ArticlePLoS pathogens2011
Structure-function analysis of the Anopheles gambiae LRIM1/APL1C complex and its interaction with complement C3-like protein TEP1.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 94 citations in OpenAlex.
- Review
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- Fluctuating Warm and Humid Conditions Differentially Impact Immunity and Development in the Malaria Vector Anopheles stephensi.Global change biology · 2025Article
- Effects of Plasmodium berghei infection on the expression of salivary gland immune-related genes in the Anopheles stephensi mosquito.Malaria journal · 2025Article
- Article
- Advances in the dissection of Anopheles-Plasmodium interactions.PLoS pathogens · 2025Review
- Comparative immunological roles of TEP1 inFrontiers in immunology · 2025Review
- Late sporogonic stages ofbioRxiv : the preprint server for biology · 2024Article
- The Anopheles leucine-rich repeat protein APL1C is a pathogen binding factor recognizing Plasmodium ookinetes and sporozoites.PLoS pathogens · 2024Article
- Late sporogonic stages ofFrontiers in cellular and infection microbiology · 2024Article
- CLIPB4 is a central node in the protease network that regulates humoral immunity in Anopheles gambiae mosquitoes.bioRxiv : the preprint server for biology · 2023Article
- Evolution and assembly ofOpen biology · 2023Article
- A rare sugar, allose, inhibits the development ofFrontiers in cellular and infection microbiology · 2023Article
- CLIPB4 Is a Central Node in the Protease Network that Regulates Humoral Immunity in Anopheles gambiae Mosquitoes.Journal of innate immunity · 2023Article
- Molecular characterization and genetic authentication assay for Anopheles 'hemocyte-like' cell lines 4a-3A and 4a-3B.Parasites & vectors · 2022Article
- Aryl hydrocarbon receptor and Krüppel like factor 10 mediate a transcriptional axis modulating immune homeostasis in mosquitoes.Scientific reports · 2022Article
- Plasmodium development in Anopheles: a tale of shared resources.Trends in parasitology · 2022Review
- C-type lectin 4 regulates broad-spectrum melanization-based refractoriness to malaria parasites.PLoS biology · 2022Article
- Knockout of Anopheles stephensi immune gene LRIM1 by CRISPR-Cas9 reveals its unexpected role in reproduction and vector competence.PLoS pathogens · 2021Article
- Transient knockdown of Anopheles stephensi LRIM1 using RNAi increases Plasmodium falciparum sporozoite salivary gland infections.Malaria journal · 2021Article
4 more citing papers are in PubMed but not listed here.
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4 authors at 1 institution in 1 country.
Funding
Abstract
Malaria threatens half the world's population and exacts a devastating human toll. The principal malaria vector in Africa, the mosquito Anopheles gambiae, encodes 24 members of a recently identified family of leucine-rich repeat proteins named LRIMs. Two members of this family, LRIM1 and APL1C, are crucial components of the mosquito complement-like pathway that is important for immune defense against Plasmodium parasites. LRIM1 and APL1C circulate in the hemolymph exclusively as a disulfide-bonded complex that specifically interacts with the mature form of the complement C3-like protein, TEP1. We have investigated the specificity of LRIM1/APL1C complex formation and which regions of these proteins are required for interactions with TEP1. To address these questions, we have generated a set of LRIM1 and APL1C alleles altering key conserved structural elements and assayed them in cell culture for complex formation and interaction with TEP1. Our data indicate that heterocomplex formation is an intrinsic ability of LRIM1 and APL1C and identify key homologous cysteine residues forming the intermolecular disulfide bond. We also demonstrate that the coiled-coil domain is the binding site for TEP1 but also contributes to the specificity of LRIM1/APL1C complex formation. In addition, we show that the LRIM1/APL1C complex interacts with the mature forms of three other TEP proteins, one of which, TEP3, we have characterized as a Plasmodium antagonist. We conclude that LRIM1 and APL1C contain three distinct modules: a C-terminal coiled-coil domain that can carry different TEP protein cargoes, potentially with distinct functions, a central cysteine-rich region that controls complex formation and an N-terminal leucine-rich repeat with a putative role in pathogen recognition.
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