Table 1.

Sialidases in skeletal muscle

	NEU1	NEU2	NEU3	NEU4
Human chromosomal localization	6p21.31	2q37.1	11q13.5	2q37.3
Human disorders due to inherited deficiency	Sialidosis and Galactosialidosis [55]	none	none	none
Sialidase animal models	NEU1 −/− mice exhibit muscle degeneration [47]	none	Transgenic NEU3 mice develop insulin resistance [126]	none
Expression in myoblasts	In vivo and in vitro[47,83,84]	In vitro[5,89,92,93,97-99,103,104,107]	In vivo and in vitro[126,137]	not detected
Role proposed in muscle cells	NEU1 regulates the ECM deposition in skeletal muscle by limiting the lysosomal exocytosis in the fibroblasts sorrounding the myofibers [47]	NEU2 silencing prevents myoblast differentiation of rat L6 myoblasts [99]	NEU3 behaves as a negative regulator of glucose uptake [126]
	NEU1 can desialylate both IR or IGF1R and influence insulin responsiveness [82]	NEU2 over-expression enhances C2C12 differentiation [98]	NEU3 is involved in C2C12 myoblast fusion by controlling the levels of GM3 [137]
	NEU1 expression increases during the early stages of mouse C2C12 myoblast differentiation [83]	NEU2 expression increases through the PI3K/AKT pathway during differentiation and hypertrophy of C2C12 myotubes [103,104]	NEU3 over-expression delays differentiation but finally promotes the formation of hypertrophic myotubes [138]
	NEU1 over-expression impairs C2C12 differentiation [84]	NEU2 is degraded through an autophagic-dependent pathway during atrophy of C2C12 myotubes [104,107]
Muscle-derived tumors: rhabdomyosarcomas	-	NEU2 expression is undetectable in the human embryonal RD cells [109]