{"entity": "publication", "iuid": "0007cf802af64e048b7ef64f029a3a3a", "timestamp": "2026-08-29T04:23:14.387Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0007cf802af64e048b7ef64f029a3a3a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0007cf802af64e048b7ef64f029a3a3a"}}, "title": "Lamin A/C promotes DNA base excision repair.", "authors": [{"family": "Maynard", "given": "Scott", "initials": "S"}, {"family": "Keijzers", "given": "Guido", "initials": "G"}, {"family": "Akbari", "given": "Mansour", "initials": "M"}, {"family": "Ezra", "given": "Michael Ben", "initials": "MB"}, {"family": "Hall", "given": "Arnaldur", "initials": "A"}, {"family": "Morevati", "given": "Marya", "initials": "M"}, {"family": "Scheibye-Knudsen", "given": "Morten", "initials": "M"}, {"family": "Gonzalo", "given": "Susana", "initials": "S"}, {"family": "Bartek", "given": "Jiri", "initials": "J"}, {"family": "Bohr", "given": "Vilhelm A", "initials": "VA"}], "type": "journal article", "published": "2019-12-16", "journal": {"title": "Nucleic Acids Res.", "issn": "1362-4962", "volume": "47", "issue": "22", "pages": "11709-11728", "issn-l": "0305-1048"}, "abstract": "The A-type lamins (lamin A/C), encoded by the LMNA gene, are important structural components of the nuclear lamina. LMNA mutations lead to degenerative disorders known as laminopathies, including the premature aging disease Hutchinson-Gilford progeria syndrome. In addition, altered lamin A/C expression is found in various cancers. Reports indicate that lamin A/C plays a role in DNA double strand break repair, but a role in DNA base excision repair (BER) has not been described. We provide evidence for reduced BER efficiency in lamin A/C-depleted cells (Lmna null MEFs and lamin A/C-knockdown U2OS). The mechanism involves impairment of the APE1 and POL\u03b2 BER activities, partly effectuated by associated reduction in poly-ADP-ribose chain formation. Also, Lmna null MEFs displayed reduced expression of several core BER enzymes (PARP1, LIG3 and POL\u03b2). Absence of Lmna led to accumulation of 8-oxoguanine (8-oxoG) lesions, and to an increased frequency of substitution mutations induced by chronic oxidative stress including GC>TA transversions (a fingerprint of 8-oxoG:A mismatches). Collectively, our results provide novel insights into the functional interplay between the nuclear lamina and cellular defenses against oxidative DNA damage, with implications for cancer and aging.", "doi": "10.1093/nar/gkz912", "pmid": "31647095", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7145687"}, {"db": "pii", "key": "5606629"}], "notes": [], "created": "2026-08-20T09:50:42.217Z", "modified": "2026-08-20T09:50:42.230Z"}