ArticleMolecular and cellular biology2012
The Abl and Arg kinases mediate distinct modes of phagocytosis and are required for maximal Leishmania infection.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Using machine learning to dissect host kinases required for Leishmania internalization and development.Molecular and biochemical parasitology · 2024Article
- Immunotherapeutic Strategies as Potential Treatment Options for Cutaneous Leishmaniasis.Vaccines · 2024Review
- Using machine learning to dissect host kinases required forbioRxiv : the preprint server for biology · 2024Article
- A Multi-Color Immunofluorescence Assay to Distinguish Intracellular From ExternalBio-protocol · 2024Article
- Src- and Abl-family kinases activate spleen tyrosine kinase to maximize phagocytosis and Leishmania infection.Journal of cell science · 2023Article
- CrkII/Abl phosphorylation cascade is critical for NLRC4 inflammasome activity and is blocked by Pseudomonas aeruginosa ExoT.Nature communications · 2022Article
- Network-Based Approaches Reveal Potential Therapeutic Targets for Host-Directed Antileishmanial Therapy Driving Drug Repurposing.Microbiology spectrum · 2021Article
- The antioxidant response favors Leishmania parasites survival, limits inflammation and reprograms the host cell metabolism.PLoS pathogens · 2021Article
- Drug-induced reactive oxygen species-mediated inhibitory effect on growth of Trypanosoma evansi in axenic culture system.Parasitology research · 2020Article
- An Antiparasitic Compound from the Medicines for Malaria Venture Pathogen Box PromotesACS infectious diseases · 2020Article
- Regulation of MT dynamics via direct binding of an Abl family kinase.The Journal of cell biology · 2019Article
- Exploiting knowledge on pharmacodynamics-pharmacokinetics for accelerated anti-leishmanial drug discovery/development.Expert opinion on drug metabolism & toxicology · 2019Review
- ABL kinase inhibition promotes lung regeneration through expansion of an SCGB1A1+ SPC+ cell population following bacterial pneumonia.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Evaluation of Different Concentrations of Imatinib on the Viability ofAdvanced biomedical research · 2019Article
- Emerging therapeutic targets for treatment of leishmaniasis.Expert opinion on therapeutic targets · 2018Review
- Analysis of Cellular Tyrosine Phosphorylation via Chemical Rescue of Conditionally Active Abl Kinase.Biochemistry · 2018Article
- Repurposing as a strategy for the discovery of new anti-leishmanials: the-state-of-the-art.Parasitology · 2018Review
- Host-Directed Drug Therapies for Neglected Tropical Diseases Caused by Protozoan Parasites.Frontiers in microbiology · 2018Review
- The Abl-1 Kinase is Dispensable for NK Cell Inhibitory Signalling and is not Involved in Murine NK Cell Education.Scandinavian journal of immunology · 2017Article
- Reciprocal stabilization of ABL and TAZ regulates osteoblastogenesis through transcription factor RUNX2.The Journal of clinical investigation · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Leishmania, an obligate intracellular parasite, binds several receptors to trigger engulfment by phagocytes, leading to cutaneous or visceral disease. These receptors include complement receptor 3 (CR3), used by promastigotes, and the Fc receptor (FcR), used by amastigotes. The mechanisms mediating uptake are not well understood. Here we show that Abl family kinases mediate both phagocytosis and the uptake of Leishmania amazonensis by macrophages (Ms). Imatinib, an Abl/Arg kinase inhibitor, decreases opsonized polystyrene bead phagocytosis and Leishmania uptake. Interestingly, phagocytosis of IgG-coated beads is decreased in Arg-deficient Ms, while that of C3bi-coated beads is unaffected. Conversely, uptake of C3bi-coated beads is decreased in Abl-deficient Ms, but that of IgG-coated beads is unaffected. Consistent with these results, Abl-deficient Ms are inefficient at C3bi-opsonized promastigote uptake, and Arg-deficient Ms are defective in IgG1-opsonized amastigote uptake. Finally, genetic loss of Abl or Arg reduces infection severity in murine cutaneous leishmaniasis, and imatinib treatment results in smaller lesions with fewer parasites than in controls. Our studies are the first to demonstrate that efficient phagocytosis and maximal Leishmania infection require Abl family kinases. These results highlight Abl family kinase-mediated signaling pathways as potential therapeutic targets for leishmaniasis.
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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.