text_1: Genomic sequences involved in alternative splicing responsible for Hutchinson-Gilford progeria syndrome (HGPS) are abundant in the ''progerinonly'' allele of Lmna knock-in models.
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.