Affinage · Plasmodium

Showing PF3D7_1335900 — TRAP is a alias.

TRAP

PF3D7_1335900 · thrombospondin-related anonymous protein

Annotated
2026-09-08
81 papers in source corpus 25 papers cited in narrative 25 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TRAP (PF3D7_1335900) is a type I transmembrane micronemal adhesin of Plasmodium sporozoites that couples host-cell recognition to the parasite's actin-myosin motor and is essential for gliding motility and productive invasion of both mosquito salivary glands and the vertebrate liver (PMID:9267031, PMID:10508153). Genetic disruption in P. berghei and P. yoelii abolishes gliding and salivary-gland invasion while leaving erythrocytic, gametocyte, and oocyst development intact, defining TRAP as a sporozoite-stage motility and invasion factor (PMID:9267031, PMID:11295181). Its ectodomain carries two independently active adhesive modules — an integrin-like von Willebrand factor A-domain and a thrombospondin type I repeat (TSR) — that engage distinct host receptors: the TSR binds heparin/heparan sulfate proteoglycans on hepatocytes through its N-terminal half (PMID:16815922, PMID:12139612), while the A-domain binds the Anopheles salivary-gland protein saglin (PMID:19148273). Structure-function mutagenesis separates roles cleanly: the two modules mediate host-cell invasion via distinct receptors, whereas the TSR is additionally required for gliding motility itself (PMID:10508153, PMID:11927544). The A-domain switches between closed and open conformations coordinated by a MIDAS Mg2+ site, and force from the motor stabilizes the open state via an extensible β-ribbon, providing a structural basis for stick-and-slip motility (PMID:23236185). On the cytoplasmic side, the C-terminal tail—via a critical penultimate tryptophan that inserts into an induced-fit pocket on aldolase overlapping its actin-binding site—bridges TRAP to the actin cytoskeleton, and this tail encodes a conserved invasion signal transferable to other invasins (PMID:12718875, PMID:17426153, PMID:12876279). Productive motility requires proteolytic shedding of TRAP by rhomboid proteases (PfROM4, with PfROM1 activity) at a transmembrane cleavage site, which breaks rearward adhesive contacts to enable continuous forward movement (PMID:17040128, PMID:22911675). The entire cycle depends on TSR glycosylation: O-fucosylation by POFUT2 and site-specific O-fucosylation (Thr256) and C-mannosylation (Trp250) are each required for TRAP folding, stability, and correct trafficking, and secretion of TRAP-containing micronemal vesicles requires the transporter PAT (PMID:28916755, PMID:27427910, PMID:40667256).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 1988 Medium

    Before any functional data, the question was what TRAP is; molecular cloning revealed a protein carrying a thrombospondin (WSPCSVTCG) motif and an RGD adhesion motif, hinting at an adhesive function.

    Evidence Gene cloning and sequencing of P. falciparum TRAP with sequence-homology analysis

    PMID:3045563

    Open questions at the time
    • No functional assay beyond sequence inference
    • Stage assignment reported as erythrocytic, later refined to sporozoite stage
  2. 1992 Medium

    To place TRAP subcellularly and test relevance to infection, immuno-EM localized it to sporozoite micronemes with stimulus-dependent surface exposure, and anti-TRAP antibodies blocked hepatocyte invasion, establishing it as an invasion-relevant surface/micronemal protein.

    Evidence Immunoelectron microscopy, live immunofluorescence, and in vitro invasion inhibition in P. falciparum

    PMID:1409621

    Open questions at the time
    • Molecular receptor not identified
    • Mechanism of surface relocalization unresolved
  3. 1993 High

    The receptor question was first addressed by showing recombinant TRAP binds sulfated glycoconjugates and hepatoma cells in a WSPCSVTCG-motif-dependent manner, defining glycosaminoglycan-type ligands as TRAP binding partners on host cells.

    Evidence Recombinant protein binding, motif-dependence and suramin/sulfatide inhibition, antisera neutralization in P. falciparum

    PMID:8392935

    Open questions at the time
    • Native protein binding not yet shown
    • In vivo relevance of the binding not established
  4. 1997 High

    Whether TRAP is genuinely essential was settled by knockout in P. berghei, which abolished gliding motility, salivary-gland invasion, and liver infectivity without disrupting other life-cycle stages, defining TRAP as a dedicated sporozoite motility/invasion factor.

