG expression implicated in long-term memory. PARP1 inhibition, silencing, or genetic deletion abrogated stimulation-induced Erk-recruitment to IEG promoters, gene expression and LTP generation in hippocampal CA3-CA1-connections. Moreover, a predominant binding of PARP1 to single-strand DNA breaks, occluding its Erk binding sites, suppressed IEG expression and prevented the generation of LTP. These findings outline a PARP1-dependent mechanism required for LTP generation, which may be implicated in long-term memory acquisition and in its deterioration in senescence.
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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.