ArticleeLife2022
Antiviral function and viral antagonism of the rapidly evolving dynein activating adaptor NINL.
Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Activation and regulation of the dynein-dynactin-NuMA complex.Nature chemical biology · 2026Article
- Synthetic cargo adaptors reveal molecular features that enhance dynein activation.Nature communications · 2026Article
- HIV-1 binds dynein directly to hijack microtubule transport machinery.Science advances · 2025Article
- Evolutionary and functional analyses reveal a role for the RHIM in tuning RIPK3 activity across vertebrates.eLife · 2025Article
- Viral warfare: unleashing engineered oncolytic viruses to outsmart cancer's defenses.Frontiers in immunology · 2025Review
- Movement of the endoplasmic reticulum is driven by multiple classes of vesicles marked by Rab-GTPases.Molecular biology of the cell · 2025Article
- Ninein domains required for its localization, association with partners dynein and ensconsin, and microtubule organization.Molecular biology of the cell · 2024Article
- Combining single-cell and bulk RNA sequencing, NK cell marker genes reveal a prognostic and immune status in pancreatic ductal adenocarcinoma.Scientific reports · 2024Article
- Proteomic analysis of crocodile white blood cells reveals insights into the mechanism of the innate immune system.Heliyon · 2024Article
- Ndel1 disfavors dynein-dynactin-adaptor complex formation in two distinct ways.The Journal of biological chemistry · 2023Article
- Ndel1 modulates dynein activation in two distinct ways.bioRxiv : the preprint server for biology · 2023Article
- Antiviral function and viral antagonism of the rapidly evolving dynein activating adaptor NINL.eLife · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Viruses interact with the intracellular transport machinery to promote viral replication. Such host-virus interactions can drive host gene adaptation, leaving signatures of pathogen-driven evolution in host genomes. Here, we leverage these genetic signatures to identify the dynein activating adaptor, ninein-like (NINL), as a critical component in the antiviral innate immune response and as a target of viral antagonism. Unique among genes encoding components of active dynein complexes, NINL has evolved under recurrent positive (diversifying) selection, particularly in its carboxy-terminal cargo-binding region. Consistent with a role for NINL in host immunity, we demonstrate that NINL knockout cells exhibit an impaired response to interferon, resulting in increased permissiveness to viral replication. Moreover, we show that proteases encoded by diverse picornaviruses and coronaviruses cleave and disrupt NINL function in a host- and virus-specific manner. Our work reveals the importance of NINL in the antiviral response and the utility of using signatures of host-virus genetic conflicts to uncover new components of antiviral immunity and targets of viral antagonism.
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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.