ArticlePloS one2013
Dissection of the beta-globin replication-initiation region reveals specific requirements for replicator elements during gene amplification.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Episomal Vectors for Stable Production of Recombinant Proteins and Engineered Antibodies.Antibodies (Basel, Switzerland) · 2024Article
- Revisiting characteristics of oncogenic extrachromosomal DNA as mobile enhancers on neuroblastoma and glioma cancers.Cancer cell international · 2022Review
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- Targeted amplification of a sequence of interest in artificial chromosome in mammalian cells.Nucleic acids research · 2019Article
- Generation and maintenance of acentric stable double minutes from chromosome arms in inter-species hybrid cells.BMC molecular and cell biology · 2019Article
- The β-globin Replicator greatly enhances the potential of S/MAR based episomal vectors for gene transfer into human haematopoietic progenitor cells.Scientific reports · 2017Article
- Amplification of a transgene within a long array of replication origins favors higher gene expression in animal cells.PloS one · 2017Article
- Reduced cohesin destabilizes high-level gene amplification by disrupting pre-replication complex bindings in human cancers with chromosomal instability.Nucleic acids research · 2016Article
- Epigenetic Repeat-Induced Gene Silencing in the Chromosomal and Extrachromosomal Contexts in Human Cells.PloS one · 2016Article
- Cloning and Characterization of a Human Genomic Sequence that Alleviates Repeat-Induced Gene Silencing.PloS one · 2016Article
- How a replication origin and matrix attachment region accelerate gene amplification under replication stress in mammalian cells.PloS one · 2014Article
- SIRT1 stabilizes extrachromosomal gene amplification and contributes to repeat-induced gene silencing.The Journal of biological chemistryArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene amplification plays a pivotal role in malignant transformation of human cells. A plasmid with both a mammalian replication-initiation region (IR)/origin/replicator and a nuclear matrix-attachment region (MAR) is spontaneously amplified in transfected cells by a mechanism that involves amplification at the extrachromosomal site, followed by amplification at the chromosomal arm, ultimately generating a long homogeneously staining region (HSR). Several observations suggest that replication initiation from IR sequences might mediate amplification. To test this idea, we previously dissected c-myc and DHFR IRs to identify the minimum sequence required to support amplification. In this study, we applied an improved analysis that discriminates between two amplification steps to the ß-globin RepP IR, which contains separate elements already known to be essential for initiation on the chromosome arm. The IR sequence was required at least for the extrachromosomal amplification step. In addition to the vector-encoded MAR, amplification also required an AT-rich region and a MAR-like element, consistent with the results regarding replicator activity on the chromosome. However, amplification did not require the AG-rich tract necessary for replicator activity, but instead required a novel sequence containing another AG-rich tract. The differential sequence requirement might be a consequence of extrachromosomal replication.
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