ArticleImmunity2015
The PIAS-like Coactivator Zmiz1 Is a Direct and Selective Cofactor of Notch1 in T Cell Development and Leukemia.
Article in Immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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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
46 citing papers in PubMed, 77 citations in OpenAlex.
- ZMIZ1 promotes aerobic glycolysis and development of hepatocellular carcinoma through inducing NOTCH1-mediated transcription of PYCR1.Journal of translational medicine · 2026Article
- Loss of Zmiz1 in Mice Leads to Impaired Cortical Development and Autistic-Like Behaviors.Biological psychiatry · 2026Article
- Article
- Genetic and functional analysis of ZMIZ1 in neurodevelopmental disorder with dysmorphic facies and distal skeletal anomalies (NEDDFSA): insights from muscle cells and signaling pathways.Pediatric research · 2026Article
- Targeting ZMIZ1 induces differentiation in acute myeloid leukemia via chromatin remodeling.Signal transduction and targeted therapy · 2026Article
- Transcriptional coregulator ZMIZ1 modulates estrogen responses that are essential for healthy endometrial function.The Journal of clinical investigation · 2025Article
- Cell-type-resolved genetic regulatory variation shapes inflammatory bowel disease risk.medRxiv : the preprint server for health sciences · 2025Article
- Native stem cell transcriptional circuits define cardinal features of high-risk leukemia.The Journal of experimental medicine · 2025Article
- Blockade of ZMIZ1-GATA4 Axis Regulation Restores Youthfulness to Aged Cartilage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- EndothelialFrontiers in cell and developmental biology · 2025Article
- Association of genetic variants, protein domains, and phenotypes in the ZMIZ1 syndromic neurodevelopmental disorder.Frontiers in neuroscience · 2025Article
- Single-cell resolution of intestinal regeneration in pythons without crypts illuminates conserved vertebrate regenerative mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of zinc finger MIZ-type containing 2 as an oncoprotein enhancing NAD-dependent protein deacetylase sirtuin-1 deacetylase activity to regulate Wnt and Hippo pathways in non-small-cell lung cancer.Cellular & molecular biology letters · 2024Article
- Endothelial Zmiz1 modulates physiological and pathophysiological angiogenesis during retinal development.bioRxiv : the preprint server for biology · 2024Article
- Targeting the ZMIZ1-Notch1 signaling axis for the treatment of tongue squamous cell carcinoma.Scientific reports · 2024Article
- Clinical report and genetic analysis of a novel variant in ZMIZ1 causing neurodevelopmental disorder with dysmorphic factors and distal skeletal anomalies in a Chinese family.Genes & genomics · 2024Review
- Development and validation of a cuproptosis-related prognostic model for acute myeloid leukemia patients using machine learning with stacking.Scientific reports · 2024Article
- Article
- Zmiz1 is a novel regulator of brain development associated with autism and intellectual disability.Frontiers in psychiatry · 2024Article
- Zmiz1 is a novel regulator of lymphatic endothelial cell gene expression and function.PloS one · 2024Article
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15 authors at 2 institutions in 1 country.
Funding
Abstract
Pan-NOTCH inhibitors are poorly tolerated in clinical trials because NOTCH signals are crucial for intestinal homeostasis. These inhibitors might also promote cancer because NOTCH can act as a tumor suppressor. We previously reported that the PIAS-like coactivator ZMIZ1 is frequently co-expressed with activated NOTCH1 in T cell acute lymphoblastic leukemia (T-ALL). Here, we show that similar to Notch1, Zmiz1 was important for T cell development and controlled the expression of certain Notch target genes, such as Myc. However, unlike Notch, Zmiz1 had no major role in intestinal homeostasis or myeloid suppression. Deletion of Zmiz1 impaired the initiation and maintenance of Notch-induced T-ALL. Zmiz1 directly interacted with Notch1 via a tetratricopeptide repeat domain at a special class of Notch-regulatory sites. In contrast to the Notch cofactor Maml, which is nonselective, Zmiz1 was selective. Thus, targeting the NOTCH1-ZMIZ1 interaction might combat leukemic growth while avoiding the intolerable toxicities of NOTCH inhibitors.
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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.