ArticleNature communications2017
NDP52 activates nuclear myosin VI to enhance RNA polymerase II transcription.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
- Myosin VI drives breast cancer progression via SP1/CA9-mediated acidic tumor microenvironment remodeling and subsequent M2 macrophage polarization.Journal for immunotherapy of cancer · 2026Article
- 3D environment favors persistent changes in cell functions and altered morphology, wrinkling, and biomechanical signature of the nucleus.Cell reports. Physical science · 2026Article
- Nuclear myosin VI cooperates with actin to promote transcriptional cluster formation at androgen receptors.The Journal of biological chemistry · 2026Article
- Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025Review
- Nuclear receptors in health and disease: signaling pathways, biological functions and pharmaceutical interventions.Signal transduction and targeted therapy · 2025Review
- Actin from within - how nuclear myosins and actin regulate nuclear architecture and mechanics.Journal of cell science · 2025Review
- MYO6 contributes to tumor progression and enzalutamide resistance in castration-resistant prostate cancer by activating the focal adhesion signaling pathway.Cell communication and signaling : CCS · 2024Article
- Motor domain phosphorylation increases nucleotide exchange and turns MYO6 into a faster and stronger motor.Nature communications · 2024Article
- Myosin VI in the nucleolus of neurosecretory PC12 cells: its involvement in the maintenance of nucleolar structure and ribosome organization.Frontiers in physiology · 2024Article
- How myosin VI traps its off-state, is activated and dimerizes.Nature communications · 2023Article
- Myosin in chromosome organisation and gene expression.Biochemical Society transactions · 2023Review
- Nuclear myosin VI maintains replication fork stability.Nature communications · 2023Article
- Autophagy receptor NDP52 alters DNA conformation to modulate RNA polymerase II transcription.Nature communications · 2023Article
- Working a second job: Cell adhesion proteins that moonlight in the nucleus.Frontiers in cell and developmental biology · 2023Review
- Binding partners regulate unfolding of myosin VI to activate the molecular motor.The Biochemical journal · 2022Article
- Myosin VI regulates the spatial organisation of mammalian transcription initiation.Nature communications · 2022Article
- Measuring Nuclear Organization of Proteins with STORM Imaging and Cluster Analysis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Measuring Nuclear Mechanics with Atomic Force Microscopy.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Mechanical Regulation of Transcription: Recent Advances.Trends in cell biology · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Myosin VI (MVI) has been found to be overexpressed in ovarian, breast and prostate cancers. Moreover, it has been shown to play a role in regulating cell proliferation and migration, and to interact with RNA Polymerase II (RNAPII). Here, we find that backfolding of MVI regulates its ability to bind DNA and that a putative transcription co-activator NDP52 relieves the auto-inhibition of MVI to enable DNA binding. Additionally, we show that the MVI-NDP52 complex binds RNAPII, which is critical for transcription, and that depletion of NDP52 or MVI reduces steady-state mRNA levels. Lastly, we demonstrate that MVI directly interacts with nuclear receptors to drive expression of target genes, thereby suggesting a link to cell proliferation and migration. Overall, we suggest MVI may function as an auxiliary motor to drive transcription.
Indexed as
Identifiers
What OpenQuestion holds
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.