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Laminin-α2 is required for the maintenance of the myotendinous junction in vivo
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DOI：10.1016/j.matbio.2026.03.003.png)
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Abstract
En 中文
• Laminin-α2 is highly concentrated at the myotendinous junction (MTJ) • Lama2 deficiency severely disrupts MTJ morphology, ultrastructure, and the localization of MTJ-specific marker proteins • Muscle unloading secondary to Lama2 deficiency partially contributes to the MTJ defects, as revealed by muscle denervation experiments • Altered muscle fiber tip morphology in Lama2-deficient and denervated mice involves a shared integrin-associated remodeling response
Keywords:
LAMA2 MD
laminin-α2
dyW/dyW mice
denervation
myotendinous junction
MTJ
extracellular matrix
ECM
collagen XXII
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