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Nuclear DNA

About: Nuclear DNA is a research topic. Over the lifetime, 3933 publications have been published within this topic receiving 185830 citations.


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Journal ArticleDOI
TL;DR: Recent advances are discussed and possible solutions to the controversial issue of HIV-1 nuclear import are suggested, which greatly enhances HIV replication and allows the virus to productively infect terminally differentiated nonproliferating cells, such as macrophages.
Abstract: As a member of the Retrovirus family, human immunodeficiency virus (HIV), a causative agent of AIDS, replicates by integrating its genome into the host cell’s nuclear DNA. However, in contrast to most retroviruses that depend on mitotic dissolution of the nuclear envelope to gain access to the host cell’s genome, the HIV pre-integration complex can enter the nucleus of the target cell during the interphase. Such capacity greatly enhances HIV replication and allows the virus to productively infect terminally differentiated nonproliferating cells, such as macrophages. Infection of macrophages is a critical factor in the pathogenesis of diseases caused by HIV-1 and other lentiviruses. The mechanisms responsible for this unusual feature of HIV have enticed researchers since the early 90s, when the first characterization of the HIV-1 pre-integration complex was reported. Several viral factors, including matrix protein, integrase, viral protein R, and central DNA flap, have been proposed as regulators of HIV-1 nuclear import, only to be later shown as nonessential for this process. As a result, after more than a decade of intense research, there is still no consensus on which HIV-1 and cellular proteins control this critical step in HIV-1 replication. In this review, we will discuss recent advances and suggest possible solutions to the controversial issue of HIV-1 nuclear import.

109 citations

Journal ArticleDOI
TL;DR: Current views focus upon cDNA as the vehicle, based upon some examples from plants, but other mechanisms, involving direct transfer of DNA from organelle chromosomes, could also account for the available data.

109 citations

Journal ArticleDOI
TL;DR: The overall results indicate that DNA degradation is influenced by multiple factors—including cellular location, chromatin structure, and transcriptional activity—factors that could be used to exploit loci for more robust forensic analysis from degraded biological material.
Abstract: Single copy nuclear loci often cannot be amplified from degraded remains, necessitating the analysis of mitochondrial DNA (mtDNA). The success in analyzing mtDNA is generally thought to result from its higher copy number in the cell; however, other factors, such as cellular location or molecular features, may be equally or more important in the superior preservation of mtDNA. To explore and compare mtDNA and nuclear DNA degradation, mouse tissues (muscle, liver, and brain) were allowed to degrade at different temperatures, and the relative degradation of a mitochondrial gene, a single copy nuclear gene, and a multi-copy nuclear gene was assayed using real-time polymerase chain reaction. The tissues were also homogenized, allowing the three loci to degrade in the same cellular environment. Gene copy number and cellular location both influence DNA recovery. In some instances, multi-copy loci could be recovered when the single copy locus could not; however, the pattern of relative DNA degradation changed between whole and homogenized tissues. The overall results indicate that DNA degradation is influenced by multiple factors-including cellular location, chromatin structure, and transcriptional activity-factors that could be used to exploit loci for more robust forensic analysis from degraded biological material.

109 citations

Journal ArticleDOI
TL;DR: V viscoelastic measurements on yeast DNA are now consistent with the idea that each chromosome contains one piece of DNA.

108 citations

Journal ArticleDOI
TL;DR: It is shown that zinc, despite completely inhibiting DNA fragmentation and the consequent loss of nuclear DNA content, does not protect rat thymocytes from spontaneous or dexamethasone-induced death and it is suggested that DNA fragmentation, although characteristic, is not a critical event for thymocyte death of apoptotic type.

108 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202361
202284
202177
202064
201966
201862