ArticleOncogene2013
Poly(ADP-ribose) polymerase family member 14 (PARP14) is a novel effector of the JNK2-dependent pro-survival signal in multiple myeloma.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 111 citations in OpenAlex.
- Tumor-intrinsic IFNγ signaling and niche adaptation drive early colonization in ovarian cancer metastasis.Nature communications · 2026Article
- Cerebral dopamine neurotrophic factor for spinal cord injury: Targeting JNK1 to relieve neuroinflammation and improve neural repair.Neural regeneration research · 2026Article
- Structure, function, regulation, evolution, and therapeutic implications of PARP14.Genes & development · 2026Review
- The RRM domains of PARP14 mediate replication fork degradation in BRCA2-deficient cells.NAR cancer · 2026Article
- Roles of ADP-Ribosyltransferases in Cancer.Oncology research · 2026Review
- Mono-ADP-ribosylating PARP enzymes in cellular signaling and disease.Journal of cell science · 2025Review
- PARP9-PARP13-PARP14 axis tunes colorectal cancer response to radiotherapy.Journal of experimental & clinical cancer research : CR · 2025Article
- PARP enzymes and mono-ADP-ribosylation: advancing the connection from interferon-signalling to cancer biology.Expert reviews in molecular medicine · 2024Review
- KH-like Domains in PARP9/DTX3L and PARP14 Coordinate Protein-Protein Interactions to Promote Cancer Cell Survival.Journal of molecular biology · 2024Article
- Exploration of glycosyltransferases mutation status in cervical cancer reveals PARP14 as a potential prognostic marker.Glycoconjugate journal · 2023Article
- Using TLC-MALDI-TOF to Interrogate In Vitro Peptidyl Proximal Preferences of PARP14 and Glycohydrolase Specificity.Molecules (Basel, Switzerland) · 2023Article
- Privileged Scaffolds for Potent and Specific Inhibitors of Mono-ADP-Ribosylating PARPs.Molecules (Basel, Switzerland) · 2023Review
- Article
- Development of a Covalent Inhibitor of c-Jun N-Terminal Protein Kinase (JNK) 2/3 with Selectivity over JNK1.Journal of medicinal chemistry · 2023Article
- An Integrated Methodology to Quantify the Glycolytic Stress in Plasma Cell Myeloma in Response to Cytotoxic Drugs.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Screening Kinase-Dependent Phosphorylation of Key Metabolic Reprogramming Regulators.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Inhibition of glutaminolysis restores mitochondrial function in senescent stem cells.Cell reports · 2022Article
- PARP10 Mediates Mono-ADP-Ribosylation of Aurora-A Regulating G2/M Transition of the Cell Cycle.Cancers · 2022Article
- The KU-PARP14 axis differentially regulates DNA resection at stalled replication forks by MRE11 and EXO1.Nature communications · 2022Article
- The Histone Demethylase Inhibitor GSK-J4 Is a Therapeutic Target for the Kidney Fibrosis of Diabetic Kidney Disease via DKK1 Modulation.International journal of molecular sciences · 2022Article
5 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Regulation of cell survival is a key part of the pathogenesis of multiple myeloma (MM). Jun N-terminal kinase (JNK) signaling has been implicated in MM pathogenesis, but its function is unclear. To elucidate the role of JNK in MM, we evaluated the specific functions of the two major JNK proteins, JNK1 and JNK2. We show here that JNK2 is constitutively activated in a panel of MM cell lines and primary tumors. Using loss-of-function studies, we demonstrate that JNK2 is required for the survival of myeloma cells and constitutively suppresses JNK1-mediated apoptosis by affecting expression of poly(ADP-ribose) polymerase (PARP)14, a key regulator of B-cell survival. Strikingly, we found that PARP14 is highly expressed in myeloma plasma cells and associated with disease progression and poor survival. Overexpression of PARP14 completely rescued myeloma cells from apoptosis induced by JNK2 knockdown, indicating that PARP14 is critically involved in JNK2-dependent survival. Mechanistically, PARP14 was found to promote the survival of myeloma cells by binding and inhibiting JNK1. Moreover, inhibition of PARP14 enhances the sensitization of MM cells to anti-myeloma agents. Our findings reveal a novel regulatory pathway in myeloma cells through which JNK2 signals cell survival via PARP14, and identify PARP14 as a potential therapeutic target in myeloma.
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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.