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Complementation of Splicing Activity by a Galectin-3 - U1 snRNP Complex on Beads
Published on: December 9, 2020
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Galectin-3: Integrator of Signaling via Hexosamine Flux
Mana Mohan Mukherjee1, Devin Biesbrock1, John Allan Hanover1
1Cell Biochemistry Section, Laboratory of Cell and Molecular Biology, National Institute of Diabetes, Digestive and Kidney Diseases (NIDDK), National Institutes of Health, Bethesda, MD 20892, USA.
Biomolecules
|July 29, 2025
Summary
Galectin-3 (Gal-3) protein levels and cell surface expression are regulated by O-GlcNAc modification. This O-GlcNAc cycling influences Gal-3 secretion, impacting cellular signaling and disease prognosis.
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Medicine
Background:
- Galectin-3 (Gal-3) is a key lectin involved in immune cell signaling and a prognostic marker for various diseases.
- Gal-3's role in cell surface signaling and receptor modulation is established, but its tissue-specific regulation is unclear.
- O-GlcNAc modification is increasingly recognized for its role in cellular regulation.
Purpose of the Study:
- To review the evidence linking O-GlcNAc modification to Gal-3 biosynthesis, secretion, and recycling.
- To explore how nutrient-driven pathways and endomembrane transport influence Gal-3 cell surface expression.
- To highlight the potential of O-GlcNAc cycling as a regulator of Gal-3 and its implications in disease.
Main Methods:
- Review of existing literature on Gal-3 function, O-GlcNAc modification, and cellular signaling pathways.
- Analysis of the interplay between the hexosamine biosynthetic pathway (HBP), endomembrane transport, and glycan synthesis.
- Integration of findings on Gal-3's prognostic value in various human diseases.
Main Results:
- O-GlcNAc cycling, influenced by nutrient availability and HBP, regulates Gal-3 synthesis and non-canonical secretion.
- Differential nucleotide sugar pools in cellular compartments modulate O-GlcNAc cycling and glycan synthesis.
- Gal-3 cell surface expression and lattice formation are constrained by O-GlcNAc cycling, acting as a homeostatic feedback mechanism.
Conclusions:
- O-GlcNAc cycling and Gal-3 synergistically regulate Gal-3 secretion and cellular signaling.
- Dysregulation of O-GlcNAc cycling and Gal-3 may contribute to pathologies like cardiovascular disease, viral infections, and neurodegeneration.
- Investigating the link between O-GlcNAc cycling and Gal-3 offers a promising avenue for understanding and potentially treating diseases.
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