Sentences with phrase «genes in mice called»

For a decade, the group at North Carolina has studied a large family of genes in mice called L1, some of which are dormant.

In earlier studies, Wang and his colleagues had revealed that a gene in mice called Pad4 (peptidylarginine deiminase 4) produces an enzyme that plays an important role in protecting the body from infection.

Not exact matches

Modifying a histone called H3K27 shuts down the activity of some imprinted genes in mice, Howard Hughes Medical Institute (HHMI) Investigator Yi Zhang and colleagues report July 19 in the journal Nature.

In 1997 Joseph Takaha - shi of the Howard Hughes Medical Institute at Northwestern University and his colleagues isolated a gene they called Clock that when mutated yielded mice with no discernible circadian rhythm.

So they developed a drug that inactivates the gene that makes FL2 and then put the drug in tiny gel capsules called nanoparticles and applied the nanoparticles to wounds on mice.

The three - day treatment reversed social deficits in mice deficient in a gene called Shank 3, an important risk factor for ASD.

The less adept mice, Rubin's team found, carry extra copies of a previously known human gene called DYRK; a mutated version of an almost identical gene in fruit flies, called minibrain, causes neurological defects.

Researchers then tested cell cultures and mouse models by using a gene editing process called CRISPR - Cas9 to demonstrate how the presence or absence of myomaker and myomerger — both individually and in unison — affect cell fusion and muscle formation.

They started with pairs of fat yellow mice known to scientists as agouti mice, so called because they carry a particular gene — the agouti gene — that in addition to making the rodents ravenous and yellow renders them prone to cancer and diabetes.

Northwestern Medicine scientists have identified a small RNA molecule called miR - 182 that can suppress cancer - causing genes in mice with glioblastoma mulitforme (GBM), a deadly and incurable type of brain tumor.

Recently he found that eight of the youngsters have a defect in a gene that codes for a receptor protein called melanocortin - 4, known to regulate eating in mice.

The first clue that digits and penises might be birds of a feather came in 1991, when a team led by developmental biologist Denis Duboule of the University of Geneva and Pierre Chambon of the Institute for Genetics and Molecular and Cellular Biology in Strasbourg, France, found that some mice with a mutated gene, called hoxd13, had abnormally small digits and malformed penises.

Indeed, the group found that the affected gene, named left - right dynein (lrd), comes on in the «node» — a key source of patterning signals — just before the appearance in the mouse embryo of the first known left - right asymmetries, the left - sided expression of two genes called nodal and lefty.

Mice without the leptin gene, called ob / ob, overeat, weigh in at three to four times normal, and develop symptoms similar to the obesity - related diabetes seen in humans.

The French team and a British group that discovered the mouse gene both decided to see if the mutation — which hampers the production of a protein called myosin VIIA — might, as in the mice, explain inherited deafness without other sensory loss.

Other researchers had linked the ank mutation to mouse chromosome 15; in this week's Science, Kingsley's team reports that it's a single typo in a previously unknown gene, which they called ank, that led to a protein about 10 % shorter than the normal version.

For both studies, Schiestl and his team used mice that had mutations in a gene called ATM, which made them susceptible to a neurologic disorder called ataxia telangiectasia.

In a related paper published online today in Nature Biotechnology, Konrad Hochedlinger of the Harvard Stem Cell Institute in Cambridge and his colleagues compared the gene expression patterns in mouse iPS cells derived from white blood cells, muscle precursor cells, immune system cells called B cells, and fibroblasts taken from tail tipIn a related paper published online today in Nature Biotechnology, Konrad Hochedlinger of the Harvard Stem Cell Institute in Cambridge and his colleagues compared the gene expression patterns in mouse iPS cells derived from white blood cells, muscle precursor cells, immune system cells called B cells, and fibroblasts taken from tail tipin Nature Biotechnology, Konrad Hochedlinger of the Harvard Stem Cell Institute in Cambridge and his colleagues compared the gene expression patterns in mouse iPS cells derived from white blood cells, muscle precursor cells, immune system cells called B cells, and fibroblasts taken from tail tipin Cambridge and his colleagues compared the gene expression patterns in mouse iPS cells derived from white blood cells, muscle precursor cells, immune system cells called B cells, and fibroblasts taken from tail tipin mouse iPS cells derived from white blood cells, muscle precursor cells, immune system cells called B cells, and fibroblasts taken from tail tips.

