DNA Damage and Deficiencies in the Mechanisms of Its Repair: Implications in the Pathogenesis of Systemic Lupus Erythematosus

Figure 1

Enzymatic deficiencies in DNA repair pathways reported in systemic lupus erythematosus. The figure shows the main proteins involved in DNA repair mechanisms and highlights in red those enzymes that have been reported abnormal in SLE. Base excision repair (BER): repair of single-strand breaks and single-base damage (e.g., 8-oxodG). Nucleotide excision repair (NER): repair of bulky lesions and cross-links (e.g., CPDs and 6-4 PPs induced by UV). Nonhomologous end-joining (NHEJ): repair of double-strand breaks. Homologous recombination (HR): repair of double-strand breaks. SLE: systemic lupus erythematosus; DNA: deoxyribonucleic acid; 8-oxodG: 8-hydroxy-2-deoxyguanosine; hOGG1: 8-oxoguanine DNA glycosylase; PARP: poly-ADP ribose polymerase; XRCC1: X-ray repair cross-complementing protein 1; ANAs: antinuclear antibodies: Pol β: polymerase beta; CPDs: pyrimidine cyclobutane dimers; 6-4 PPs: 6-4-pyrimidine pyrimidone photoproducts; UV: ultraviolet radiation; XPA: xeroderma pigmentosum complementation group A; XPC: xeroderma pigmentosum complementation group C; XPE: Xeroderma pigmentosum complementation group E; DDB1 DNA damage-binding protein 1.