ArticleNature communications2016
Dephosphorylated parafibromin is a transcriptional coactivator of the Wnt/Hedgehog/Notch pathways.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Intestinal epithelial cells in health and disease.Tissue barriers · 2026Review
- Mechanisms and Functions of the RNA Polymerase II General Transcription Machinery during the Transcription Cycle.Biomolecules · 2024Review
- Cdc73 protects Notch-induced T-cell leukemia cells from DNA damage and mitochondrial stress.Blood · 2023Article
- Phenotypic Profiling and Molecular Mechanisms in Hyperparathyroidism-jaw Tumor Syndrome.The Journal of clinical endocrinology and metabolism · 2023Article
- Molecular and Clinical Spectrum of Primary Hyperparathyroidism.Endocrine reviews · 2023Article
- POFUT1 promotes gastric cancer progression through Notch/Wnt dual signaling pathways dependent on the parafibromin-NICD1-β-catenin complex.Journal of the Chinese Medical Association : JCMA · 2023Article
- Translocation of cytosolic human Cdc73 to stress granules plays a role in arsenic stress-induced stabilization of p53 mRNA.Journal of cell science · 2023Article
- The clinicopathological and prognostic significances of CDC73 expression in breast cancer: A pathological and bioinformatics analysis.Histology and histopathology · 2023Article
- Association Between Parafibromin Expression and Presence of Brown Tumors and Jaw Tumors in Patients with Primary Hyperparathyroidism: Series of Cases with Review of the Literature.The American journal of case reports · 2022Review
- UBR5 targets tumor suppressor CDC73 proteolytically to promote aggressive breast cancer.Cell death & disease · 2022Article
- The roles of the tumor suppressor parafibromin in cancer.Frontiers in cell and developmental biology · 2022Review
- Biochemical insights into Paf1 complex-induced stimulation of Rad6/Bre1-mediated H2B monoubiquitination.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Paf1 Complex: A Keystone of Nuclear Regulation Operating at the Interface of Transcription and Chromatin.Journal of molecular biology · 2021Review
- Genomics and Epigenomics in Parathyroid Neoplasia: from Bench to Surgical Pathology Practice.Endocrine pathology · 2021Review
- Article
- Targeting protein tyrosine kinase 6 in cancer.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- Molecular anatomy and pathogenic actions of Helicobacter pylori CagA that underpin gastric carcinogenesis.Cellular & molecular immunology · 2020Review
- PSPC1-interchanged interactions with PTK6 and β-catenin synergize oncogenic subcellular translocations and tumor progression.Nature communications · 2019Article
- MEIS2C and MEIS2D promote tumor progression via Wnt/β-catenin and hippo/YAP signaling in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2019Article
- Parafibromin immunostainings of parathyroid tumors in clinical routine: a near-decade experience from a tertiary center.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evolutionally conserved Wnt, Hedgehog (Hh) and Notch morphogen pathways play essential roles in the development, homeostasis and pathogenesis of multicellular organisms. Nevertheless, mechanisms that intracellularly coordinate these signal inputs remain poorly understood. Here we found that parafibromin, a component of the PAF complex, competitively interacts with β-catenin and Gli1, thereby potentiating transactivation of Wnt- and Hh-target genes in a mutually exclusive manner. Parafibromin also binds to the Notch intracellular domain (NICD), enabling concerted activation of Wnt- and Notch-target genes. The transcriptional platform function of parafibromin is potentiated by tyrosine dephosphorylation, mediated by SHP2 phosphatase, while it is attenuated by tyrosine phosphorylation, mediated by PTK6 kinase. Consequently, acute loss of parafibromin in mice disorganizes the normal epithelial architecture of the intestine, which requires coordinated activation/inactivation of Wnt, Hh and/or Notch signalling. Parafibromin integrates and converts signals conveyed by these morphogen pathways into appropriate transcriptional outputs in a tyrosine phosphorylation/dephosphorylation-regulated manner.
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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.