    Evidence Homologous-recombination knockout plus gliding and infectivity assays in P. berghei

    PMID:9251640 PMID:9267031

    Open questions at the time
    • Does not distinguish adhesion from motility from invasion roles
    • No molecular mechanism of motor coupling
  5. 2001 Medium

    To confirm the phenotype was not species-idiosyncratic, TRAP disruption in P. yoelii reproduced the non-gliding, non-invasive sporozoite phenotype, generalizing TRAP's essential role across rodent malaria species.

    Evidence Site-specific knockout, gliding and salivary-gland invasion assays in P. yoelii

    PMID:11295181

    Open questions at the time
    • Does not address vertebrate-cell-type specificity
    • No domain-level dissection
  6. 2002 High

    The functional question of what each ectodomain module does was answered by mutagenesis showing the A-domain and TSR act as independent binding modules for distinct receptors, and that loss of both blocks invasion of all host cell types without affecting motility or adhesion.

    Evidence Site-directed mutagenesis of ectodomain modules with multi-cell-type invasion and motility assays in P. berghei; plus cell-type-specific GAG-binding of recombinant TRAP on primary liver cells

    PMID:11927544 PMID:12139612

    Open questions at the time
    • Identity of the A-domain host receptor not yet known
    • Cross-talk between modules unresolved
  7. 2003 High

    How the extracellular adhesin transmits force inward was addressed by identifying aldolase as the cytoplasmic-tail partner bridging TRAP to actin, dependent on a critical C-terminal tryptophan, and by showing the tail carries a transferable, conserved invasion signal.

    Evidence Co-IP, pulldown and tryptophan mutagenesis (aldolase); EBA-175/TRAP cytoplasmic domain swap in P. falciparum

    PMID:12718875 PMID:12876279

    Open questions at the time
    • Direct demonstration of force transmission in vivo not shown
    • Full glideosome composition not defined here
  8. 2007 High

    The structural basis of the TRAP-aldolase link was resolved: the penultimate tryptophan of TRAP inserts into an induced-fit pocket on aldolase that overlaps the actin-binding site, explaining how the adhesin engages the motor.

    Evidence X-ray crystallography of PfAldo with TRAP C-terminal peptide plus aldolase mutagenesis

    PMID:17426153

    Open questions at the time
    • Stoichiometry within the intact glideosome unresolved
    • Regulation of the interaction during motility not addressed
  9. 2006 High

    The TSR structure and its receptor engagement were defined by NMR, revealing a Trp-Arg-ladder/disulfide-stabilized fold with heparin binding localized to the N-terminal half, mapping the hepatocyte-receptor contact.

    Evidence NMR solution structure and heparin-fragment binding mapping of the P. falciparum TSR domain

    PMID:16815922

    Open questions at the time
    • Structure of full ectodomain not resolved here
    • In vivo relevance of the minimal tetrasaccharide binding not shown
  10. 2006 Medium

    The enzymatic basis of TRAP turnover at the surface was addressed by showing rhomboid proteases PfROM4 (and PfROM1) cleave TRAP in a transmembrane-domain-dependent manner, nominating the sheddases responsible for releasing TRAP.

    Evidence Heterologous rhomboid cleavage assay with transmembrane-domain swaps

    PMID:17040128

    Open questions at the time
    • Physiological relevance shown only in heterologous system
    • Relative in vivo contribution of PfROM4 vs PfROM1 not established
  11. 2010 Medium

    To pinpoint when TRAP acts during locomotion, TIRF and flow imaging placed TRAP in the earliest adhesion step of a multistep, developmentally regulated adhesion process.

    Evidence TIRF microscopy and flow adhesion assays with TRAP and S6 mutants in P. berghei

    PMID:20159960

    Open questions at the time
    • Molecular receptor for initial adhesion not identified
    • Contribution relative to other adhesins not quantified
  12. 2012 High

    Two complementary studies answered how motility is mechanically regulated: crystal structures revealed a MIDAS-controlled closed/open A-domain switch stabilized by tensile force via an extensible β-ribbon, and cleavage-site mutagenesis showed rhomboid shedding of TRAP is required to break adhesive contacts for continuous movement.

