text_1: Lmna knock-in models are appropriate for testing therapeutic approaches against Hutchinson-Gilford progeria syndrome (HGPS).
text_2: The HGPS mutation activates an aberrant cryptic splice site in LMNA pre-mRNA, leading to synthesis of a truncated lamin A protein and concomitant reduction in wild-type lamin A. Fibroblasts from individuals with HGPS have severe morphological abnormalities in nuclear envelope structure.