Monday, May 23, 2016

Nature Reviews Molecular Cell Biology contents June 2016 Volume 17 Number 6 pp 329-394

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Nature Reviews Molecular Cell Biology


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TABLE OF CONTENTS
 
June 2016 Volume 17 Number 6Advertisement
Nature Reviews Molecular Cell Biology cover
Impact Factor 37.806 *
In this issue
Research Highlights
Comment
Focus on: DNA damage repair
Reviews

Also this month
 Featured article:
Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers
Petra Schwertman, Simon Bekker-Jensen & Niels Mailand
 Focus on:
DNA damage repair
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RESEARCH HIGHLIGHTSTop

DNA damage response: Controlling ubiquitylation at DNA lesions
p329 | doi:10.1038/nrm.2016.59
Two studies now provide new insights into the complex and multi-level regulation of ubiquitylation in the DNA damage response.
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Non-coding RNA: LINP1 joins ends with triple-negative effect
p330 | doi:10.1038/nrm.2016.60
The long non-coding RNA LINP1 facilitates double-strand break repair in triple-negative breast cancer through non-homologous end joining, by recruiting DNA-PKcs to sites of damage.
PDF


Autophagy: Inflammatory pathology of Fanconi anaemia
p330 | doi:10.1038/nrm.2016.64
The Fanconi anaemia DNA repair pathway also has cytoplasmic functions in selective autophagy that might contribute to Fanconi anaemia disease.
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Ageing: The yin and yang of mitochondrial dysfunction
p331 | doi:10.1038/nrm.2016.71
Three studies provide important insights into mitochondrial function during ageing – they reveal a connection to stem cell senescence and shed light on the epigenetic mechanisms underlying UPRmt activation and stress-induced longevity.
PDF


DNA Replication: Looping smoothens repetitive DNA replication
p332 | doi:10.1038/nrm.2016.61
DNA supercoiling and the formation of loops suppresses the ATR checkpoint and is required for proper replication of centromeric DNA.
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JOURNAL CLUB
The rule of three
p333 | doi:10.1038/nrm.2016.57
As far as James Haber is concerned, the big picture is all he wants of protein structures. This was not the case, however, with the structure of RecA, published in 2008.
PDF


Cytoskeleton: Microtubules set the beat
p333 | doi:10.1038/nrm.2016.63
Microtubule detyrosination is shown to influence mechanical properties of cardiomyocytes, as detyrosinated microtubules resist the force of contraction by undergoing buckling.
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IN BRIEF

Genome engineering: Presenting Argonaute, the genome editor | Ion transporters: Potassium channel regulates ciliogenesis | DNA damage response: p53 curbs topological stress
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Comment: The world of DNA in glycol solution
Tomas Lindahl
p335 | doi:10.1038/nrm.2016.66
Tomas Lindahl presents a case for keeping DNA in the organic solvent glycol, in which it keeps its activity and is better protected from contamination and, potentially, radiation.
Abstract | Full Text | PDF
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  Focus on: DNA damage repair
REVIEWSTop
The Fanconi anaemia pathway: new players and new functions
Raphael Ceccaldi, Prabha Sarangi & Alan D. D'Andrea
p337 | doi:10.1038/nrm.2016.48
Proteins of the Fanconi anaemia pathway are master regulators of genomic integrity through their interactions with other DNA repair pathways to repair interstrand crosslinks, stabilize replication forks and regulate cytokinesis.
Abstract | Full Text | PDF
Processing ribonucleotides incorporated during eukaryotic DNA replication
Jessica S. Williams, Scott A. Lujan & Thomas A. Kunkel
p350 | doi:10.1038/nrm.2016.37
Ribonucleotides are incorporated into DNA by various mechanisms, including by DNA polymerases during replication. Such ribonucleotides may have physiological functions, but their presence is typically associated with diverse structural aberrations and interferes with fundamental processes, including DNA replication, repair and transcription. Thus, efficient mechanisms of ribonucleotide removal are key to maintaining genomic integrity and functionality.
Abstract | Full Text | PDF
Stop pulling my strings – what telomeres taught us about the DNA damage response
Eros Lazzerini-Denchi & Agnel Sfeir
p364 | doi:10.1038/nrm.2016.43
Double-strand break (DSB) repair at telomeres – the ends of linear chromosomes – can cause chromosome end fusions and genomic instability, which drives tumorigenesis. As several mechanisms protect mammalian telomeres from the DNA damage response, telomeres have emerged as a system to uncover key steps in DSB repair.
Abstract | Full Text | PDF
Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers
Petra Schwertman, Simon Bekker-Jensen & Niels Mailand
p379 | doi:10.1038/nrm.2016.58
Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs), and crosstalk between these modifications, underlies cellular responses to DNA double-strand breaks (DSBs). Important insights have been gained into the mechanisms by which ubiquitin and UBLs regulate protein interactions at DSB sites to enable accurate repair in mammalian cells, thereby protecting genome integrity.
Abstract | Full Text | PDF
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