ArticleThe Journal of cell biology1997
Cellular localization, expression, and structure of the nuclear dot protein 52.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 47 citations in OpenAlex.
- PEDV Nsp14 induces mitophagy-mediated degradation of MAVS to antagonize host innate immunity and facilitate viral proliferation.Journal of virology · 2025Article
- NDP52 and its emerging role in pathogenesis.Cell death & disease · 2025Review
- Autophagy receptor NDP52 alters DNA conformation to modulate RNA polymerase II transcription.Nature communications · 2023Article
- Crosstalk Between NDP52 and LUBAC in Innate Immune Responses, Cell Death, and Xenophagy.Frontiers in immunology · 2021Article
- CALCOCO1 acts with VAMP-associated proteins to mediate ER-phagy.The EMBO journal · 2020Article
- The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections.International journal of molecular sciences · 2020Review
- Competition between two high- and low-affinity protein-binding sites in myosin VI controls its cellular function.The Journal of biological chemistry · 2020Article
- Mechanistic insights into the interactions of NAP1 with the SKICH domains of NDP52 and TAX1BP1.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- NDP52 activates nuclear myosin VI to enhance RNA polymerase II transcription.Nature communications · 2017Article
- SUMO Ligase Protein Inhibitor of Activated STAT1 (PIAS1) Is a Constituent Promyelocytic Leukemia Nuclear Body Protein That Contributes to the Intrinsic Antiviral Immune Response to Herpes Simplex Virus 1.Journal of virology · 2016Article
- Mechanisms of Selective Autophagy.Journal of molecular biology · 2016Review
- Regulation of Toll-like receptor signaling by NDP52-mediated selective autophagy is normally inactivated by A20.Cellular and molecular life sciences : CMLS · 2012Article
- Transcriptional activation of the adenoviral genome is mediated by capsid protein VI.PLoS pathogens · 2012Article
- The TBK1 adaptor and autophagy receptor NDP52 restricts the proliferation of ubiquitin-coated bacteria.Nature immunology · 2009Article
- T6BP and NDP52 are myosin VI binding partners with potential roles in cytokine signalling and cell adhesion.Journal of cell science · 2007Article
- Subcellular localization of EEN/endophilin A2, a fusion partner gene in leukaemia.The Biochemical journal · 2004Article
- Essential role of survivin, an inhibitor of apoptosis protein, in T cell development, maturation, and homeostasis.The Journal of experimental medicine · 2004Article
- Differential expression profiling of head and neck squamous cell carcinoma (HNSCC).British journal of cancer · 2003Article
- Overexpression of the human MNB/DYRK1A gene induces formation of multinucleate cells through overduplication of the centrosome.BMC cell biology · 2003Article
- Evidence for covalent modification of the nuclear dot-associated proteins PML and Sp100 by PIC1/SUMO-1.The Journal of cell biology · 1997Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear dots containing PML and Sp100 proteins (NDs) play a role in the development of acute promyelocytic leukemia, are modified after infection with various viruses, and are autoimmunogenic in patients with primary biliary cirrhosis (PBC). PML and Sp100 gene expression is strongly enhanced by interferons (IFN). Based on immunostaining with a monoclonal antibody (mAb C8A2), a third protein, nuclear dot protein 52 (NDP52), was recently localized in NDs. Here we analyzed the cellular localization, expression, and structure of NDP52 in more detail. Our NDP52-specific sera revealed mainly cytoplasmic staining but no ND pattern, neither in untreated nor in IFN-treated cells. Cells transfected with NDP52 expression vectors showed exclusively cytoplasmic staining. In subcellular fractionation experiments, NDP52 was found in cytoplasmic and nuclear fractions. Unlike as described for Sp100 and PML, NDP52 mRNA and protein levels were only marginally enhanced by IFN gamma and not enhanced at all by IFN beta. NDP52 homodimerization but no heterodimerization with Sp100 or PML could be demonstrated. None of the 93 PBC sera tested contained autoantibodies against NDP52. Finally, mAb C8A2 reacted not only with NDP52 but also with a conformation-dependent epitope on the Sp100 protein. These data imply that NDP52 forms homodimers but no heterodimers with Sp100 and PML, lacks autoantigenicity in PBC, localizes mainly in the cytoplasm, and is associated with the nucleus, but not with NDs. Finally, unlike Sp100 and PML, NDP52 expression is neither markedly enhanced nor localization detectably altered by type I and II IFNs.
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