Idioma:

THE INVOLVEMENT OF ACTIVE DNA-SYNTHESIS IN CAMPTOTHECIN-INDUCED G2 ARREST - ALTERED REGULATION OF P34CDC2 CYCLIN-B

TSAO, YP ; DARPA, P ; LIU, LF

Cancer research (Chicago, Ill.), 1992-04, Vol.52 (7), p.1823-1829 [Periódico revisado por pares]

PHILADELPHIA: Amer Assoc Cancer Research

Texto completo disponível

Citações Citado por

Enviar para

Título:
THE INVOLVEMENT OF ACTIVE DNA-SYNTHESIS IN CAMPTOTHECIN-INDUCED G2 ARREST - ALTERED REGULATION OF P34CDC2 CYCLIN-B
Autor: TSAO, YP ; DARPA, P ; LIU, LF
Assuntos: Aphidicolin - pharmacology ; Camptothecin - pharmacology ; CDC2 Protein Kinase - metabolism ; Cyclins - metabolism ; Dimethyl Sulfoxide - pharmacology ; DNA Damage ; DNA Replication ; DNA Topoisomerases, Type I - metabolism ; G2 Phase - drug effects ; HeLa Cells ; Humans ; Kinetics ; Life Sciences & Biomedicine ; Methionine - metabolism ; Models, Biological ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - isolation & purification ; Oncology ; Protamine Kinase - metabolism ; S Phase - drug effects ; Science & Technology
É parte de: Cancer research (Chicago, Ill.), 1992-04, Vol.52 (7), p.1823-1829
Notas: Medline
NIH RePORTER
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Descrição: Cell cycle arrest in G2 phase is a common response to a variety of DNA-damaging agents. The coupling between DNA damage and G2 arrest was studied in synchronized HeLa cells using camptothecin, a highly specific inhibitor of topoisomerase I that damages DNA through the formation of reversible topoisomerase I-DNA cleavable complexes. Brief camptothecin treatment of early S-phase HeLa cells caused arrest at G2 phase and abolished the activation of p34cdc2 protein kinase. Both tyrosine dephosphorylation of p34cdc2 and cyclin B accumulation were altered. These cell cycle-dependent changes were not observed when DNA replication was inhibited by aphidicolin during the brief camptothecin treatment. Our results suggest that to produce G2 arrest, active DNA synthesis is required at the time of camptothecin treatment, as was previously shown for camptothecin-induced cytotoxicity. Furthermore, our results suggest that the interaction of the replication fork with DNA damage may ultimately trigger altered regulation of p34cdc2/cyclin B, leading to cell cycle arrest at the G2 phase.
Editor: PHILADELPHIA: Amer Assoc Cancer Research
Idioma: Inglês

Links

View this record in MEDLINE/PubMed

Voltar para lista de resultados

Realização: Logos de Redes Sociais:

THE INVOLVEMENT OF ACTIVE DNA-SYNTHESIS IN CAMPTOTHECIN-INDUCED G2 ARREST - ALTERED REGULATION OF P34CDC2 CYCLIN-B

TSAO, YP ; DARPA, P ; LIU, LF

PHILADELPHIA: Amer Assoc Cancer Research

Buscando em bases de dados remotas. Favor aguardar.