ArticleEuropean journal of immunology2021
Cereblon regulates NK cell cytotoxicity and migration via Rac1 activation.
Article in European journal of immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- TNF-α deficiency underlies NK cell dysfunction in colorectal cancer.Oncoimmunology · 2026Article
- Implications of Rho GTPase signaling in cancer immunotherapy.Biochemical Society transactions · 2026Review
- NKG2D triggering hampers DNAM-1-mediated signaling in human NK cells.Frontiers in immunology · 2025Article
- RAC1 serves as a prognostic factor and correlated with immune infiltration in liver hepatocellular carcinoma.Journal of cancer research and clinical oncology · 2024Article
- Excessive endometrial PlGF- Rac1 signalling underlies endometrial cell stiffness linked to pre-eclampsia.Communications biology · 2024Article
- Activin A, a Novel Chemokine, Induces Mouse NK Cell Migration via AKT and Calcium Signaling.Cells · 2024Article
- Rac1: A Regulator of Cell Migration and a Potential Target for Cancer Therapy.Molecules (Basel, Switzerland) · 2023Review
- Single-cell RNA sequencing of CSF reveals neuroprotective RAC1Frontiers in immunology · 2022Article
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
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Abstract
Rearrangement of the actin cytoskeleton is critical for cytotoxic and immunoregulatory functions as well as migration of natural killer (NK) cells. However, dynamic reorganization of actin is a complex process, which remains largely unknown. Here, we investigated the role of the protein Cereblon (CRBN), an E3 ubiquitin ligase complex co-receptor and the primary target of the immunomodulatory drugs, in NK cells. We observed that CRBN partially colocalizes with F-actin in chemokine-treated NK cells and is recruited to the immunological synapse, thus suggesting a role for this protein in cytoskeleton reorganization. Accordingly, silencing of CRBN in NK cells results in a reduced cytotoxicity that correlates with a defect in conjugate and lytic synapse formation. Moreover, CRBN depletion significantly impairs the ability of NK cells to migrate and reduces the enhancing effect of lenalidomide on NK cell migration. Finally, we provided evidence that CRBN is required for activation of the small GTPase Rac1, a critical mediator of cytoskeleton dynamics. Indeed, in CRBN-depleted NK cells, chemokine-mediated or target cell-mediated Rac1 activation is significantly reduced. Altogether our data identify a critical role for CRBN in regulating NK cell functions and suggest that this protein may mediate the stimulatory effect of lenalidomide on NK cells.
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