ArticleThe Journal of cell biology2004
c-Abl phosphorylates Dok1 to promote filopodia during cell spreading.
Article in The Journal of cell biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 76 citations in OpenAlex.
- c-Abl Tyrosine Kinase Is Required for BDNF-Induced Dendritic Branching and Growth.International journal of molecular sciences · 2023Article
- Nck adaptors at a glance.Journal of cell science · 2021Article
- Nck adapter proteins promote podosome biogenesis facilitating extracellular matrix degradation and cancer invasion.Cancer medicine · 2019Article
- Selective Regulation of Cytoskeletal Dynamics and Filopodia Formation by Teleost Leukocyte Immune-Type Receptors Differentially Contributes to Target Capture During the Phagocytic Process.Frontiers in immunology · 2018Article
- Differential signaling through p190 and p210 BCR-ABL fusion proteins revealed by interactome and phosphoproteome analysis.Leukemia · 2017Article
- Critical role of actin-associated proteins in smooth muscle contraction, cell proliferation, airway hyperresponsiveness and airway remodeling.Respiratory research · 2015Review
- Targeting Abl kinases to regulate vascular leak during sepsis and acute respiratory distress syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2015Review
- Phosphorylation of the cytoskeletal protein CAP1 controls its association with cofilin and actin.Journal of cell science · 2014Article
- mRNA expression of DOK1-6 in human breast cancer.World journal of clinical oncology · 2014Article
- Role of c-Abl tyrosine kinase in smooth muscle cell migration.American journal of physiology. Cell physiology · 2014Article
- BRK targets Dok1 for ubiquitin-mediated proteasomal degradation to promote cell proliferation and migration.PloS one · 2014Article
- Gleevec, an Abl family inhibitor, produces a profound change in cell shape and migration.PloS one · 2013Article
- Transcriptional regulation of the human tumor suppressor DOK1 by E2F1.Molecular and cellular biology · 2012Article
- Activation of abl family kinases in solid tumors.Genes & cancer · 2012Article
- Characterization of DOK1, a candidate tumor suppressor gene, in epithelial ovarian cancer.Molecular oncology · 2011Article
- Oncogenic tyrosine kinases target Dok-1 for ubiquitin-mediated proteasomal degradation to promote cell transformation.Molecular and cellular biology · 2011Article
- Rif-mDia1 interaction is involved in filopodium formation independent of Cdc42 and Rac effectors.The Journal of biological chemistry · 2011Article
- The Cain and Abl of epithelial-mesenchymal transition and transforming growth factor-β in mammary epithelial cells.Cells, tissues, organs · 2011Review
- Downstream of tyrosine kinase 1 and 2 play opposing roles in CD200 receptor signaling.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- ABL tyrosine kinases: evolution of function, regulation, and specificity.Science signaling · 2010Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
Abstract
Filopodia are dynamic F-actin structures that cells use to explore their environment. c-Abl tyrosine kinase promotes filopodia during cell spreading through an unknown mechanism that does not require Cdc42 activity. Using an unbiased approach, we identified Dok1 as a specific c-Abl substrate in spreading fibroblasts. When activated by cell adhesion, c-Abl phosphorylates Y361 of Dok1, promoting its association with the Src homology 2 domain (SH2)/SH3 adaptor protein Nck. Each signaling component was critical for filopodia formation during cell spreading, as evidenced by the finding that mouse fibroblasts lacking c-Abl, Dok1, or Nck had fewer filopodia than cells reexpressing the product of the disrupted gene. Dok1 and c-Abl stimulated filopodia in a mutually interdependent manner, indicating that they function in the same signaling pathway. Dok1 and c-Abl were both detected in filopodia of spreading cells, and therefore may act locally to modulate actin. Our data suggest a novel pathway by which c-Abl transduces signals to the actin cytoskeleton through phosphorylating Dok1 Y361 and recruiting Nck.
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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.