ArticleScientific reports2025
A lectin produced by a Streptomyces species targets mammalian pancreatic acinar cells in mice and humans.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lectins are produced in almost all life forms, can interact with targets (glycans) in a cross-kingdom manner and have served as valuable tools for studying glycobiology. Previously, a bacterial lectin, named Streptomyces hemagglutinin (SHA), was found to agglutinate human type B erythrocytes. However, the binding of SHA to mammalian cell types other than human erythrocytes has not been explored. To address this, we produced a recombinant fusion protein, with the mCherry reporter protein proceeding the SHA protein (referred to as mCherry-SHA), and performed co-immunofluorescence staining analysis. We focused on the normal pancreas in this study because glycans on pancreatic cells have been associated with initiation and progression of pancreatic cancer, a deadly disease. We found that only acinar, but not ductal or endocrine cells were stained positively with mCherry-SHA from embryonic day (E) 18.5 to 35 weeks old mice; in contrast, E12.5 and E15.5 pancreas display minimal mCherry-SHA binding. In adult humans, mCherry-SHA also targeted acinar cells specifically; however, only tissue from blood type B donors, but not type A or O donors, showed positivity. Together, these results demonstrate that SHA can bind to normal murine and human pancreatic acinar cells and that SHA-binding glycans are developmentally regulated.
Indexed as
Identifiers
What OpenQuestion holds
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.