ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Essential role of Elmo1 in Dock2-dependent lymphocyte migration.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
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- Dock2 Protects Colitis by Facilitating Akkermansia Colonization via Suppressing IL-22-Reg3 Activity.Inflammation · 2026Article
- Complement-mediated ADCP as a distinct and finite cytotoxic mechanism of monoclonal antibodies.Frontiers in immunology · 2026Article
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- The Progression of Mycosis Fungoides During Treatment with Mogamulizumab: A BIO-MUSE Case Study of the Tumor and Immune Response in Peripheral Blood and Tissue.Biomedicines · 2025Article
- Single-Cell Transcriptomics Reveals a Pivotal Role of DOCK2 in Sjögren Disease.ACR open rheumatology · 2024Article
- Chemokine-mediated F-actin dynamics, polarity, and migration in B lymphocytes depend on WNK1 signaling.Science signaling · 2024Article
- Engulfment and cell motility protein 1 fosters reprogramming of tumor-associated macrophages in colorectal cancer.Cancer science · 2023Article
- Molecular complexity and gene expression controlling cell turnover during a digestive cycle of carnivorous sponge Lycopodina hypogea.Cell and tissue research · 2022Article
- Functional Verification of NovelFrontiers in cell and developmental biology · 2021Article
- Macrophage hypophagia as a mechanism of innate immune exhaustion in mAb-induced cell clearance.Blood · 2020Article
- DOCK family proteins: key players in immune surveillance mechanisms.International immunology · 2020Review
- Loci Associated With Antibody Response in Feral Swine (Frontiers in veterinary science · 2020Article
- CaJournal of clinical medicine · 2019Review
- Molecular Profiling and Functional Analysis of Macrophage-Derived Tumor Extracellular Vesicles.Cell reports · 2019Article
- How do chemokines navigate neutrophils to the target site: Dissecting the structural mechanisms and signaling pathways.Cellular signalling · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Elmo1 and Elmo2 are highly homologous cytoplasmic adaptor proteins that interact with Dock family guanine nucleotide exchange factors to promote activation of the small GTPase Rac. In T lymphocytes, Dock2 is essential for CCR7- and CXCR4-dependent Rac activation and chemotaxis, but the role of Elmo proteins in regulating Dock2 function in primary T cells is not known. In this article, we show that endogenous Elmo1, but not Elmo2, interacts constitutively with Dock2 in mouse and human primary T cells. CD4(+) T cells from Elmo1(-/-) mice were profoundly impaired in polarization, Rac activation, and chemotaxis in response to CCR7 and CXCR4 stimulation. Transfection of full-length Elmo1, but not Elmo2 or a Dock2-binding mutant of Elmo1, rescued defective migration of Elmo1(-/-) T cells. Interestingly, Dock2 protein levels were reduced by 4-fold in Elmo1(-/-) lymphocytes despite normal levels of Dock2 mRNA. Dock2 polyubiquitination was increased in Elmo1(-/-) T cells, and treatment with proteasome inhibitors partially restored Dock2 levels in Elmo1(-/-) T cells. Finally, we show that Dock2 is directly ubiquitinated in CD4(+) T cells and that Elmo1 expression in heterologous cells inhibits ubiquitination of Dock2. Taken together, these findings reveal a previously unknown, nonredundant role for Elmo1 in controlling Dock2 levels and Dock2-dependent T cell migration in primary lymphocytes. Inhibition of Dock2 has therapeutic potential as a means to control recruitment of pathogenic lymphocytes in diseased tissues. This work provides valuable insights into the molecular regulation of Dock2 by Elmo1 that can be used to design improved inhibitors that target the Elmo-Dock-Rac signaling complex.
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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.