    Evidence X-ray crystallography of VWA/TSR domains from P. vivax and P. falciparum; cleavage-site mutagenesis with shedding, motility, and infectivity assays in P. berghei

    PMID:22911675 PMID:23236185

    Open questions at the time
    • Direct measurement of force-dependent conformational switching in living parasites not achieved
    • In vivo identity of the sheddase not genetically confirmed here
  13. 2009 High

    The mosquito-side receptor question was answered by identifying saglin as the A-domain-binding salivary-gland partner whose knockdown blocks sporozoite invasion, defining the receptor for salivary-gland tropism.

    Evidence SM1 mimotope crosslinking, competition, A-domain point mutation, and in vivo saglin RNAi in P. falciparum

    PMID:19148273

    Open questions at the time
    • Affinity and structural basis of the TRAP-saglin interaction not resolved
    • Whether saglin is the sole salivary-gland receptor unknown
  14. 2016 Medium

    Native-state questions were addressed by demonstrating TRAP is glycosylated and surface-exposed on live salivary-gland sporozoites, and that secretion of TRAP-containing micronemal vesicles requires the transporter PAT.

    Evidence Surface chemical labeling and mass spectrometry on live P. falciparum sporozoites; PAT knockout with TRAP secretion and motility assays in P. berghei

    PMID:27128092 PMID:27427910

    Open questions at the time
    • Glycan structures not mapped at this stage
    • Mechanism by which PAT enables microneme exocytosis unresolved
  15. 2017 High

    The enzyme responsible for TRAP TSR glycosylation and its functional importance were established: POFUT2 O-fucosylates TRAP, and its loss destabilizes and mis-traffics TRAP, impairing motility, traversal, and hepatocyte invasion, linking glycosylation to ER quality control.

    Evidence POFUT2 genetic disruption with TRAP stability/trafficking, motility, traversal, invasion assays and humanized-liver mouse model in P. falciparum

    PMID:28916755

    Open questions at the time
    • Site of O-fucosylation on TRAP not pinpointed in this study
    • Direct structural consequence of the modification on folding unresolved
  16. 2025 High

    The specific glycosylation residues were dissected, showing O-fucosylation at Thr256 and C-mannosylation at Trp250 are each individually required for TRAP protein stability and for salivary-gland colonization, gliding, and hepatocyte invasion.

    Evidence CRISPR/Cas9 T256A and W250F mutants with protein-abundance quantification and functional assays in P. falciparum NF54 (preprint)

    PMID:40667256

    Open questions at the time
    • Preprint, not yet peer-reviewed
    • Structural mechanism by which each glycan stabilizes the TSR fold not resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the A-domain force-driven conformational switch, TSR receptor engagement, rhomboid shedding, and aldolase-mediated motor coupling are temporally coordinated during a single traction cycle in the living sporozoite remains unresolved.
  • No integrated real-time measurement of conformational state, receptor binding, and shedding during motility
  • In vivo hierarchy of hepatocyte receptors versus saglin not established
  • Structural basis of the TRAP-saglin interaction unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification
Partners
ALDOLASE (PFALDO) — BINDS TRAP C-TERMINAL CYTOPLASMIC TAIL, BRIDGING TO ACTIN [#7, #8, #11]CHONDROITIN SULFATE PROTEOGLYCANS ON STELLATE CELLS [#18]HEPARAN SULFATE / SULFATED GLYCOCONJUGATE PROTEOGLYCANS ON HEPATOCYTES — TSR LIGAND [#2, #3, #10, #18]PAT PUTATIVE PANTOTHENATE TRANSPORTER — REQUIRED FOR TRAP MICRONEMAL SECRETION [#21]PFROM4 / PFROM1 RHOMBOID PROTEASES — CLEAVE/SHED TRAP [#9, #14]POFUT2 O-FUCOSYLTRANSFERASE — MODIFIES TRAP TSR [#20, #23]S6 — CO-PARTICIPANT IN EARLY SPOROZOITE ADHESION [#22]SAGLIN (ANOPHELES SALIVARY GLAND PROTEIN) — A-DOMAIN RECEPTOR [#12]
Complex memberships
Glideosome / actin-myosin motor complex (linked via aldolase to the TRAP cytoplasmic tail)

