Featured
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News |
Bomb-blast brain injuries explained
Researchers identify protein pathway involved in traumatic brain injury.
- Gwyneth Dickey Zakaib
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Outlook |
Dementia: A problem for our age
As the number of Alzheimer's cases rises rapidly in an ageing global population, the need to understand this puzzling disease is growing.
- Alison Abbott
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News & Views |
Alcohol, DNA and disease
Acetaldehyde, a reactive metabolite of ethanol, can damage DNA unless properly processed. A biochemical pathway involved in Fanconi anaemia seems to be essential for protection against such damage. See Article p.53
- Hans Joenje
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Letter |
Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein
- Kasia Hrecka
- , Caili Hao
- & Jacek Skowronski
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Letter |
Modelling schizophrenia using human induced pluripotent stem cells
- Kristen J. Brennand
- , Anthony Simone
- & Fred H. Gage
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Perspective |
Charting a course for genomic medicine from base pairs to bedside
- Eric D. Green
- , Mark S. Guyer
- & Jane L. Peterson
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Review Article |
Pervasive roles of microRNAs in cardiovascular biology
- Eric M. Small
- & Eric N. Olson
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News & Views |
Angelman syndrome connections
Neuronal networks in the brain that develop early in life underlie our ability to learn, remember and communicate. Genetic defects that perturb the fine-tuning of such neuronal connectivity can cause disease.
- Peter Scheiffele
- & Asim A. Beg
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Article |
Reversing EphB2 depletion rescues cognitive functions in Alzheimer model
It is shown that amyloid-β oligomers interact with the receptor tyrosine kinase EphB2 and trigger its degradation. EphB2 regulates NMDA-type glutamate receptors and its depletion in normal mice reduces NMDA receptor currents and impairs long-term potentiation, both of which are important for memory formation. Increasing EphB2 levels in a mouse model of Alzheimer's disease improves memory.
- Moustapha Cissé
- , Brian Halabisky
- & Lennart Mucke
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News |
Disease-in-a-dish approach gives clues to Rett syndrome
Unregulated jumping genes are a possible culprit for the debilitating disease.
- David Cyranoski
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Letter |
Anthrax toxins cooperatively inhibit endocytic recycling by the Rab11/Sec15 exocyst
During infection, Bacillus anthracis secretes two potent toxins called lethal factor and oedema factor. Using Drosophila melanogaster as a model system, these authors show that these toxins interact with the Rab11/Sec15 exocyst, which is involved in endocytic recycling. This interaction may explain vascular leakage during infection.
- Annabel Guichard
- , Shauna M. McGillivray
- & Ethan Bier
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News |
The skin disease that cures itself
Diseased cells have harnessed a cancer-causing mechanism to banish a mutant gene.
- Ewen Callaway
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Article |
Ataxin-2 intermediate-length polyglutamine expansions are associated with increased risk for ALS
The causes of the neurodegenerative disease amyotrophic lateral sclerosis (ALS) are poorly understood, although the protein TDP-43 seems to be involved. These authors show that the polyglutamine-containing protein ataxin 2 interacts with TDP-43 and is a potent modifier of TDP-43 toxicity. Moreover, intermediate-length polyglutamine expansions in the ataxin 2 gene significantly associate with ALS. These data establish the ataxin 2 gene as a new and relatively common ALS disease susceptibility gene.
- Andrew C. Elden
- , Hyung-Jun Kim
- & Aaron D. Gitler
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Letter |
Genome-wide association study in alopecia areata implicates both innate and adaptive immunity
The genetic basis of alopecia areata, one of the most common human autoimmune diseases, is largely unknown. This study reports a genome-wide association for this trait that implies the involvement of acquired and innate immunity. Among significant associations are the cytomegalovirus UL16-binding protein genes, which encode activating ligands for the natural killer cell receptor, NKG2D, here implicated for the first time in any autoimmune disease.
- Lynn Petukhova
- , Madeleine Duvic
- & Angela M. Christiano
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News & Views |
Extreme makeover of pancreatic α-cells
Most insulin-secreting pancreatic β-cells are irreplaceably lost in type 1 diabetes. In a mouse model, pancreatic α-cells seem to sacrifice their identity to replenish the low stock of β-cells
1 . Two experts discuss what this means for understanding the basic cell biology involved and its relevance to treating diabetes.boxed-text - Kenneth S. Zaret
- & Morris F. White
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Review Article |
Neural mechanisms of ageing and cognitive decline
- Nicholas A. Bishop
- , Tao Lu
- & Bruce A. Yankner
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News & Views |
Mitochondrial damage control
Defects in mitochondria are implicated in Parkinson's disease. Study of a quality-control pathway involving the proteins PINK1 and Parkin provides further clues about the mechanism involved.
- Asa Abeliovich