ArticleNature communications2013
Miz1 is required to maintain autophagic flux.
Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 54 citations in OpenAlex.
- MIZ-1 controls transcriptional programs required for BCR signaling, actin dynamics, and naïve B cell survival.Frontiers in immunology · 2026Article
- Unraveling Novel Strategies: Targeting Miz1 for Degradation to Enhance Antiviral Defense against Influenza A Virus.Journal of respiratory biology and translational medicine · 2024Article
- Regulation of BCR-mediated CaScience immunology · 2024Article
- Review
- In vivo screening characterizes chromatin factor functions during normal and malignant hematopoiesis.Nature genetics · 2023Article
- Time-of-day defines NADNature communications · 2023Article
- Lessons in aging from Myc knockout mouse models.Frontiers in cell and developmental biology · 2023Review
- AMBRA1 and its role as a target for anticancer therapy.Frontiers in oncology · 2022Review
- Targeting cancer stem cells in medulloblastoma by inhibiting AMBRA1 dual function in autophagy and STAT3 signalling.Acta neuropathologica · 2021Article
- MYC- and MIZ1-Dependent Vesicular Transport of Double-Strand RNA Controls Immune Evasion in Pancreatic Ductal Adenocarcinoma.Cancer research · 2021Article
- Zinc Finger Proteins in Neuro-Related Diseases Progression.Frontiers in neuroscience · 2021Review
- Identification of the transcription factor Miz1 as an essential regulator of diphthamide biosynthesis using a CRISPR-mediated genome-wide screen.PLoS genetics · 2020Article
- Epithelial cell-specific loss of function ofScience advances · 2020Article
- Developmental vascular regression is regulated by a Wnt/β-catenin, MYC and CDKN1A pathway that controls cell proliferation and cell death.Development (Cambridge, England) · 2018Article
- Miz1 Controls Schwann Cell Proliferation via H3K36The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Convergence of Cancer Metabolism and Immunity: an Overview.Biomolecules & therapeutics · 2018Review
- Increased expression of Myc-interacting zinc finger protein 1 in APP/PS1 mice.Experimental and therapeutic medicine · 2017Article
- Structural Insights into c-Myc-interacting Zinc Finger Protein-1 (Miz-1) Delineate Domains Required for DNA Scanning and Sequence-specific Binding.The Journal of biological chemistry · 2017Article
- MYC/MIZ1-dependent gene repression inversely coordinates the circadian clock with cell cycle and proliferation.Nature communications · 2016Article
- Convergence of cMyc and β-catenin on Tcf7l1 enables endoderm specification.The EMBO journal · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Miz1 is a zinc finger protein that regulates the expression of cell cycle inhibitors as part of a complex with Myc. Cell cycle-independent functions of Miz1 are poorly understood. Here we use a Nestin-Cre transgene to delete an essential domain of Miz1 in the central nervous system (Miz1(ΔPOZNes)). Miz1(ΔPOZNes) mice display cerebellar neurodegeneration characterized by the progressive loss of Purkinje cells. Chromatin immunoprecipitation sequencing and biochemical analyses show that Miz1 activates transcription upon binding to a non-palindromic sequence present in core promoters. Target genes of Miz1 encode regulators of autophagy and proteins involved in vesicular transport that are required for autophagy. Miz1(ΔPOZ) neuronal progenitors and fibroblasts show reduced autophagic flux. Consistently, polyubiquitinated proteins and p62/Sqtm1 accumulate in the cerebella of Miz1(ΔPOZNes) mice, characteristic features of defective autophagy. Our data suggest that Miz1 may link cell growth and ribosome biogenesis to the transcriptional regulation of vesicular transport and autophagy.
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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.