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 TRAP is essential for sporozoite gliding motility in vitro and for infection of mosquito salivary glands and the vertebrate liver, as demonstrated by gene disruption (knockout) in Plasmodium berghei, which abolished gliding motility and infectivity while leaving erythrocytic cycle and oocyst development intact. Gene targeting / homologous recombination knockout in P. berghei; in vitro gliding motility assay; sporozoite infectivity assays in mosquitoes and rodents Cell High 9267031
1988 TRAP (PF3D7_1335900) was cloned and sequenced from P. falciparum; it encodes a protein containing the WSPCSVTCG thrombospondin motif (also found in circumsporozoite proteins and properdin) and an RGD cell-recognition motif, and is expressed during the erythrocytic stage. Gene cloning, DNA sequencing, sequence homology analysis Nature Medium 3045563
1993 Recombinant TRAP constructs expressed in E. coli bind specifically to sulfated glycoconjugates (sulfatides) and to the surface of HepG2 hepatoma cells; these interactions depend on the conserved WSPCSVTCG motif and are inhibited by sulfated glycoconjugates and suramin. Antisera against TRAP constructs inhibit sporozoite invasion of HepG2 cells. Recombinant protein binding assays (sulfatide binding, HepG2 cell binding); inhibition assays with sulfated glycoconjugates and suramin; neutralization assays with antisera The EMBO journal High 8392935
1995 Recombinant TRAP binds to the basolateral cell membrane of human hepatocytes in the Disse's space, with sulfated glycoconjugates functioning as TRAP ligands on hepatocytes. TRAP expression in P. falciparum sporozoites is absent in oocysts, variable in hemocoel sporozoites, and uniform in salivary gland sporozoites, indicating developmentally regulated expression linked to infectivity. Recombinant TRAP binding assays on hepatocytes; immunofluorescence and localization studies during sporozoite development in mosquito stages The EMBO journal Medium 7664729
1992 TRAP (PfSSP2) localizes to sporozoite micronemes by immunoelectron microscopy and to the surface membrane by live immunofluorescence; antibodies against recombinant TRAP inhibit sporozoite invasion and development in hepatocytes in vitro. Immunoelectron microscopy; live immunofluorescence; in vitro sporozoite invasion inhibition assay Proceedings of the National Academy of Sciences of the United States of America Medium 1409621
1999 The A-domain and TSR motif of P. falciparum TRAP are both required for mosquito salivary gland invasion. Transgenic P. berghei expressing PfTRAP with a point mutation in the conserved A-domain residue or a deletion in the TSP motif showed impaired salivary gland invasion; midgut sporozoites with A-domain mutation retained motility while TSP motif deletion abolished gliding motility. Both mutants remained able to infect mice from the midgut stage. Gene replacement in P. berghei with site-directed mutant PfTRAP constructs; gliding motility assay; salivary gland invasion assay; mouse infectivity assay The EMBO journal High 10508153
2002 Loss-of-function mutations in the integrin-like A-domain and the thrombospondin type I repeat (TSR) of TRAP's ectodomain specifically decrease sporozoite invasion of host cells (mosquito salivary glands and vertebrate cells) without affecting gliding motility or cell adhesion; mutations in both modules render sporozoites non-invasive in all host cell types tested. The two adhesive modules act as independently active binding domains interacting with distinct cell receptors. Site-directed mutagenesis of TRAP ectodomain modules in P. berghei; sporozoite invasion assays in multiple cell types (mosquito salivary glands, CHO cells, human/hamster hepatoma cells); gliding motility assays The EMBO journal High 11927544
2003 Aldolase specifically interacts with the C-terminal cytoplasmic domain of TRAP family adhesins, including TRAP; this interaction is disrupted by mutation of a critical tryptophan in the C-terminal domain previously shown to be essential for parasite motility, identifying aldolase as a bridge between TRAP and the actin cytoskeleton. Co-immunoprecipitation; pulldown assays; site-directed mutagenesis of the C-terminal tryptophan residue Molecular cell High 12718875
