Home LiteratureArticle Details
PMID: 2431928 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Increased nuclear cyclin/PCNA antigen staining of non S-phase transformed human amnion cells engaged in nucleotide excision DNA repair.

FEBS letters ·Vol. 209 ·No. 2 ·1986-12-15 ·Pages 277-83

Celis JE, Madsen P

Abstract

PCNA autoantibodies specific for cyclin/PCNA were used to determine the nuclear distribution of this protein in transformed human amnion cells (AMA) irradiated with ultraviolet light (254 nm) under conditions that induced nucleotide excision DNA repair synthesis. The results showed a striking increase in nuclear cyclin/PCNA antigen staining of non S-phase cells that was not abolished by cycloheximide (20 micrograms/ml, added 2 h before irradiation), and that is most likely due to a redistribution of pre-existing cyclin. These observations raise the possibility that cyclin/PCNA may play a role in nucleotide excision DNA repair synthesis in addition to its putative role in replicative DNA synthesis.

MeSH Terms
Amniotic Fluid/cytology,radiation effects Autoantigens/analysis Cell Nucleus/immunology,radiation effects Cell Transformation, Neoplastic DNA Repair Female Fluorescent Antibody Technique Humans Nucleoproteins/analysis Pregnancy Proliferating Cell Nuclear Antigen Staining and Labeling Ultraviolet Rays
Chemicals
Autoantigens Nucleoproteins Proliferating Cell Nuclear Antigen
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Celis J E
Madsen P
Article Info
Journal
FEBS letters
Abbr.
FEBS Lett
ISSN
0014-5793
Published
1986-12-15
Pages
277-83
Language
English
Region
England
NLM ID
0155157
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]