ArticleScientific reports2017
Emerging Role for the PERK/eIF2α/ATF4 in Human Cutaneous Leishmaniasis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Article
- Activating transcription factors: Orchestrators of macrophage biology in pathological settings (Review).International journal of molecular medicine · 2026Review
- The integrated stress response in apicomplexan and trypanosomatid parasites: balancing survival and pathogenesis.Frontiers in immunology · 2026Review
- Inhibition of PERK-eIF2α-ATF4 signaling enhances the antiviral effects of resveratrol-loaded nanoparticles against enterovirus 71 in hand, foot, and mouth disease.Archives of virology · 2025Article
- Unraveling the Role of Proteinopathies in Parasitic Infections.Biomedicines · 2025Review
- Advance in Nrf2 Signaling Pathway in Leishmaniasis.Biomedicines · 2024Review
- Proteome profiling of cutaneous leishmaniasis lesions due to dermotropic Leishmania donovani in Sri Lanka.Clinical proteomics · 2024Article
- Review
- Activity of the Di-Substituted Urea-Derived Compound I-17 inPathogens (Basel, Switzerland) · 2024Article
- Proteome profiling of cutaneous leishmaniasis lesions due to dermotropicbioRxiv : the preprint server for biology · 2024Article
- Unfolded protein response pathway in leishmaniasis: A review.Parasite immunology · 2023Review
- Unfolded protein response is involved in resistance to Neospora caninum infection via IRE1α-XBP1s-NOD2 Axis.Parasitology research · 2023Article
- Roles of Oxidative Stress and Nrf2 Signaling in Pathogenic and Non-Pathogenic Cells: A Possible General Mechanism of Resistance to Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- Endoplasmic Stress Affects the Coinfection of Leishmania Amazonensis and the Phlebovirus (Bunyaviridae) Icoaraci.Viruses · 2022Article
- Article
- The host micro-RNA cfa-miR-346 is induced in canine leishmaniasis.BMC veterinary research · 2022Article
- Therapeutic effect and mechanism of 4-phenyl butyric acid on renal ischemia-reperfusion injury in mice.Experimental and therapeutic medicine · 2022Article
- Albendazole reduces hepatic inflammation and endoplasmic reticulum-stress in a mouse model of chronic Echinococcus multilocularis infection.PLoS neglected tropical diseases · 2022Article
- GSK2606414 attenuates PERK/p-eIF2α/ATF4/CHOP axis and augments mitochondrial function to mitigate high glucose induced neurotoxicity in N2A cells.Current research in pharmacology and drug discovery · 2022Article
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 4 countries.
Funding
Abstract
Leishmania parasites utilize adaptive evasion mechanisms in infected macrophages to overcome host defenses and proliferate. We report here that the PERK/eIF2α/ATF4 signaling branch of the integrated endoplasmic reticulum stress response (IERSR) is activated by Leishmania and this pathway is important for Leishmania amazonensis infection. Knocking down PERK or ATF4 expression or inhibiting PERK kinase activity diminished L. amazonensis infection. Knocking down ATF4 decreased NRF2 expression and its nuclear translocation, reduced HO-1 expression and increased nitric oxide production. Meanwhile, the increased expression of ATF4 and HO-1 mRNAs were observed in lesions derived from patients infected with the prevalent related species L.(V.) braziliensis. Our data demonstrates that Leishmania parasites activate the PERK/eIF2α/ATF-4 pathway in cultured macrophages and infected human tissue and that this pathway is important for parasite survival and progression of the infection.
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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.