2005 The cytoplasmic tail of TRAP binds the actin-bridging protein aldolase in vitro, linking the extracellular adhesin to the actin-myosin motor complex. Homologues of glideosome-associated proteins (GAP40, GAP50) and a merozoite TRAP homologue (MTRAP) sharing TRAP's key features (thrombospondin repeat, rhomboid-protease cleavage site, aldolase-binding cytoplasmic tail) are present in P. falciparum merozoites. In vitro aldolase binding assay with TRAP cytoplasmic tail; comparative genomic and protein domain analysis; localization studies The Journal of biological chemistry Medium 16321976
2006 P. falciparum rhomboid protease PfROM4 cleaves TRAP in a heterologous assay, dependent on the TRAP transmembrane domain; PfROM1 also shows activity toward TRAP. This identifies rhomboid proteases as the enzymes responsible for TRAP shedding during sporozoite invasion. Heterologous rhomboid cleavage assay; transmembrane domain swap experiments establishing substrate specificity PLoS pathogens Medium 17040128
2006 The NMR solution structure of the TSR domain of P. falciparum TRAP reveals an elongated structure stabilized by a tryptophan-arginine ladder and disulfide bonds; heparin binding maps to the N-terminal half of the TSR domain with a tetrasaccharide as the minimal binding fragment. Solution NMR structure determination; chemical shift mapping of heparin binding epitope; heparin fragment binding assays Protein science : a publication of the Protein Society High 16815922
2007 Crystal structures of P. falciparum aldolase (PfAldo) at 2.4 Å and 2.7 Å resolution with the C-terminal hexapeptide of TRAP (from P. berghei) show that the penultimate tryptophan of TRAP fits into a newly formed induced-fit hydrophobic pocket on aldolase delimited by hydrophilic residues (two arginines, one glutamate, one glutamine). Mutagenesis of PfAldo residues in and near this induced pocket reduces TRAP binding; the TRAP- and actin-binding sites on aldolase overlap. X-ray crystallography (2.4 Å and 2.7 Å); site-directed mutagenesis of aldolase residues; structural comparison with unliganded PfAldo Proceedings of the National Academy of Sciences of the United States of America High 17426153
2009 TRAP interacts with the Anopheles salivary gland protein saglin; point mutations in TRAP's A-domain binding domain abolish saglin binding, and the SM1 peptide (a mimotope of TRAP) competes for binding. In vivo knockdown of saglin strongly inhibits salivary gland invasion by Plasmodium sporozoites. UV-crosslinking of SM1 peptide to salivary gland target; anti-SM1 antibody identification of TRAP as mimotope; binding competition assays; point mutation analysis of TRAP A-domain; in vivo saglin RNAi knockdown PLoS pathogens High 19148273
2012 Crystal structures of TRAP VWA and TSR domains from P. vivax and P. falciparum reveal that the VWA domain adopts closed and open conformations with Mg2+ binding at a MIDAS; in the open conformation, an extensible β-ribbon (disulfide-bonded segments flanking the VWA domain) is extended 15 Å and the TSR domain becomes ordered. The open conformation is stabilized by tensile force from the actin motility apparatus, providing a structural mechanism for 'stick-and-slip' motility regulation. X-ray crystallography (multiple crystal forms); structural comparison of closed vs. open states; identification of MIDAS metal coordination Proceedings of the National Academy of Sciences of the United States of America High 23236185
2012 Shedding of TRAP by a rhomboid protease is essential for sporozoite gliding motility and infectivity. Mutations introduced into the TRAP rhomboid-cleavage site within the transmembrane domain resulted in defective TRAP shedding, slow staccato motility, and reduced infectivity. Mutation of both the rhomboid-cleavage site and an alternate cleavage site produced non-motile, non-infectious sporozoites, demonstrating that TRAP removal from the sporozoite surface by proteolytic shedding is required to break adhesive contacts and enable continuous forward movement. Site-directed mutagenesis of rhomboid cleavage site and alternate cleavage site in TRAP transmembrane domain in P. berghei; TRAP shedding assay; gliding motility assay; infectivity assays (intradermal and intravenous inoculation) PLoS pathogens High 22911675
2001 Gene disruption of TRAP in P. yoelii phenocopies P. berghei TRAP knockout: TRAP-null sporozoites fail to glide and cannot invade mosquito salivary glands, while erythrocytic cycle, gametocyte, and oocyst development are unaffected. Sporozoite morphology appears normal. Gene targeting by site-specific integration in P. yoelii; gliding motility assay; salivary gland invasion assay Molecular and biochemical parasitology Medium 11295181
