ArticleProceedings of the National Academy of Sciences of the United States of America2007
A viral adaptor protein modulating casein kinase II activity induces cytopathic effects in permissive cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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Who cites it
32 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Review
- The role of post-translational modifications in parvovirus life cycle.Frontiers in veterinary science · 2025Review
- Parvoviruses NS1 oncolytic attributes: mechanistic insights and synergistic anti-tumor therapeutic strategies.Frontiers in microbiology · 2025Review
- Minute virus of mice NS1 redirects casein kinase 2 specificity to suppress the ATR DNA damage response pathway during infection.Journal of virology · 2024Article
- Novel mutation N588 residue in the NS1 protein of feline parvovirus greatly augments viral replication.Journal of virology · 2024Article
- Development of a Double-Antibody Sandwich ELISA Based on a Monoclonal Antibody against the Viral NS1 Protein for the Detection of Chicken Parvovirus.Pathogens (Basel, Switzerland) · 2024Article
- The Autonomous Parvovirus Minute Virus of Mice Localizes to Cellular Sites of DNA Damage Using ATR Signaling.Viruses · 2023Article
- Design and Characterization of Mutated Variants of the Oncotoxic Parvoviral Protein NS1.Viruses · 2023Article
- Parvovirus nonstructural protein 2 interacts with chromatin-regulating cellular proteins.PLoS pathogens · 2022Article
- Review
- Canine Parvovirus and Its Non-Structural Gene 1 as Oncolytic Agents: Mechanism of Action and Induction of Anti-Tumor Immune Response.Frontiers in oncology · 2021Review
- The NS1 protein of the parvovirus MVM Aids in the localization of the viral genome to cellular sites of DNA damage.PLoS pathogens · 2020Article
- Tropomyosin pseudo-phosphorylation results in dilated cardiomyopathy.The Journal of biological chemistry · 2019Article
- Viral genes as oncolytic agents for cancer therapy.Cellular and molecular life sciences : CMLS · 2015Review
- PKCη/Rdx-driven phosphorylation of PDK1: a novel mechanism promoting cancer cell survival and permissiveness for parvovirus-induced lysis.PLoS pathogens · 2015Article
- Oncolytic parvoviruses: from basic virology to clinical applications.Virology journal · 2015Review
- Tumor Selectivity of Oncolytic Parvoviruses: From in vitro and Animal Models to Cancer Patients.Frontiers in bioengineering and biotechnology · 2015Review
- Complementary induction of immunogenic cell death by oncolytic parvovirus H-1PV and gemcitabine in pancreatic cancer.Journal of virology · 2014Article
- Role of mitochondria in parvovirus pathology.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autonomous parvoviruses induce severe morphological and physiological alterations in permissive host cells, eventually leading to cell lysis and release of progeny virions. Viral cytopathic effects (CPE) result from specific rearrangements and destruction of cytoskeletal micro- and intermediate filaments. We recently reported that inhibition of endogenous casein kinase II (CKII) protects target cells from parvovirus minute virus of mice (MVM)-induced CPE, pointing to this kinase as an effector of MVM toxicity. The present work shows that the parvoviral NS1 protein mediates CKII-dependent cytoskeletal alterations and cell death. NS1 can act as an adaptor molecule, linking the cellular protein kinase CKIIalpha to tropomyosin and thus modulating the substrate specificity of the kinase. This action results in an altered tropomyosin phosphorylation pattern both in vitro and in living cells. The capacity of NS1 to induce CPE was impaired by mutations abolishing binding with either CKIIalpha or tropomyosin. The cytotoxic adaptor function of NS1 was confirmed with fusion peptides, where the tropomyosin-binding domain of NS1 and CKIIalpha are physically linked. These adaptor peptides were able to mimic NS1 in its ability to induce death of transformed MVM-permissive cells.
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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.