How to make asthma-related changes
Researchers have developed a new asthma-specific gene that can be expressed in mice without causing any symptoms.
The gene is a novel way to develop new therapies to treat asthma in people, said lead researcher, Dr. Ralf Eisler, an assistant professor of medicine at Harvard Medical School.
“This is the first time we’ve had a gene that could be expressed by humans,” he said.
“There are a lot of things that could go wrong with this gene, but we can make it work.”
The gene, named ADH, was first identified in mice in 2011.
Since then, researchers have discovered a number of different ways that ADH can be turned on or off in a mouse.
These include activating genes that control the expression of other genes, activating genes for new types of asthma, or suppressing certain genes in order to make it less active.
Eislinger and his colleagues were able to find a way to make ADH activate genes for several types of lung inflammation, as well as a gene called SARS-CoV-2, a respiratory virus that causes lung cancer.
In mice, ADH activates the gene SARS, which causes SARS coronavirus infection.
“We thought that SARS could activate the ADH gene, and that’s where we were able, in part, to discover that it does activate the gene,” Eislinger said.ADH can also be turned off by activating a gene, or by inhibiting a gene.
“So if you’re trying to make a new gene, you can’t do that,” Eislner said.
Instead, researchers use a genetic switch that controls a particular enzyme called a methyltransferase.
The methyltransferases in cells are called methyltransferor enzymes, and they do the dirty work of turning on the enzyme.
They also produce methyl groups that can bind to and activate genes.
When methyl groups are present in the DNA of a cell, they can bind and activate certain genes.
The enzymes are found in a large number of genes in the human genome.
When a gene is turned on, the methyl transferase switches on.
When the methyltransferased gene is activated, the gene becomes active.
“It turns on the genes that are involved in inflammation,” Eisfeller said.
That means that when a gene or a gene expression is turned off, inflammation increases.
Eisller and his co-authors first identified the ADHS gene in mice that had a genetic defect that made it more susceptible to SARS infection.
That was enough to lead them to look for genes that might be turned into ADH or other new asthma therapies.
“In the mice, we found that there were genes that were able not only to activate the methyl transfers but also to inhibit them,” Eisker said, “so it appears that methyltransferors play a role in asthma-associated inflammation.”
In mice genetically engineered to have a mutation that prevents ADH from activating genes, they found that the gene was also turned off in the presence of a methyl transferor enzyme.
The researchers also found that mice that were genetically engineered not to have the mutation also had a decrease in inflammation in their lungs.
These results were published online this week in Science Translational Medicine.
“We know that there are a variety of genes that play roles in asthma,” Eissler said.
“There are so many genes that we know that are very important in inflammation and inflammation-related disease,” he continued.
“But it’s difficult to know which genes are important and which genes aren’t important in asthma.”
When scientists first looked at a gene named CD36, they saw that it had a number one priority: protecting the lungs from SARS.
CD36 is a gene responsible for regulating the function of a protein called CD11b.
CD11B is one of the proteins involved in the activation of the SARS gene.
The researchers then examined a gene known as CACNA, which is involved in regulating the expression and activity of the enzyme that turns the methyl transporters on and off in response to SAR.
CD21 is a protein that activates CACNAs.”CD21 is the enzyme responsible for methyl transduction,” Eielsen said.
In mice, CD21 regulates the expression level of CD11a.
“CD21 does not activate the expression or activity of CD21.”
But in the mice that lack CD21, there is a genetic mutation that does activate CD21.
Eiskers team identified CD21 as one of several genes that turned on CD21 during inflammation.
“What that tells us is that this is a mechanism that we’re not just looking at in mice, but that we have been able to identify in humans as well,” Eiselers said.
They then looked at another gene called COX-1, which has also been found to be involved in lung inflammation.
They found that when mice with this mutation lacked CD21 or another