Study Finds Tar-Like Peptides Block Nucleic Acids, Leading to Motor Neuron Death in Familial ALS
May 12, 2021
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Research by scientists at the Spanish National Cancer Research Centre (CNIO) has uncovered a mechanism that may explain what causes neuronal cell death in cases of amyotrophic lateral sclerosis (ALS) that are associated with mutations in a gene known as C9ORF72. The findings suggest that the C9ORF72 gene mutations are toxic because they induce the cell to produce small proteins or peptides that are very rich in arginine, an amino acid that, due to its positive charge and chemical nature, binds very avidly to nucleic acids, including DNA and RNA. The resulting peptides stick to the DNA “like a kind of tar,” effectively blocking them from their normal interactions with other proteins, and disrupting fundamental cell processes.
University of Seville
The two meters of -stretched- DNA contained in human cells are continuously twisting and untwisting to give access to genetic information: when a gene is expressed to generate a protein, the two strands of DNA are separated to give access to all the machinery necessary for this expression, resulting in an excessive accumulation of coiling that needs to be resolved later. The paper that has now been published by the team led by Felipe Cortés, head of the DNA Topology and Breaks Group at the Spanish National Cancer Research Centre (CNIO), in collaboration with Silvia Jimeno González, professor at the University of Seville and head of the mRNA Transcription and Processing Group at the Andalusian Centre for Molecular Biology and Regenerative Medicine (CABIMER), shows that this supercoiling characteristic of DNA’s structure controls gene expression rather than being a mere collateral damage to be solved, as had been thought to date. The results are reported in t
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The two meters of -stretched- DNA contained in human cells are continuously twisting and untwisting to give access to genetic information: when a gene is expressed to generate a protein, the two strands of DNA are separated to give access to all the machinery necessary for this expression, resulting in an excessive accumulation of coiling that needs to be resolved later. The paper that has now been published by the team led by Felipe Cortés, head of the DNA Topology and Breaks Group at the Spanish National Cancer Research Centre (CNIO), in collaboration with Silvia Jimeno González, professor at the University of Seville and head of the mRNA Transcription and Processing Group at the Andalusian Centre for Molecular Biology and Regenerative Medicine (CABIMER), shows that this supercoiling characteristic of DNA s structure controls gene expression rather than being a mere collateral damage to be solved, as had been thought to date. The results are reported in the journal Cell
Apr 26, 2021
Here s today s feel-good story:
Obesity is known to be an inflammatory disease, a defensive reaction of the body to stress by excess nutrients.
With this knowledge, a group of researchers at the Spanish National Cancer Research Centre decided to try to find a way to fight obesity by preventing inflammation.
They found out that the drug Digoxin, used for heart disease, reduces inflammation and leads to 40% weight loss in mice that are obese with no side effects.
“Since no effective treatments for obesity and metabolic syndrome are available, digoxin may represent an effective therapeutic option,” the researchers wrote.
Apr 26, 2021
Here s today s feel-good story:
Obesity is known to be an inflammatory disease, a defensive reaction of the body to stress by excess nutrients.
With this knowledge, a group of researchers at the Spanish National Cancer Research Centre decided to try to find a way to fight obesity by preventing inflammation.
They found out that the drug Digoxin, used for heart disease, reduces inflammation and leads to 40% weight loss in mice that are obese with no side effects.
“Since no effective treatments for obesity and metabolic syndrome are available, digoxin may represent an effective therapeutic option,” the researchers wrote.