The enzyme does not act on 4-O-acetylated sialic acids. endo-alpha-Sialidase activity is listed as EC 3.2.1.129, endo-alpha-sialidase. See also EC 4.2.2.15 anhydrosialidase.
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SYSTEMATIC NAME
IUBMB Comments
acetylneuraminyl hydrolase
The enzyme does not act on 4-O-acetylated sialic acids. endo-alpha-Sialidase activity is listed as EC 3.2.1.129, endo-alpha-sialidase. See also EC 4.2.2.15 anhydrosialidase.
isoform Neu3 plays a key role in skeletal muscle differentiation by strictly modulating the ganglioside content of adjacent cells, with special regard to GM3
the absence of Neu1 results in the increased sialylation of the cell surface proteins, probably affecting multiple receptors for phagocytosis. Macrophages from the Neu1-deficient mice show increased sialylation and impaired phosphorylation of FcgammaRas well as markedly reduced phosphorylation of Syk kinase in response to treatment with immunoglobulin G-opsonized beads
treatment of the cells with purified mouse Neu1 reduces surface sialylation and restores phagocytosis. Cell surface Neu1 activates the phagocytosis in macrophages and dendritic cells through desialylation of surface receptors, thus, contributing to their functional integrity
in macrophages from isoform Neu1 deficient mice, a model for sialidosis, oversialylated lysosomal membrane protein Lamp-1 enhances lysosomal exocytosis. Silencing of Lamp-1 reverts this phenotype by interfering with the docking of lysosomes at the plasma membrane. In Neu1-/- mice the excessive exocytosis of serine proteases in the bone niche leads to inactivation of extracellular serpins, premature degradation of VCAM-1, and loss of bone marrow retention
neuramindase-1 deficiency in mice results in a tight-skin phenotype. Normal septation of Neu-1 null mice does not occur in neonatal mice, resulting in enlarged alveoli that are maintained in adults. Elastin fibers develop abnormally and elastin, fibrillin-1, fibrillin-2, and fibrillin-5 show overlapping distributions. Myofibroblasts distribute randomly around the alveolar walls. Concentration of elastin is significantly reduced in the aorta of mutant mice
in macrophages from isoform Neu1 deficient mice, a model for sialidosis, oversialylated lysosomal membrane protein Lamp-1 enhances lysosomal exocytosis. Silencing of Lamp-1 reverts this phenotype by interfering with the docking of lysosomes at the plasma membrane. In Neu1-/- mice the excessive exocytosis of serine proteases in the bone niche leads to inactivation of extracellular serpins, premature degradation of VCAM-1, and loss of bone marrow retention
isoform Neu3 plays a key role in skeletal muscle differentiation by strictly modulating the ganglioside content of adjacent cells, with special regard to GM3. Induced down-regulation of NEU3, even when partial, totally inhibits cell's capability to differentiate by increasing the GM3 level above a critical point, which causes epidermal growth factor receptor inhibition and ultimately its down-regulation and an higher responsiveness of myoblasts to the apoptotic stimuli
The plasma membrane-associated sialidase MmNEU3 modifies the ganglioside pattern of adjacent cells supporting its involvement in cell-to-cell interactions