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. 2020 Jul 23;13:118. doi: 10.3389/fnmol.2020.00118

Table 2.

LAMA2 mouse models.

Lama2 Mouse Mutation Laminin-α2 levels CNS Involvement
Myelination deficits BBB Deficits Other
dy/dy (Michelson et al., 1955) Spontaneous mutation Substantially reduced Impaired oligodendrogenesis and myelination (Chun et al., 2003; Relucio et al., 2009). Unknown Elevated audiometric threshold response, degeneration of cochlear and vestibular structures (Pillers et al., 2002). Atrophy of motor neurons and abnormal neurotrophic factor expression in CNS (Sakuma et al., 2002)
dy2J/dy2J (Meier and Southard, 1970) Spontaneous mutation; abnormal splicing and subsequent instability leads to a truncated protein that lacks the N-terminus Expressed but lacking LN domain; modest reduction in levels Unknown Unknown Long term plasticity was disrupted (Anderson et al., 2005).
dyW/dyW (Kuang et al., 1998) Targeted knock-out; truncated protein Very low to absent Unknown Unknown
dy3k/dy3k (Miyagoe et al., 1997) Targeted knock-out Absent Impaired oligodendrogenesis and myelination (Relucio et al., 2012). BBB dysfunction and increased permeability (Menezes et al., 2014). Impaired NSC proliferation and attachment within the ventricular zone (Loulier et al., 2009; Relucio et al., 2012).