ArticleMolecular biology of the cell2003
The interplay between folding-facilitating mechanisms in Trypanosoma cruzi endoplasmic reticulum.
Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Glycocalyx-Driven Immunomodulation in Trypanosoma cruzi: Structures, Host Responses, Diagnostic and Therapeutic Targeting.Parasite immunology · 2026Review
- Inhibition of calreticulin by protein nanoparticles carrying antisense oligonucleotides reduce gene expression and infection ofNanomedicine (London, England) · 2025Article
- Mechanical effect of protein glycosylation on BiP-mediated post-translational translocation and folding in the endoplasmic reticulum.Biophysical reviews · 2025Review
- Common and unique features of glycosylation and glycosyltransferases in African trypanosomes.The Biochemical journal · 2022Article
- The endoplasmic reticulum of trypanosomatids: An unrevealed road for chemotherapy.Frontiers in cellular and infection microbiology · 2022Review
- To the Surface and Back: Exo- and Endocytic Pathways inFrontiers in cell and developmental biology · 2021Review
- Article
- Origin and Evolution of Two Independently Duplicated Genes Encoding UDP- Glucose: Glycoprotein Glucosyltransferases inG3 (Bethesda, Md.) · 2020Article
- Endoplasmic reticulum-associated degradation and disposal of misfolded GPI-anchored proteins in Trypanosoma brucei.Molecular biology of the cell · 2018Article
- Article
- Review
- Immune complexes in chronic Chagas disease patients are formed by exovesicles from Trypanosoma cruzi carrying the conserved MASP N-terminal region.Scientific reports · 2017Article
- Surface proteins, ERAD and antigenic variation in Trypanosoma brucei.Cellular microbiology · 2016Article
- Is the Antitumor Property of Trypanosoma cruzi Infection Mediated by Its Calreticulin?Frontiers in immunology · 2016Review
- Depletion of UDP-Glucose and UDP-Galactose Using a Degron System Leads to Growth Cessation of Leishmania major.PLoS neglected tropical diseases · 2015Article
- Calcium signaling in trypanosomatid parasites.Cell calcium · 2015Review
- Article
- Knockout of the dhfr-ts gene in Trypanosoma cruzi generates attenuated parasites able to confer protection against a virulent challenge.PLoS neglected tropical diseases · 2011Article
- Functional cooperation between BiP and calreticulin in the folding maturation of a glycoprotein in Trypanosoma cruzi.Molecular and biochemical parasitology · 2011Article
- The two Caenorhabditis elegans UDP-glucose:glycoprotein glucosyltransferase homologues have distinct biological functions.PloS one · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lectin (calreticulin [CRT])-N-glycan-mediated quality control of glycoprotein folding is operative in trypanosomatid protozoa but protein-linked monoglucosylated N-glycans are exclusively formed in these microorganisms by UDP-Glc:glycoprotein glucosyltransferase (GT)-dependent glucosylation. The gene coding for this enzyme in the human pathogen Trypanosoma cruzi was identified and sequenced. Even though several of this parasite glycoproteins have been identified as essential components of differentiation and mammalian cell invasion processes, disruption of both GT-encoding alleles did not affect cell growth rate of epimastigote form parasites and only partially affected differentiation and mammalian cell invasion. The cellular content of one of the already identified T. cruzi glycoprotein virulence factors (cruzipain, a lysosomal proteinase) only showed a partial (5-20%) decrease in GT null mutants in spite of the fact that >90% of all cruzipain molecules interacted with CRT during their folding process in wild-type cells. Although extremely mild cell lysis and immunoprecipitation procedures were used, no CRT-cruzipain interaction was detected in GT null mutants but secretion of the proteinase was nevertheless delayed because of a lengthened interaction with Grp78/BiP probably caused by the detected induction of this chaperone in GT null mutants. This result provides a rationale for the absence of a more drastic consequence of GT absence. It was concluded that T. cruzi endoplasmic reticulum folding machinery presents an exquisite plasticity that allows the parasite to surmount the absence of the glycoprotein-specific folding facilitation mechanism.
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