ArticleThe Journal of biological chemistry
The 89-kDa PARP1 cleavage fragment serves as a cytoplasmic PAR carrier to induce AIF-mediated apoptosis.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers, 1 of them a synthesis that pooled it.
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Who cites it
130 citing papers in PubMed, 1 synthesis or guideline pooled it, 224 citations in OpenAlex.
- Comprehensive analysis of regulated cell death pathways: intrinsic disorder, protein-protein interactions, and cross-pathway communication.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- The calcium channel blocker diltiazem ameliorates parthanatos in juvenile neuronal ceroid lipofuscinosis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Defining early carcinogenic markers for the prediction of the hazard potential of mineral fibres in an in vitro human 3D bronchial model.Archives of toxicology · 2026Article
- circSCAF11 Attenuates TGF-β/SMAD2/3 Signaling to Suppress Colorectal Cancer Progression.Cancers · 2026Article
- Antiproliferation and Anti-invasion Activity of Binuclear Copper(II) Complex in BRAFi-Resistant Melanoma Cells.ACS pharmacology & translational science · 2026Article
- HIRA-SETDB1-H3K9me3 axis regulates chromatin architecture in leukemia cells.The Journal of biological chemistry · 2026Article
- Article
- Folic Acid-Guided PLGA-Zein Core-Shell Nanoparticles for Co-Delivery of Temozolomide and Ellagic Acid to Overcome PARP-Mediated Chemoresistance in Glioblastoma.Pharmaceutics · 2026Article
- Repetitive transcranial magnetic stimulation is associated with improved functional recovery and time-dependent changes in apoptosis-related execution-phase markers after spinal cord injury.Scientific reports · 2026Article
- ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway.International journal of molecular sciences · 2026Article
- Resveratrol potentiates chemotherapeutic efficacy of olaparib in MCF7 human breast cancer cells by inducing apoptosis.Irish journal of medical science · 2026Article
- Non-pyroptotic caspase-11 activity regulates osteoclastogenesis and pathological bone loss.Cell death and differentiation · 2026Article
- Cleavage and inactivation of poly(ADP-ribose) polymerase in peripheral blood mononuclear cells of patients with acute respiratory distress syndrome.Respiratory research · 2026Article
- Structure-Activity Relationship Studies Enable Optimization of a Small-Molecule Autophagy Activator and Evaluation of Effects on Cell Death Pathways.ACS pharmacology & translational science · 2026Article
- Article
- Novel quinoxaline-based survivin degraders overcome docetaxel-resistance in castration-resistant prostate cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2026Review
- Article
- The effect of PARP and PLK1 dual inhibition on the expression of important protein signaling pathways, DNA damage, and molecular docking scores against MCF-7 and MDA-MB-231 breast cancer cell lines.Irish journal of medical science · 2026Article
- Article
- PARP-1 prevents osteoarthritis pathogenesis by inhibiting apoptosis in chondrocytes: an animal study.Arthritis research & therapy · 2026Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Poly(ADP-ribose) polymerase 1 (PARP1) is a nuclear protein that is activated by binding to DNA lesions and catalyzes poly(ADP-ribosyl)ation of nuclear acceptor proteins, including PARP1 itself, to recruit DNA repair machinery to DNA lesions. When excessive DNA damage occurs, poly(ADP-ribose) (PAR) produced by PARP1 is translocated to the cytoplasm, changing the activity and localization of cytoplasmic proteins, e.g., apoptosis-inducing factor (AIF), hexokinase, and resulting in cell death. This cascade, termed parthanatos, is a caspase-independent programmed cell death distinct from necrosis and apoptosis. In contrast, PARP1 is a substrate of activated caspases 3 and 7 in caspase-dependent apoptosis. Once cleaved, PARP1 loses its activity, thereby suppressing DNA repair. Caspase cleavage of PARP1 occurs within a nuclear localization signal near the DNA-binding domain, resulting in the formation of 24-kDa and 89-kDa fragments. In the present study, we found that caspase activation by staurosporine- and actinomycin D-induced PARP1 autopoly(ADP-ribosyl)ation and fragmentation, generating poly(ADP-ribosyl)ated 89-kDa and 24-kDa PARP1 fragments. The 89-kDa PARP1 fragments with covalently attached PAR polymers were translocated to the cytoplasm, whereas 24-kDa fragments remained associated with DNA lesions. In the cytoplasm, AIF binding to PAR attached to the 89-kDa PARP1 fragment facilitated its translocation to the nucleus. Thus, the 89-kDa PARP1 fragment is a PAR carrier to the cytoplasm, inducing AIF release from mitochondria. Elucidation of the caspase-mediated interaction between apoptosis and parthanatos pathways extend the current knowledge on mechanisms underlying programmed cell death and may lead to new therapeutic targets.
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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.