ArticleThe Journal of experimental medicine2013
Poly(ADP-ribose) polymerase 1 regulates nuclear reprogramming and promotes iPSC generation without c-Myc.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
The trial behind it
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Who cites it
49 citing papers in PubMed, 95 citations in OpenAlex.
- A synthetic benzoxazine dimer derivative targets c-Myc to inhibit colorectal cancer progression.Molecular oncology · 2026Article
- ACYP2 Induces Temozolomide Resistance in Glioblastoma by Promoting PARP1-Mediated DNA Damage Repair.Molecular cancer research : MCR · 2026Article
- CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025Review
- Proteogenomic reprogramming to a functional human blastomere-like stem cell state via a PARP-DUX4 regulatory axis.Cell reports · 2025Article
- Covalent PARylation of DNA base excision repair proteins regulates DNA demethylation.Nature communications · 2024Article
- ZSCAN4 interacts with PARP1 to promote DNA repair in mouse embryonic stem cells.Cell & bioscience · 2023Article
- Crosstalk of moderate ROS and PARP-1 contributes to sustainable proliferation of conditionally reprogrammed keratinocytes.Journal of biochemical and molecular toxicology · 2023Article
- Multiomics analysis of the NADGenes & development · 2022Article
- PARP1-PKM2 Axis Mediates Right Ventricular Failure Associated With Pulmonary Arterial Hypertension.JACC. Basic to translational science · 2022Article
- Article
- MyoD induces ARTD1 and nucleoplasmic poly-ADP-ribosylation during fibroblast to myoblast transdifferentiation.iScience · 2021Article
- p66ShcA potentiates the cytotoxic response of triple-negative breast cancers to PARP inhibitors.JCI insight · 2021Article
- The role of Trop2 in prostate cancer: an oncogene, biomarker, and therapeutic target.American journal of clinical and experimental urology · 2021Article
- Different regulation of PARP1, PARP2, PARP3 and TRPM2 genes expression in acute myeloid leukemia cells.BMC cancer · 2020Article
- Review
- PARPs and ADP-ribosylation in RNA biology: from RNA expression and processing to protein translation and proteostasis.Genes & development · 2020Review
- Trop2 is a driver of metastatic prostate cancer with neuroendocrine phenotype via PARP1.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Defective neurogenesis and schizophrenia-like behavior in PARP-1-deficient mice.Cell death & disease · 2019Article
- Ash2l interacts with Oct4-stemness circuitry to promote super-enhancer-driven pluripotency network.Nucleic acids research · 2019Article
- Oncogenic activity of poly (ADP-ribose) glycohydrolase.Oncogene · 2019Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Poly(ADP-ribose) polymerase 1 (Parp1) catalyzes poly(ADP-ribosylation) (PARylation) and induces replication networks involved in multiple nuclear events. Using mass spectrometry and Western blotting, Parp1 and PARylation activity were intensively detected in induced pluripotent stem cells (iPSCs) and embryonic stem cells, but they were lower in mouse embryonic fibroblasts (MEFs) and differentiated cells. We show that knockdown of Parp1 and pharmacological inhibition of PARylation both reduced the efficiency of iPSC generation induced by Oct4/Sox2/Klf4/c-Myc. Furthermore, Parp1 is able to replace Klf4 or c-Myc to enhance the efficiency of iPSC generation. In addition, mouse iPSCs generated from Oct4/Sox2/Parp1-overexpressing MEFs formed chimeric offspring. Notably, the endogenous Parp1 and PARylation activity was enhanced by overexpression of c-Myc and repressed by c-Myc knockdown. A chromatin immunoprecipitation assay revealed a direct interaction of c-Myc with the Parp1 promoter. PAR-resin pulldown, followed by proteomic analysis, demonstrated high levels of PARylated Chd1L, DNA ligase III, SSrp1, Xrcc-6/Ku70, and Parp2 in pluripotent cells, which decreased during the differentiation process. These data show that the activation of Parp1, partly regulated by endogenous c-Myc, effectively promotes iPSC production and helps to maintain a pluripotent state by posttranslationally modulating protein PARylation.
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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.