2003 The cytoplasmic domain of TRAP can functionally substitute for the cytoplasmic domain of EBA-175 in P. falciparum merozoite invasion of erythrocytes, demonstrating that the TRAP cytoplasmic domain encodes a conserved signal recognized by the parasite's invasion machinery regardless of the invasive stage. Cytoplasmic domain swap (chimeric EBA-175 with TRAP cytoplasmic tail) in P. falciparum; erythrocyte invasion assay The Journal of cell biology Medium 12876279
2000 Antibodies against TRAP (A-domain, conserved N-terminus, and repeat region) have no effect on sporozoite gliding motility or infectivity to mice in vivo. TRAP is normally located in micronemes and is present at very low levels on the sporozoite surface; calcium ionophore treatment or contact with hepatoma cells induces dramatic relocalization of TRAP to the parasite surface. In vivo mouse sporozoite challenge after immunization; monoclonal and polyclonal antibody gliding inhibition assays; immunofluorescence localization; calcium ionophore treatment Infection and immunity Medium 10816526
2002 Recombinant P. falciparum TRAP binds to heparan sulphate proteoglycans on hepatocytes and both heparan and chondroitin sulphate proteoglycans on stellate cells; TRAP binding to Kupffer cells is glycosaminoglycan-independent. Recombinant TRAP binding assays on primary liver cells (Kupffer cells, hepatocytes, stellate cells, sinusoidal endothelia); competitive inhibition with specific glycosaminoglycans Molecular microbiology Medium 12139612
2016 Mass spectrometry of chemically labeled P. falciparum salivary gland sporozoites provides the first direct evidence that TRAP is glycosylated on the sporozoite surface; TRAP was surface-exposed and accessible to antibodies on live sporozoites. Chemical surface labeling of live sporozoites; mass spectrometry-based proteomics; antibody accessibility assay PLoS pathogens Medium 27128092
2017 POFUT2 (Plasmodium protein O-fucosyltransferase 2) is responsible for O-fucosylation of TRAP. Genetic disruption of POFUT2 in P. falciparum results in destabilization and incorrect trafficking of TRAP (and other TSR-bearing proteins), impairing gliding motility, cell traversal, hepatocyte invasion, and production of exoerythrocytic forms. Genetic disruption of POFUT2; assessment of TRAP stability and trafficking; gliding motility assay; cell traversal assay; hepatocyte invasion assay; humanized chimeric liver mouse model Nature communications High 28916755
2016 A putative pantothenate transporter PAT is a membrane component of sporozoite micronemes and is required for secretion of TRAP-containing vesicles to the sporozoite surface; PAT-deficient P. berghei sporozoites fail to secrete TRAP, are immotile, and unable to infect the rodent host. Gene disruption of PAT in P. berghei; TRAP secretion assay; gliding motility assay; rodent infectivity assay; localization by immunofluorescence PLoS pathogens Medium 27427910
2010 TRAP (together with S6) is important for initial adhesion of sporozoites to flat surfaces; total internal reflection fluorescence microscopy and flow experiments reveal that sporozoite adhesion is a multistep, developmentally regulated process in which TRAP participates in the earliest adhesion step. Total internal reflection fluorescence (TIRF) microscopy; sporozoite flow assays; genetic analysis of TRAP and S6 surface proteins FASEB journal Medium 20159960
2025 O-fucosylation (at Thr256) and C-mannosylation (at Trp250) of the TSR domain of P. falciparum TRAP are both individually required for TRAP protein stability and function: CRISPR/Cas9-generated glyco-null mutants (T256A and W250F) show significantly reduced TRAP protein abundance despite normal transcript levels, are unable to colonize mosquito salivary glands, and are severely impaired in gliding motility and hepatocyte invasion in vitro. CRISPR/Cas9 site-directed mutagenesis of glycosylation sites in P. falciparum TRAP; western blot quantification of TRAP protein abundance; gliding motility assay; salivary gland colonization assay; hepatocyte invasion assay; comparison with TRAP knockout line bioRxiv : the preprint server for biologypreprint High 40667256
1997 Transgenic P. berghei sporozoites with TRAP disrupted by gene targeting fail to glide and fail to invade mosquito salivary glands but develop normally through erythrocytic, gametocyte, and oocyst stages, directly confirming TRAP's essential role in sporozoite-stage motility. Gene targeting by homologous recombination in P. berghei; gliding motility assay; salivary gland invasion assay; blood stage and mosquito stage phenotyping Lancet (London, England) Medium 9251640

