ArticleThe Journal of experimental medicine2001
Phosphoinositide 3-kinase-dependent membrane recruitment of p62(dok) is essential for its negative effect on mitogen-activated protein (MAP) kinase activation.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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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Who cites it
28 citing papers in PubMed, 66 citations in OpenAlex.
- Lyn, Lupus, and (B) Lymphocytes, a Lesson on the Critical Balance of Kinase Signaling in Immunity.Frontiers in immunology · 2018Review
- A splicing variant of NME1 negatively regulates NF-κB signaling and inhibits cancer metastasis by interacting with IKKβ.The Journal of biological chemistry · 2014Article
- BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.PloS one · 2014Article
- DOK2 inhibits EGFR-mutated lung adenocarcinoma.PloS one · 2013Article
- Article
- Oncogenic tyrosine kinases target Dok-1 for ubiquitin-mediated proteasomal degradation to promote cell transformation.Molecular and cellular biology · 2011Article
- The conundrum of inhibitory signaling by ITAM-containing immunoreceptors: potential molecular mechanisms.FEBS letters · 2010Review
- Molecular underpinning of B-cell anergy.Immunological reviews · 2010Review
- Analysis of DOK-6 function in downstream signaling of RET in human neuroblastoma cells.Cancer science · 2010Article
- The insulin-like growth factor (IGF) receptor type 1 (IGF1R) as an essential component of the signalling network regulating neurogenesis.Molecular neurobiology · 2009Review
- 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
- Investigation of protein-tyrosine phosphatase 1B function by quantitative proteomics.Molecular & cellular proteomics : MCP · 2008Article
- p21 Ras/impedes mitogenic signal propagation regulates cytokine production and migration in CD4 T cells.The Journal of biological chemistry · 2008Article
- Regulation of hematopoietic cell function by inhibitory immunoglobulin G receptors and their inositol lipid phosphatase effectors.Immunological reviews · 2008Review
- A nuclear export signal and phosphorylation regulate Dok1 subcellular localization and functions.Molecular and cellular biology · 2006Article
- Dok-1 independently attenuates Ras/mitogen-activated protein kinase and Src/c-myc pathways to inhibit platelet-derived growth factor-induced mitogenesis.Molecular and cellular biology · 2006Article
- Divergent roles of c-Src in controlling platelet-derived growth factor-dependent signaling in fibroblasts.Molecular biology of the cell · 2005Article
- Dok-R mediates attenuation of epidermal growth factor-dependent mitogen-activated protein kinase and Akt activation through processive recruitment of c-Src and Csk.Molecular and cellular biology · 2005Article
- Role of Dok-1 and Dok-2 in myeloid homeostasis and suppression of leukemia.The Journal of experimental medicine · 2004Article
- Role of Dok-1 and Dok-2 in leukemia suppression.The Journal of experimental medicine · 2004Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
A major pathway by which growth factors, such as platelet-derived growth factor (PDGF), regulate cell proliferation is via the receptor tyrosine kinase/Ras/mitogen-activated protein kinase (MAPK) signaling cascade. The output of this pathway is subjected to tight regulation of both positive and negative regulators. One such regulator is p62(dok), the prototype of a newly identified family of adaptor proteins. We recently provided evidence, through the use of p62(dok)-deficient cells, that p62(dok) acts as a negative regulator of growth factor-induced cell proliferation and the Ras/MAPK pathway. We show here that reintroduction of p62(dok) into p62(dok)-(/)- cells can suppress the increased cell proliferation and prolonged MAPK activity seen in these cells, and that plasma membrane recruitment of p62(dok) is essential for its function. We also show that the PDGF-triggered plasma membrane translocation of p62(dok) requires activation of phosphoinositide 3-kinase (PI3-kinase) and binding of its pleckstrin homology (PH) domain to 3'-phosphorylated phosphoinositides. Furthermore, we demonstrate that p62(dok) can exert its negative effect on the PDGFR/MAPK pathway independently of its ability to associate with RasGAP and Nck. We conclude that p62(dok) functions as a negative regulator of the PDGFR/Ras/MAPK signaling pathway through a mechanism involving PI3-kinase-dependent recruitment of p62(dok) to the plasma membrane.
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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.