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Mol Biol Cell ; 32(20): br6, 2021 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-34379448

RESUMO

On induction of DNA damage with 405-nm laser light, proteins involved in base excision repair (BER) are recruited to DNA lesions. We find that the dynamics of factors typical of either short-patch (XRCC1) or long-patch (PCNA) BER are altered by chemicals that perturb actin or tubulin polymerization in human cells. Whereas the destabilization of actin filaments by latrunculin B, cytochalasin B, or Jasplakinolide decreases BER factor accumulation at laser-induced damage, inhibition of tubulin polymerization by nocodazole increases it. We detect no recruitment of actin to sites of laser-induced DNA damage, yet the depolymerization of cytoplasmic actin filaments elevates both actin and tubulin signals in the nucleus. While published evidence suggested a positive role for F-actin in double-strand break repair in mammals, the enrichment of actin in budding yeast nuclei interferes with BER, augmenting sensitivity to Zeocin. Our quantitative imaging results suggest that the depolymerization of cytoplasmic actin may compromise BER efficiency in mammals not only due to elevated levels of nuclear actin but also of tubulin, linking cytoskeletal integrity to BER.


Assuntos
Reparo do DNA/fisiologia , Antígeno Nuclear de Célula em Proliferação/metabolismo , Proteína 1 Complementadora Cruzada de Reparo de Raio-X/metabolismo , Actinas/metabolismo , Linhagem Celular Tumoral , Núcleo Celular/metabolismo , Citoesqueleto/fisiologia , DNA/metabolismo , Dano ao DNA/genética , Dano ao DNA/fisiologia , Reparo do DNA/genética , Proteínas de Ligação a DNA/metabolismo , Células HeLa , Humanos , Antígeno Nuclear de Célula em Proliferação/fisiologia , Tubulina (Proteína)/metabolismo , Proteína 1 Complementadora Cruzada de Reparo de Raio-X/fisiologia
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