Source papers

Stage 0 corpus · 81 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 TRAP is necessary for gliding motility and infectivity of plasmodium sporozoites. Cell 508 9267031
1988 A highly conserved amino-acid sequence in thrombospondin, properdin and in proteins from sporozoites and blood stages of a human malaria parasite. Nature 346 3045563
2005 A conserved molecular motor drives cell invasion and gliding motility across malaria life cycle stages and other apicomplexan parasites. The Journal of biological chemistry 291 16321976
2003 Aldolase forms a bridge between cell surface adhesins and the actin cytoskeleton in apicomplexan parasites. Molecular cell 266 12718875
2002 Hepatocyte CD81 is required for Plasmodium falciparum and Plasmodium yoelii sporozoite infectivity. Nature medicine 262 12483205
2017 Enhancing protective immunity to malaria with a highly immunogenic virus-like particle vaccine. Scientific reports 210 28422178
1992 Characterization of Plasmodium falciparum sporozoite surface protein 2. Proceedings of the National Academy of Sciences of the United States of America 194 1409621
2006 Two Plasmodium rhomboid proteases preferentially cleave different adhesins implicated in all invasive stages of malaria. PLoS pathogens 180 17040128
2012 Clinical assessment of a recombinant simian adenovirus ChAd63: a potent new vaccine vector. The Journal of infectious diseases 178 22275401
1993 Thrombospondin related anonymous protein (TRAP) of Plasmodium falciparum binds specifically to sulfated glycoconjugates and to HepG2 hepatoma cells suggesting a role for this molecule in sporozoite invasion of hepatocytes. The EMBO journal 170 8392935
1995 Natural selection on Plasmodium surface proteins. Molecular and biochemical parasitology 163 7630387
2010 Prime-boost vectored malaria vaccines: progress and prospects. Human vaccines 161 20061802
2016 Interrogating the Plasmodium Sporozoite Surface: Identification of Surface-Exposed Proteins and Demonstration of Glycosylation on CSP and TRAP by Mass Spectrometry-Based Proteomics. PLoS pathogens 153 27128092
2002 Plasmodium sporozoite invasion into insect and mammalian cells is directed by the same dual binding system. The EMBO journal 139 11927544
1995 Thrombospondin-related adhesive protein (TRAP) of Plasmodium falciparum: expression during sporozoite ontogeny and binding to human hepatocytes. The EMBO journal 137 7664729
1995 Identification of conserved antigenic components for a cytotoxic T lymphocyte-inducing vaccine against malaria. Lancet (London, England) 130 7536870
2004 Plasmodium sporozoite molecular cell biology. Annual review of cell and developmental biology 119 15473834
2008 No TRAP, no invasion. Trends in parasitology 117 19101208
2015 Prime-boost vaccination with chimpanzee adenovirus and modified vaccinia Ankara encoding TRAP provides partial protection against Plasmodium falciparum infection in Kenyan adults. Science translational medicine 110 25947165
1999 The A-domain and the thrombospondin-related motif of Plasmodium falciparum TRAP are implicated in the invasion process of mosquito salivary glands. The EMBO journal 110 10508153
1997 Gene targeting in malaria parasites. Methods (San Diego, Calif.) 109 9405198
2009 Malaria parasite invasion of the mosquito salivary gland requires interaction between the Plasmodium TRAP and the Anopheles saglin proteins. PLoS pathogens 106 19148273
2008 The Plasmodium TRAP/MIC2 family member, TRAP-Like Protein (TLP), is involved in tissue traversal by sporozoites. Cellular microbiology 95 18346224
2002 Proteoglycans mediate malaria sporozoite targeting to the liver. Molecular microbiology 95 12139612
2005 Synergistic DNA-MVA prime-boost vaccination regimes for malaria and tuberculosis. Vaccine 91 16150517
2000 Developmental arrest of the human malaria parasite Plasmodium falciparum within the mosquito midgut via CTRP gene disruption. Molecular microbiology 91 10760158
