ArticleMolecular and cellular biology2004
Negative control of the Myc protein by the stress-responsive kinase Pak2.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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Who cites it
40 citing papers in PubMed, 85 citations in OpenAlex.
- PPP1R12B inhibits cell proliferation by inducing G0/G1 phase arrest via PAK2/β-catenin axis in hepatocellular carcinoma.Frontiers in cell and developmental biology · 2025Article
- Regulation of Cancer Metastasis by PAK2.International journal of molecular sciences · 2024Review
- Regulation of Vascular Injury and Repair by P21-Activated Kinase 1 and P21-Activated Kinase 2: Therapeutic Potential and Challenges.Biomolecules · 2024Review
- The Interplay Between theInternational journal of molecular sciences · 2024Review
- Role of activated p21-activated kinase 2 in methylmercury-induced embryotoxic effects on mouse blastocysts.Toxicology research · 2023Article
- When Just One Phosphate Is One Too Many: The Multifaceted Interplay between Myc and Kinases.International journal of molecular sciences · 2023Review
- Demystifying the Druggability of the MYC Family of Oncogenes.Journal of the American Chemical Society · 2023Review
- Role of caspase-3-cleaved/activated PAK2 in brusatol-triggered apoptosis of human lung cancer A549 cells.Toxicology research · 2022Article
- The MYC oncoprotein directly interacts with its chromatin cofactor PNUTS to recruit PP1 phosphatase.Nucleic acids research · 2022Article
- Review
- New Therapeutic Opportunities for the Treatment of Squamous Cell Carcinomas: A Focus on Novel Driver Kinases.International journal of molecular sciences · 2021Review
- Structural and Biophysical Insights into the Function of the Intrinsically Disordered Myc Oncoprotein.Cells · 2020Review
- The draft genome of a wild barley genotype reveals its enrichment in genes related to biotic and abiotic stresses compared to cultivated barley.Plant biotechnology journal · 2020Article
- Crystal Structures and Nuclear Magnetic Resonance Studies of the Apo Form of the c-MYC:MAX bHLHZip Complex Reveal a Helical Basic Region in the Absence of DNA.Biochemistry · 2019Article
- MYC dephosphorylation by the PP1/PNUTS phosphatase complex regulates chromatin binding and protein stability.Nature communications · 2018Article
- Myc phosphorylation in its basic helix-loop-helix region destabilizes transient α-helical structures, disrupting Max and DNA binding.The Journal of biological chemistry · 2018Article
- Expansion of BCR/ABL1British journal of haematology · 2017Article
- MYC Deregulation in Primary Human Cancers.Genes · 2017Review
- KRAS-dependent suppression of MYC enhances the sensitivity of cancer cells to cytotoxic agents.Oncotarget · 2017Article
- Silencing of CDK2, but not CDK1, separates mitogenic from anti-apoptotic signaling, sensitizing p53 defective cells for synthetic lethality.Cell cycle (Georgetown, Tex.) · 2016Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Pak2 is a serine/threonine kinase that participates in the cellular response to stress. Among the potential substrates for Pak2 is the protein Myc, encoded by the proto-oncogene MYC. Here we demonstrate that Pak2 phosphorylates Myc at three sites (T358, S373, and T400) and affects Myc functions both in vitro and in vivo. Phosphorylation at all three residues reduces the binding of Myc to DNA, either by blocking the requisite dimerization with Max (through phosphorylation at S373 and T400) or by interfering directly with binding to DNA (through phosphorylation at T358). Phosphorylation by Pak2 inhibits the ability of Myc to activate transcription, to sustain cellular proliferation, to transform NIH 3T3 cells in culture, and to elicit apoptosis on serum withdrawal. These results indicate that Pak2 is a negative regulator of Myc, suggest that inhibition of Myc plays a role in the cellular response to stress, and raise the possibility that Pak2 may be the product of a tumor suppressor gene.
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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.