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001-es BibID:	BIBFORM085922
035-os BibID:	(Cikkazonosító)43156 (WOS)000394534200001 (Scopus)85013667550
Első szerző:	Qiu, Zhijun
Cím:	Generation of Gross Chromosomal Rearrangements by a Single Engineered DNA Double Strand Break / Zhijun Qiu, Zhenhua Zhang, Anna Roschke, Tamas Varga, Peter D. Aplan
Dátum:	2017
ISSN:	2045-2322
Megjegyzések:	Gross chromosomal rearrangements (GCRs), including translocations, inversions amplifications, and deletions, can be causal events leading to malignant transformation. GCRs are thought to be triggered by DNA double strand breaks (DSBs), which in turn can be spontaneous or induced by external agents (eg. cytotoxic chemotherapy, ionizing radiation). It has been shown that induction of DNA DSBs at two defined loci can produce stable balanced chromosomal translocations, however, a single engineered DNA DSB could not. Herein, we report that although a single engineered DNA DSB in H2AX "knockdown" cells did not generate GCRs, repair of a single engineered DNA DSB in fibroblasts that had ablated H2ax did produce clonal, stable GCRs, including balanced translocations and megabase-pair inversions. Upon correction of the H2ax deficiency, cells no longer generated GCRs following a single engineered DNA DSB. These findings demonstrate that clonal, stable GCRs can be produced by a single engineered DNA DSB in H2ax knockout cells, and that the production of these GCRs is ameliorated by H2ax expression.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Scientific Reports. - 7 : 1 (2017), p. 1-10. -
További szerzők:	Zhang, Zhenhua Roschke, Anna Varga Tamás (1971-) (biológus) Aplan, Peter D.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM016570
Első szerző:	Varga Tamás (biológus)
Cím:	Chromosomal aberrations induced by double strand DNA breaks / Varga Tamas, Aplan Peter D.
Dátum:	2005
ISSN:	1568-7864
Megjegyzések:	It has been suggested that introduction of double-strand DNA breaks into mammalian chromosomes can lead to gross chromosomal rearrangements through improper DNA repair. To study this phenomenon, we employed a model system in which a double-strand DNA break (DSB) can be produced in human cells in vivo at a predetermined location. The ensuing chromosomal changes flanking the breakage site can then be cloned and characterized. In this system, the recognition site for the I-SceI endonuclease, whose 18 bp recognition sequence is not normally found in the human genome, is placed between a strong constitutive promoter and the Herpes simplex virus thymidine kinase (HSV-tk) gene, which serves as a negative selectable marker. We found that the most common mutation following aberrant DSB repair was an interstitial deletion; these deletions typically showed features of non-homologous end joining (NHEJ), such as microhomologies and insertions of direct or inverted repeat sequences. We also detected more complex rearrangements, including large insertions from adjacent or distant genomic regions. The insertion events that involved distant genomic regions typically represented transcribed sequences, and included both L1 LINE elements and sequences known to be involved in genomic rearrangements. This type of aberrant repair could potentially lead to gene inactivation via deletion of coding or regulatory sequences, or production of oncogenic fusion genes via insertion of coding sequences.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Chromosomal rearrangement Double strand DNA break I-SceI Insertion Non-homologous end joining
Megjelenés:	Dna Repair. - 4 : 9 (2005), p. 1038-1046. -
További szerzők:	Aplan, Peter D.
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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