2016 Immune Escape Strategies of Malaria Parasites. Frontiers in microbiology 90 27799922
2012 Shedding of TRAP by a rhomboid protease from the malaria sporozoite surface is essential for gliding motility and sporozoite infectivity. PLoS pathogens 90 22911675
2000 Antibodies against thrombospondin-related anonymous protein do not inhibit Plasmodium sporozoite infectivity in vivo. Infection and immunity 90 10816526
2002 PCR diagnostics underestimate the prevalence of avian malaria (Plasmodium relictum) in experimentally-infected passerines. The Journal of parasitology 89 12053956
2016 Safety and High Level Efficacy of the Combination Malaria Vaccine Regimen of RTS,S/AS01B With Chimpanzee Adenovirus 63 and Modified Vaccinia Ankara Vectored Vaccines Expressing ME-TRAP. The Journal of infectious diseases 84 27307573
1995 Molecular cloning of a gene from Plasmodium falciparum that codes for a protein sharing motifs found in adhesive molecules from mammals and plasmodia. Molecular and biochemical parasitology 78 8719155
1990 Polymorphism of the TRAP gene of Plasmodium falciparum. Proceedings. Biological sciences 71 1983036
2003 The cytoplasmic domain of the Plasmodium falciparum ligand EBA-175 is essential for invasion but not protein trafficking. The Journal of cell biology 68 12876279
2007 Aldolase provides an unusual binding site for thrombospondin-related anonymous protein in the invasion machinery of the malaria parasite. Proceedings of the National Academy of Sciences of the United States of America 67 17426153
1992 Characterization of the gene encoding sporozoite surface protein 2, a protective Plasmodium yoelii sporozoite antigen. Molecular and biochemical parasitology 67 1501644
2010 Multistep adhesion of Plasmodium sporozoites. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 65 20159960
1997 Cloning and cross-species comparison of the thrombospondin-related anonymous protein (TRAP) gene from Plasmodium knowlesi, Plasmodium vivax and Plasmodium gallinaceum. Molecular and biochemical parasitology 65 9041517
2007 Malaria vaccines: are we getting closer? Current opinion in molecular therapeutics 63 17330398
2017 Proteogenomic analysis of the total and surface-exposed proteomes of Plasmodium vivax salivary gland sporozoites. PLoS neglected tropical diseases 62 28759593
2012 Shape change in the receptor for gliding motility in Plasmodium sporozoites. Proceedings of the National Academy of Sciences of the United States of America 62 23236185
2012 Semaphorin-7A is an erythrocyte receptor for P. falciparum merozoite-specific TRAP homolog, MTRAP. PLoS pathogens 61 23166499
2006 The layered fold of the TSR domain of P. falciparum TRAP contains a heparin binding site. Protein science : a publication of the Protein Society 60 16815922
1999 Plasmodium falciparum parasites in French Guiana: limited genetic diversity and high selfing rate. The American journal of tropical medicine and hygiene 58 10674682
2013 Safety and immunogenicity of heterologous prime-boost immunisation with Plasmodium falciparum malaria candidate vaccines, ChAd63 ME-TRAP and MVA ME-TRAP, in healthy Gambian and Kenyan adults. PloS one 56 23526949
2011 Environmental constraints guide migration of malaria parasites during transmission. PLoS pathogens 54 21698220
2008 TREP, a novel protein necessary for gliding motility of the malaria sporozoite. International journal for parasitology 54 19000911
2017 Motility precedes egress of malaria parasites from oocysts. eLife 53 28115054
2016 Plasmodium Merozoite TRAP Family Protein Is Essential for Vacuole Membrane Disruption and Gamete Egress from Erythrocytes. Cell host & microbe 53 27832590
2020 SARS-CoV-2 and Plasmodium falciparum common immunodominant regions may explain low COVID-19 incidence in the malaria-endemic belt. New microbes and new infections 52 33230417
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