ArticleThe Journal of experimental medicine2004
Role of Dok-1 and Dok-2 in myeloid homeostasis and suppression of leukemia.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 107 citations in OpenAlex.
- CD200R1-CD200 checkpoint inhibits phagocytosis differently from SIRPα-CD47 to suppress tumor growth.Nature communications · 2025Article
- DOK1 and DOK2 regulate CD8 T cell signaling and memory formation without affecting tumor cell killing.Scientific reports · 2024Article
- Loss of Dok-3 in Non-tumor Cells Induces Malignant Transformation of Benign Epithelial Tumor Cells of the Intestine.Cancer research communications · 2022Article
- Plasma exosomal DOK3 reflects immunological states in lung tumor and predicts prognosis of gefitinib treatment.Cancer science · 2022Article
- DOK2 Has Prognostic and Immunologic Significance in Adults With Acute Myeloid Leukemia: A Novel Immune-Related Therapeutic Target.Frontiers in medicine · 2022Article
- Introduction to DOK2 and its potential role in cancer.Physiological research · 2021Review
- DOK7 Inhibits Cell Proliferation, Migration, and Invasion of Breast Cancer via the PI3K/PTEN/AKT Pathway.Journal of oncology · 2021Article
- Article
- Emerging Roles of Downstream of Kinase 3 in Cell Signaling.Frontiers in immunology · 2020Review
- DOK6 promoter methylation serves as a potential biomarker affecting prognosis in de novo acute myeloid leukemia.Cancer medicine · 2019Article
- Article
- A Threshold Model for T-Cell Activation in the Era of Checkpoint Blockade Immunotherapy.Frontiers in immunology · 2019Review
- Methylation-associated DOK1 and DOK2 down-regulation: Potential biomarkers for predicting adverse prognosis in acute myeloid leukemia.Journal of cellular physiology · 2018Article
- Purification of zebrafish erythrocytes as a means of identifying a novel regulator of haematopoiesis.British journal of haematology · 2018Article
- Region-Specific Dok2 Overexpression Associates with Poor Prognosis in Human Astrocytoma.Molecular neurobiology · 2018Article
- Dok-1 and Dok-2 Are Required To Maintain Herpes Simplex Virus 1-Specific CD8Journal of virology · 2017Article
- Turning the tide in myelodysplastic/myeloproliferative neoplasms.Nature reviews. Cancer · 2017Review
- Effects of expressing human T-cell leukemia virus type 1 (HTLV-I) oncoprotein Tax on DOK1, DOK2 and DOK3 gene expression in mice.The Journal of veterinary medical science · 2017Article
- Subcellular compartmentalization of docking protein-1 contributes to progression in colorectal cancer.EBioMedicine · 2016Article
- The right and wrong of DOKing the nuclear receptor.EBioMedicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dok-1 and Dok-2 are closely related rasGAP-associated docking proteins expressed preferentially in hematopoietic cells. Although they are phosphorylated upon activation of many protein tyrosine kinases (PTKs), including those coupled with cytokine receptors and oncogenic PTKs like Bcr-Abl, their physiological roles are largely unidentified. Here, we generated mice lacking Dok-1 and/or Dok-2, which included the double-deficient mice succumbed to myeloproliferative disease resembling human chronic myelogenous leukemia (CML) and chronic myelomonocytic leukemia. The double-deficient mice displayed medullary and extramedullary hyperplasia of granulocyte/macrophage progenitors with leukemic potential, and their myeloid cells showed hyperproliferation and hypo-apoptosis upon treatment and deprivation of cytokines, respectively. Consistently, the mutant myeloid cells showed enhanced Erk and Akt activation upon cytokine stimulation. Moreover, loss of Dok-1 and/or Dok-2 induced blastic transformation of chronic phase CML-like disease in mice carrying the bcr-abl gene, a cause of CML. These findings demonstrate that Dok-1 and Dok-2 are key negative regulators of cytokine responses and are essential for myeloid homeostasis and suppression of leukemia.
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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.