We recently reported that anti-CD13 mAbs induce homotypic aggregation of monocytic cells. This phenomenon is signal transduction dependent and does not require CD13 aminopeptidase activity. Since CD13 is heavily glycosylated and a member of the galectin family (galectin-4) has been shown to associate with CD13 in the intestinal epithelium, we hypothesized that CD13-mediated aggregation might proceed through a carbohydrate-dependent mechanism involving galectin-3, the most highly expressed galectin on monocytes. We report here that lactose and anti-galectin-3 antibodies completely abrogate homotypic aggregation induced by anti-CD13 antibodies. Furthermore, galectin-3 co-immunoprecipitates with CD13 from resting U-937 cells and this association decreases during the aggregation process, a phenomenon that may have functional implications. Together, the results presented here point to a key role for galectin-3 in CD13-mediated homotypic aggregation of monocytic cells.
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http://dx.doi.org/10.1016/j.bbrc.2006.12.081 | DOI Listing |
J Biol Chem
January 2025
Genomics Research Center, Academia Sinica, Taipei, Taiwan; Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Yang Ming Chiao Tung University and Academia Sinica, Taipei, Taiwan; Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan; Chemical Biology and Molecular Biophysics Program, Taiwan International Graduate Program, Institute of Biological Chemistry, Academia Sinica; Institute of Biochemical Sciences, National Taiwan University; Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Taiwan University and Academia Sinica, Taipei, Taiwan. Electronic address:
Tauopathies cover a range of neurodegenerative diseases in which natively unfolded tau protein aggregates and spreads in the brain during disease progression. To gain insights into the mechanism of tau structure and spreading, here, we examined the biochemical and cellular properties of human full-length wild-type and familial mutant tau, ΔK280, with a deletion at lysine 280. Our results showed that both wild-type and mutant tau are predominantly monomeric by analytical ultracentrifugation.
View Article and Find Full Text PDFJ Control Release
December 2024
Jiangsu Key Laboratory of Neuropsychiatric Diseases Research, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China; Jiangsu Province Engineering Research Center of Precision Diagnostics and Therapeutics Development, Soochow University, Suzhou 215123, China. Electronic address:
Many brain-targeting drug delivery strategies have been reported to permeate the blood-brain barrier (BBB) via hijacking receptor-mediated transport. However, these receptor-based strategies could mediate whole-brain BBB crossing due to the wide intracranial expression of target receptors and lead to unwanted accumulation and side effects on healthy brain tissues. Inspired by brain metastatic processes and the selectivity of brain metastatic cancer cells for the inflammatory BBB, a biomimetic nanoparticle was developed by coating drug-loaded core with the inflammatory BBB-seeking erythrocyte-brain metastatic hybrid membrane, which can resist homotypic aggregation and specially bind and permeate the inflammatory BBB for specific drug delivery.
View Article and Find Full Text PDFNature
January 2025
Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Proc Natl Acad Sci U S A
July 2024
Department of Biochemistry and Molecular Biology, School of Neurobiology, Biochemistry and Biophysics, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 6997801, Israel.
In the developing human brain, only 53 stochastically expressed clustered protocadherin (cPcdh) isoforms enable neurites from individual neurons to recognize and self-avoid while simultaneously maintaining contact with neurites from other neurons. Cell assays have demonstrated that self-recognition occurs only when all cPcdh isoforms perfectly match across the cell boundary, with a single mismatch in the cPcdh expression profile interfering with recognition. It remains unclear, however, how a single mismatched isoform between neighboring cells is sufficient to block erroneous recognitions.
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