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Table 1 Sialidases in skeletal muscle

From: Implications for the mammalian sialidases in the physiopathology of 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]

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