ArticleInternational journal of molecular sciences2019
TIM-1 As a Signal Receptor Triggers Dengue Virus-Induced Autophagy.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- Autophagy in emerging and highly concerned severe zoonotic infectious diseases.Frontiers in immunology · 2026Review
- Review
- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- Review
- Quantification of the interaction forces between dengue virus and dopamine type-2 receptor using optical tweezers.Virology journal · 2024Article
- Role of angiotensin II in cellular entry and replication of dengue virus.Archives of virology · 2024Review
- Angiotensin II and dengue.Archives of virology · 2023Review
- Article
- Single Nucleotide Variants of the Human TIM-1 IgV Domain with Reduced Ability to Promote Viral Entry into Cells.Viruses · 2022Article
- Identification of stage-related and severity-related biomarkers and exploration of immune landscape for Dengue by comprehensive analyses.Virology journal · 2022Article
- The role of phosphatidylserine on the membrane in immunity and blood coagulation.Biomarker research · 2022Review
- Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy.Central-European journal of immunology · 2021Article
- The Mechanism of the Zika Virus Crossing the Placental Barrier and the Blood-Brain Barrier.Frontiers in microbiology · 2020Article
- Comprehensive Analysis of the Expression, Relationship to Immune Infiltration and Prognosis of TIM-1 in Cancer.Frontiers in oncology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Dengue virus (DENV) infection triggers the activation of autophagy to facilitate the viral replication cycle from various aspects. Although a number of stimulators are proposed to activate autophagy, none of them appears prior to the uncoating process. Given that T-cell immunoglobulin and mucin domain 1 (TIM-1) receptor is a putative DENV receptor and promotes apoptotic body clearance by autophagy induction, it raises the possibility that TIM-1 may participate in the activation of DENV-induced autophagy. In this study, confocal images first revealed the co-localization of TIM-1 with autophagosomes in DENV-induced autophagy rather than rapamycin-induced autophagy, suggesting the co-transportation of TIM-1 with DENV during infection. The treatment of siRNA to knockdown TIM-1 expression in DENV-infected GFP-microtubule-associated protein light chain 3 (LC3)-Huh7.5 cells revealed that TIM-1 is required not only for DENV cellular internalization but also for autophagy activation. Furthermore, knockdown p85, a subunit of phosphoinositide 3-kinases (PI3Ks), which is co-localized with TIM-1 at rab5-positive endosomes caused the reduction of autophagy, indicating that TIM-1-mediated DENV-induced autophagy requires p85. Taken together, the current study uncovered TIM-1 as a novel factor for triggering autophagy in DENV infection through TIM-1-p85 axis, in addition to serving as a DENV receptor.
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