ArticleMolecular cell2020
Zmat3 Is a Key Splicing Regulator in the p53 Tumor Suppression Program.
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Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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66citing papers in PubMed
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66 citing papers in PubMed, 117 citations in OpenAlex.
- P-selectin delineates conserved functional heterogeneity in early hematopoietic stem cell aging in humans and mice.The EMBO journal · 2026Article
- ZMAT3 alleviates cell death in Fanconi anemia via adaptation of sphingolipid metabolism.Science advances · 2026Article
- Splice-altering TP53 missense mutations as drivers of dysfunction and targets for RNA-based therapy.Stem cell research & therapy · 2026Article
- Covalent inhibitors of human papillomavirus type 16 E6 protein restore p53 function and suppress growth of HPV-driven tumors in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
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- Pharmacological targeting of SF3a1-MDM4 splicing vulnerability in ovarian cancer with rifaximin and antisense oligonucleotide.Journal of translational medicine · 2026Article
- Spatial single cell transcriptomic analysis informs tumor developmental hierarchy of DICER1 syndrome related sarcoma.Nature communications · 2026Article
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- p53 Drives Lung Cancer Regression through a TSC2/TFEB-dependent Senescence Program.Cancer discovery · 2026Article
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- Splicing factor FUS facilitates the progression of PIT1-lineage PitNETs by upregulating MDM2.Theranostics · 2026Article
- Integrative multiomic approaches reveal ZMAT3 and p21 as conserved hubs in the p53 tumor suppression network.Cell death and differentiation · 2025Article
- Identification of radiation-sensitive genes as biomarkers for biodosimetry: an ex vivo analysis of TNFRSF10B, ZMAT3, POLH, and PLK2 in human blood samples.BMC medical genomics · 2025Article
- Transcriptomic profiles of susceptibility and resilience to stress in the amygdala and hippocampus of male rats.Neurobiology of stress · 2025Article
- Extracellular vesicle-mediated delivery of circp53 suppresses the progression of multiple cancers by activating the CypD/TRAP/HSP90 pathway.Experimental & molecular medicine · 2025Article
- A base editing platform for the correction of cancer driver mutations unmasks conserved p53 transcription programs.Genome biology · 2025Article
- Ribosomal RNA transcription regulates splicing through ribosomal protein RPL22.Cell chemical biology · 2025Article
- Transcriptomic Insights Into Serum-Free Medium Adaptation and Temperature Reduction in Chinese Hamster Ovary Cell Cultures.Biotechnology journal · 2025Article
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- FN1 shapes the behavior of papillary thyroid carcinoma through alternative splicing of EDB region.Scientific reports · 2025Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 4 institutions in 1 country.
Kathryn T Bieging-RolettDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Alyssa M KaiserDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
David W MorgensDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Anthony M BoutelleDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Jose A SeoaneDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Eric L Van NostrandDepartment of Cellular and Molecular Medicine & Institute for Genomic Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Changyu ZhuCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Shauna L HoulihanCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Stephano S MelloDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Brian A YeeDepartment of Cellular and Molecular Medicine & Institute for Genomic Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Jacob McClendonDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Sarah E PierceDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ian P WintersDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Mengxiong WangDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Andrew J ConnollyDepartment of Pathology, UCSF School of Medicine, San Francisco, CA 94143, USA.
Scott W LoweCancer Biology and Genetics Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Christina CurtisDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Gene W YeoDepartment of Cellular and Molecular Medicine & Institute for Genomic Medicine, University of California San Diego, La Jolla, CA 92037, USA.
Monte M WinslowDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michael C BassikDepartment of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
Laura D AttardiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: attardi@stanford.edu.
Stanford University · USMemorial Sloan Kettering Cancer Center · USUniversity of California, San Diego · USUniversity of California, San Francisco · US
Funding
X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4MVIRAL MALIGNANCYP30CA023100 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Jesse Nodora · 1985 to 2026
$124.9MTranslational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Vittorio Sebastiano · 2007 to 2026
$71.4MScientific ReagentsP01CA087497 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI LOWE, SCOTT W. · 2000 to 2021
$35.4MLeveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1MIntegrative approaches to elucidate p53 transcriptional networks during carcinogenesisR35CA197591 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI · 2015 to 2026
$11.6MRapid and flexible precision oncology mouse models of epithelial malignancies epithelial malignanciesR01CA233944 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LOWE, SCOTT W. · 2020 to 2024
$2.4MRobust, high-throughput identification of RNA processing regulators and regulatory networks genome-wideK99HG009530 · NHGRI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI VAN NOSTRAND, ERIC LYMAN · 2017 to 2018
$250kIdentifying novel p53 target genes that mediate tumor suppressionF32CA162681 · NCI · STANFORD UNIVERSITY · PI BIEGING, KATHRYN · 2011 to 2012
$64kNCI NIH HHS F32 CA162681NCI NIH HHS P01 CA087497NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA023100NCI NIH HHS R01 CA233944NCI NIH HHS R35 CA197591NCI NIH HHS T32 CA009302NHGRI NIH HHS K99 HG009530
Abstract
Although TP53 is the most commonly mutated gene in human cancers, the p53-dependent transcriptional programs mediating tumor suppression remain incompletely understood. Here, to uncover critical components downstream of p53 in tumor suppression, we perform unbiased RNAi and CRISPR-Cas9-based genetic screens in vivo. These screens converge upon the p53-inducible gene Zmat3, encoding an RNA-binding protein, and we demonstrate that ZMAT3 is an important tumor suppressor downstream of p53 in mouse Kras
Indexed as
AdenocarcinomaAlternative SplicingAnimalsCell Cycle ProteinsExonsGene Expression ProfilingGenes, Tumor SuppressorHumansLiver NeoplasmsMaleMiceMice, Inbred ICRMice, SCIDRNA-Binding ProteinsRNA InterferenceRNA SplicingCell Cycle ProteinsRNA-Binding ProteinsTumor Suppressor Protein p53ZMAT3 protein, humanalternative splicingCRISPR screenhepatocellular carcinomalung adenocarcinomaMdm4p53RBPRNAi screentumor suppressionZmat3
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