Aggregator
How a scientist–pop industry partnership slashed a live gig’s carbon emissions by 98%
Life-giving oxygen is wafting out of lakes worldwide
Ancient shackles testify to brutality of Egypt’s gold mines
Fasting for weight loss is all the rage: what are the health benefits?
Climate change will send home insurance spiralling. Here’s how to control costs
How the Atlantic jet stream has changed in 600 years — and what it means for weather
Why is my cello howling?
MFSD6 is an entry receptor for enterovirus D68
Microbes can capture carbon and degrade plastic — why aren’t we using them more?
How to get more women into mining
Lesotho matters
Give grants to female scientists in war zones
Lessons from Portugal on effects of cutting research funding
A year later, cow flu origins are an unsettling puzzle
It's still unclear how H5N1 virus jumped into U.S. cattle—and why it keeps doing so
Saying ‘pandemic is over,’ NIH starts cutting COVID-19 research
Grant terminations halt research on improving vaccinations and preventing future pandemics
Trump cuts damage global efforts to track diseases, prevent outbreaks
Disease surveillance programs worldwide are suddenly in limbo
Mexican whale researchers sound the alarm on an energy megaproject
A planned gas terminal would routinely send huge tankers through a marine mammal oasis, scientists fear
Ca<sub>V</sub>2.1 mediates presynaptic dysfunction induced by amyloid β oligomers
Synaptic dysfunction is an early pathological phenotype of Alzheimer's disease (AD) that is initiated by oligomers of amyloid β peptide (Aβ(o)s). Treatments aimed at correcting synaptic dysfunction could be beneficial in preventing disease progression, but mechanisms underlying Aβ(o)-induced synaptic defects remain incompletely understood. Here, we uncover an epithelial sodium channel (ENaC) - Ca(V)2.3 - protein kinase C (PKC) - glycogen synthase kinase-3β (GSK-3β) signal transduction pathway...
Targeted degradation of α-Synuclein using an evolved botulinum toxin protease
There is considerable interest in the targeted degradation of proteins implicated in human disease. The use of sequence-specific proteases for this purpose is severely limited by the difficulty in engineering the numerous enzyme-substrate interactions required to yield highly selective proteases while maintaining catalytic activity. Herein, we report a strategy to evolve a protease for the programmed degradation of α-Synuclein, a presynaptic protein closely linked to Parkinson's disease. Our...
Correction to: White matter lipid alterations during aging in the rhesus monkey brain
No abstract