Important molecular machines routinely crash into one another while plying their trades on DNA. New research shows that the enzymes that copy DNA before cell division, called replisomes, are the kings of this road, kicking aside machines that are performing less critical tasks, such as transcribing instructions for proteins.
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Scientists crash test DNA’s replication machinery
Armed with the latest high-tech DNA analysis techniques, two New York City high school students examined every nook and cranny of their homes and were astonished to discover a veritable zoo of 95 animal species surrounding them, in everything from fridges to furniture.
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DNA ‘barcoding’ reveals 95 species of life in NYC homes, students show
On average, our cells encounter a very lethal form of DNA damage 10 times a day. Lucky for us, we have the capacity to repair each and every one of them. New research now reveals exactly how two well-known proteins are involved in the process, a finding that not only helps shed light on cancer but also on how our cells maintain the integrity of our genome.
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Two proteins act as molecular tailors in DNA repair
Over the decades, scientists have learned a lot about the basic life processes shared by many animals — including people — by manipulating the DNA of the “lower” species, such as mice and worms. But to date, they have been unable to readily probe the genetic contribution to one higher cognitive capacity of particular interest — the ability to learn language from one another. Now scientists have worked out a method for altering the genes of the zebra finch, one of the handful of social animals that learn to “speak” in a way that is analogous to humans. 
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Transgenic songbirds provide new tool to understand the brain
Restenosis rate following vascular interventions still limits their long-term success. Oxidative stress plays a relevant role in this pathophysiological phenomenon, but less attention has been devoted to its effects on DNA damage and to the subsequent mechanisms of repair.
We analysed in a model of arteriotomy-induced stenosis in rat carotids the time-dependent expression of DNA damage markers and of DNA repair genes, together with the assessment of proliferation and apoptosis indexes.
The expression of the oxidative DNA damage marker 7,8-dihydro-8-oxo-2’-deoxyguanosine was increased at 3 and 7 days after arteriotomy, with immunostaining distributed in the injured vascular wall and in perivascular tissue. The expression of the DNA damage marker phospho-H2A.X was less relevant but increasing from 4 hrs to 7 days after arteriotomy, with immunostaining prevalently present in the adventitia and, to a lesser extent, in medial smooth muscle cells at the injury site.
RT-PCR indicated a decrease of 8 out of 12 genes of the DNA repair machinery we selected from 4 hrs to 7 days after arteriotomy with the exception of increased Muyth and Slk genes (p<0.05).
Western Blot revealed a decrease of p53 and catalase at 3 days after arteriotomy (p<0.05).
A maximal 7% of BrdU-positive cells in endothelium and media occurred at 7 days after arteriotomy, while the apoptotic index peaked at 3 days after injury (p<0.05).
Our results highlight a persistent DNA damage presumably related to a temporary decreased expression of the DNA repair machinery and of the antioxidant enzyme catalase, playing a role in stenosis progression.
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DNA damage and repair in a model of rat vascular injury
Spectrophotometric evaluation of genomic DNA quantity and quality using a nanodrop ND-1000 microvolumetric spectrophotometer, a implemented by the Molecular Biology Laboratory of the Universidad Autónoma de San Luis Potosi Medical Faculty.
Free licenses for CodonCode Aligner, a leading software program for DNA sequence assembly and analysis, will be made available to selected applicants under CodonCode Corporation’s new License Grant Program.
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CodonCode Corporation Announces Free License Program For DNA Sequence Assembly Software
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