ArticleCancer research2014
NACK is an integral component of the Notch transcriptional activation complex and is critical for development and tumorigenesis.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- A tandem recruitment site in the pseudokinase scaffold PEAK3 is subject to phosphorylation-dependent regulation and cancer-associated mutations.The Journal of biological chemistry · 2026Article
- Targeting notch signaling pathway in esophageal cancer: from molecular insights to therapies.Oncology reviews · 2026Review
- Notch NICD domains form biomolecular condensates.Journal of cell communication and signaling · 2025Article
- Current understanding of PEAK family members in regulation of cellular signaling pathways and cancer therapy.Molecular and cellular biochemistry · 2025Review
- A comparative analysis of paxillin and Hic-5 proximity interactomes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Candidate Genes for IgA Nephropathy in Pediatric Patients: Exome-Wide Association Study.International journal of molecular sciences · 2023Article
- Structural mapping of PEAK pseudokinase interactions identifies 14-3-3 as a molecular switch for PEAK3 signaling.Nature communications · 2023Article
- A novel chemical attack on Notch-mediated transcription by targeting the NACK ATPase.Molecular therapy oncolytics · 2023Article
- Twinkle twinkle brittle star: the draft genome of Ophioderma brevispinum (Echinodermata: Ophiuroidea) as a resource for regeneration research.BMC genomics · 2022Article
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- NACK and INTEGRATOR act coordinately to activate Notch-mediated transcription in tumorigenesis.Cell communication and signaling : CCS · 2021Article
- Pharmacological Disruption of the Notch1 Transcriptional Complex Inhibits Tumor Growth by Selectively Targeting Cancer Stem Cells.Cancer research · 2021Article
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- PEAK3/C19orf35 pseudokinase, a new NFK3 kinase family member, inhibits CrkII through dimerization.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- SHEDding light on the role of Pragmin pseudo-kinases in cancer.American journal of cancer research · 2019Article
- The Role of Notch Signaling and Leptin-Notch Crosstalk in Pancreatic Cancer.Medicines (Basel, Switzerland) · 2018Review
- The pseudokinases SgK269 and SgK223: A novel oncogenic alliance in human cancer.Cell adhesion & migration · 2018Review
- Notch Represses Transcription by PRC2 Recruitment to the Ternary Complex.Molecular cancer research : MCR · 2017Article
- The Small Molecule IMR-1 Inhibits the Notch Transcriptional Activation Complex to Suppress Tumorigenesis.Cancer research · 2016Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
The Notch signaling pathway governs many distinct cellular processes by regulating transcriptional programs. The transcriptional response initiated by Notch is highly cell context dependent, indicating that multiple factors influence Notch target gene selection and activity. However, the mechanism by which Notch drives target gene transcription is not well understood. Herein, we identify and characterize a novel Notch-interacting protein, Notch activation complex kinase (NACK), which acts as a Notch transcriptional coactivator. We show that NACK associates with the Notch transcriptional activation complex on DNA, mediates Notch transcriptional activity, and is required for Notch-mediated tumorigenesis. We demonstrate that Notch1 and NACK are coexpressed during mouse development and that homozygous loss of NACK is embryonic lethal. Finally, we show that NACK is also a Notch target gene, establishing a feed-forward loop. Thus, our data indicate that NACK is a key component of the Notch transcriptional complex and is an essential regulator of Notch-mediated tumorigenesis and development.
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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.