ArticleThe Journal of experimental medicine2001
p62(dok), a negative regulator of Ras and mitogen-activated protein kinase (MAPK) activity, opposes leukemogenesis by p210(bcr-abl).
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 51 papers.
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Who cites it
51 citing papers in PubMed, 105 citations in OpenAlex.
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- DOK6 promoter methylation serves as a potential biomarker affecting prognosis in de novo acute myeloid leukemia.Cancer medicine · 2019Article
- Rasal2 deficiency reduces adipogenesis and occurrence of obesity-related disorders.Molecular metabolism · 2017Article
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- The non-genomic loss of function of tumor suppressors: an essential role in the pathogenesis of chronic myeloid leukemia chronic phase.BMC cancer · 2016Review
- Dok-1 negatively regulates platelet integrin αIIbβ3 outside-in signalling and inhibits thrombosis in mice.Thrombosis and haemostasis · 2016Article
- Grb10 is involved in BCR-ABL-positive leukemia in mice.Leukemia · 2015Article
- mRNA expression of DOK1-6 in human breast cancer.World journal of clinical oncology · 2014Article
- Epstein-Barr virus down-regulates tumor suppressor DOK1 expression.PLoS pathogens · 2014Article
- BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.PloS one · 2014Article
- Modulation of the transcriptional activity of peroxisome proliferator-activated receptor gamma by protein-protein interactions and post-translational modifications.Yonsei medical journal · 2013Review
- Transcriptional regulation of the human tumor suppressor DOK1 by E2F1.Molecular and cellular biology · 2012Article
- Inactivation of the putative suppressor gene DOK1 by promoter hypermethylation in primary human cancers.International journal of cancer · 2012Article
- The inositol 5-phosphatase SHIP-1 and adaptors Dok-1 and 2 play central roles in CD4-mediated inhibitory signaling.Immunology letters · 2012Article
- Enhanced ABL-inhibitor-induced MAPK-activation in T315I-BCR-ABL-expressing cells: a potential mechanism of altered leukemogenicity.Journal of cancer research and clinical oncology · 2012Article
- Feedback circuits monitor and adjust basal Lck-dependent events in T cell receptor signaling.Science signaling · 2011Article
- Oncogenic tyrosine kinases target Dok-1 for ubiquitin-mediated proteasomal degradation to promote cell transformation.Molecular and cellular biology · 2011Article
- The proximal signaling network of the BCR-ABL1 oncogene shows a modular organization.Oncogene · 2010Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
p62(dok) has been identified as a substrate of many oncogenic tyrosine kinases such as the chronic myelogenous leukemia (CML) chimeric p210(bcr-abl) oncoprotein. It is also phosphorylated upon activation of many receptors and cytoplamic tyrosine kinases. However, the biological functions of p62(dok) in normal cell signaling as well as in p210(bcr-abl) leukemogenesis are as yet not fully understood. Here we show, in hemopoietic and nonhemopoietic cells derived from p62(dok)-(/)- mice, that the loss of p62(dok) results in increased cell proliferation upon growth factor treatment. Moreover, Ras and mitogen-activated protein kinase (MAPK) activation is markedly sustained in p62(dok)-(/)- cells after the removal of growth factor. However, p62(dok) inactivation does not affect DNA damage and growth factor deprivation-induced apoptosis. Furthermore, p62(dok) inactivation causes a significant shortening in the latency of the fatal myeloproliferative disease induced by retroviral-mediated transduction of p210(bcr-abl) in bone marrow cells. These data indicate that p62(dok) acts as a negative regulator of growth factor-induced cell proliferation, at least in part through downregulating Ras/MAPK signaling pathway, and that p62(dok) can oppose leukemogenesis by p210(bcr-abl).
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