LGALS3 Antibody (C-term) [AMM06263G]

Tissue Location: A major expression is found in the colonic epithelium. It is also abundant in the activated macrophages. Expressed in fetal membranes.

We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality LGALS3 Antibody (C-term) [AMM06263G].

Galectin-3, Gal-3, 35 kDa lectin, Carbohydrate-binding protein 35, CBP 35, Galactose-specific lectin 3, Galactoside-binding protein, GALBP, IgE-binding protein, L-31, Laminin-binding protein, Lectin L-29, Mac-2 antigen, LGALS3, MAC2

Cytoplasm. Nucleus. Secreted. Note=Secreted by a non- classical secretory pathway and associates with the cell surface. Can be secreted; the secretion is dependent on protein unfolding and facilitated by the cargo receptor TMED10; it results in protein translocation from the cytoplasm into the ERGIC (endoplasmic reticulum- Golgi intermediate compartment) followed by vesicle entry and secretion (PubMed:32272059) .

Purified monoclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS.

Galactose-specific lectin which binds IgE. May mediate with the alpha-3, beta-1 integrin the stimulation by CSPG4 of endothelial cells migration. Together with DMBT1, required for terminal differentiation of columnar epithelial cells during early embryogenesis (By similarity) . In the nucleus: acts as a pre-mRNA splicing factor. Involved in acute inflammatory responses including neutrophil activation and adhesion, chemoattraction of monocytes macrophages, opsonization of apoptotic neutrophils, and activation of mast cells. Together with TRIM16, coordinates the recognition of membrane damage with mobilization of the core autophagy regulators ATG16L1 and BECN1 in response to damaged endomembranes.