ArticleProceedings of the National Academy of Sciences of the United States of America2004
IkappaB kinase beta phosphorylates Dok1 serines in response to TNF, IL-1, or gamma radiation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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
25 citing papers in PubMed, 46 citations in OpenAlex.
- Nuclear Factor κB (NF-κB)-Mediated Inflammation in Multiple Sclerosis.Frontiers in immunology · 2020Review
- Advances and challenges in targeting IRF5, a key regulator of inflammation.The FEBS journal · 2019Review
- The crossroads of breast cancer progression: insights into the modulation of major signaling pathways.OncoTargets and therapy · 2017Review
- Breaking the mold: transcription factors in the anucleate platelet and platelet-derived microparticles.Frontiers in immunology · 2015Review
- A splicing variant of NME1 negatively regulates NF-κB signaling and inhibits cancer metastasis by interacting with IKKβ.The Journal of biological chemistry · 2014Article
- Epstein-Barr virus down-regulates tumor suppressor DOK1 expression.PLoS pathogens · 2014Article
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- The IκB kinase complex in NF-κB regulation and beyond.EMBO reports · 2014Review
- Integration of apoptosis signal-regulating kinase 1-mediated stress signaling with the Akt/protein kinase B-IκB kinase cascade.Molecular and cellular biology · 2013Article
- Epstein - Barr virus transforming protein LMP-1 alters B cells gene expression by promoting accumulation of the oncoprotein ΔNp73α.PLoS pathogens · 2013Article
- IKK biology.Immunological reviews · 2012Review
- IKKα activation of NOTCH links tumorigenesis via FOXA2 suppression.Molecular cell · 2012Article
- Characterization of DOK1, a candidate tumor suppressor gene, in epithelial ovarian cancer.Molecular oncology · 2011Article
- Crosstalk in NF-κB signaling pathways.Nature immunology · 2011Review
- IkappaB kinase beta promotes cell survival by antagonizing p53 functions through DeltaNp73alpha phosphorylation and stabilization.Molecular and cellular biology · 2011Article
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- Phosphorylation of ARD1 by IKKbeta contributes to its destabilization and degradation.Biochemical and biophysical research communications · 2009Article
- Advances in targeting IKK and IKK-related kinases for cancer therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Review
- Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
Abstract
Dok1 is an abundant Ras-GTPase-activating protein-associated tyrosine kinase substrate that negatively regulates cell growth and promotes migration. We now find that IkappaB kinase beta (IKKbeta) associated with and phosphorylated Dok1 in human epithelial cells and B lymphocytes. IKKbeta phosphorylation of Dok1 depended on Dok1 S(439), S(443), S(446), and S(450). Recombinant IKKbeta also phosphorylated Dok1 or Dok1 amino acids 430-481 in vitro. TNF-alpha, IL-1, gamma radiation, or IKKbeta overexpression phosphorylated Dok1 S(443), S(446), and S(450) in vivo, as detected with Dok1 phospho-S site-specific antisera. Moreover, Dok1 with S(439), S(443), S(446), and S(450) mutated to A was not phosphorylated by IKKbeta in vivo. Surprisingly, mutant Dok1 A(439), A(443), A(446), and A(450) differed from wild-type Dok1 in not inhibiting platelet-derived growth factor-induced extracellular signal-regulated kinase 1/2 phosphorylation or cell growth. Mutant Dok1 A(439), A(443), A(446), and A(450) also did not promote cell motility, whereas wild-type Dok1 promoted cell motility, and Dok1 E(439), E(443), E(446), and E(450) further enhanced cell motility. These data indicate that IKKbeta phosphorylates Dok1 S(439)S(443) and S(446)S(450) after TNF-alpha, IL-1, or gamma-radiation and implicate the critical Dok1 serines in Dok1 effects after tyrosine kinase activation.
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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.