In a study published earlier this year, Jiang and other collaborators at Duke described a mouse model of autism in which they deleted a prominent autism gene called SHANK3, which is mutated in 1 percent of people with the disordeIn a study published earlier this year, Jiang and other collaborators at Duke described a mouse model of autism in which they deleted a prominent autism gene called SHANK3, which is mutated in 1 percent of people with the disordein which they deleted a prominent autism gene called SHANK3, which is mutated in 1 percent of people with the disordein 1 percent of people with the disorder.

The second was the existence in laboratory mice of a large mutation called an inversion that affects several million nucleotides near the KITLG gene.

They used a somewhat bizarre technique in which two mice were sutured together in such as way that they shared a circulatory system (known as parabiosis), and found old mice joined to their youthful counterparts showed changes in gene activity in a brain region called the hippocampus as well as increased neural connections and enhanced «synaptic plasticity» — a mechanism believed to underlie learning and memory in which the strength of neural connections change in response to experience.

Mice with mutations in what is called the nude gene don't fully develop the thymus, a small organ in the chest cavity that plays a key role in the maturation of infection - fighting T cells.

Researchers analyzed the genomes of 16 related orange and white tigers in captivity, fully mapping those of the three parent tigers to show that a mutation in one pigment gene called SLC45A2 is at play — the very same gene that drives lighter coloring in people of European ancestry, chickens, and some mice.

Although that marker, called IL21, had not previously been associated with autoimmune diseases, the gene that produces it sits right in the stretch of DNA known to make these mice vulnerable to diabetes, suggesting that IL21 might make a drug target, says Sarvetnick.Furthermore, by giving the animals a shot of dead bacteria — similar to an immunization in humans — when they were newborns, Sarvetnick and her colleagues prevented a surfeit of CD4 + and CD8 + cells.

A study published by Cell Press November 7th in the journal Cell has revealed that an evolutionarily conserved gene called Lin28a, which is very active in embryos but not in adults, enhances tissue repair after injury when reactivated in adult mice.

Based on experiments with mice, some scientists had speculated that cilia nestled in a dimple at the top of the embryo called the node might push fluid down the left side of the embryo, carrying a signal that somehow triggers certain genes to activate.

In a search for mutant mice that might be missing the gene, Banfi and colleagues came upon a strain called head slant.

Now, a new study in mice shows how a gene, called FOXP2, implicated in a language disorder may have changed between humans and chimps to make learning to speak possible — or at least a little easier.

In mice engineered without a muscle - building gene called IL - 15R - alpha, fast - twitch muscles in their front legs acted more like slow - twitch fiberIn mice engineered without a muscle - building gene called IL - 15R - alpha, fast - twitch muscles in their front legs acted more like slow - twitch fiberin their front legs acted more like slow - twitch fibers.

With chronically infected mice as their model, the researchers used a new technology called ATAC - seq to map the regulatory regions of the genome — the sections of DNA involved in switching genes on and off — in the animals» exhausted and functional CD8 + T cells.

Mutations in a gene called progranulin (GRN) are commonly associated with frontotemporal dementia, but GRN mutations in mice do not mimic all the features of the human disorder, which has limited progress in the development of effective treatments.

The team knocked out the gene for a protein called nuclear receptor corepressor 1 (NCoR1) in the muscles of mice.

William Shawlot and Richard Behringer of the University of Texas M. D. Anderson Cancer Center in Houston created 125 headless mice by knocking out a gene called Lim1 in the developing embryos.

UBC Psychiatry Professor Dr. Weihong Song and Neurology Professor Yan - Jiang Wang at Third Military Medical University in Chongqing attached normal mice, which don't naturally develop Alzheimer's disease, to mice modified to carry a mutant human gene that produces high levels of a protein called amyloid - beta.

Studying mice, the researchers found that a gene called Phr1 plays a major role in governing the self - destruction of injured axons.

But in addition to Brg1's role in forming IPMN lesions, Hebrok discovered that when the gene is knocked out in mice that have an activated gene called KRAS, whose role is to help regulate cell division, PanIN lesions occur less frequently.

The gene they found, dubbed Odysseus, contains a so - called homeodomain, a stretch of DNA that usually changes very little even in creatures as distantly related as worms and mice.

In a closing set of experiments, the researchers examined neurons obtained from mice with the most common inherited form of ALS, one caused by mutations in a gene called SODIn a closing set of experiments, the researchers examined neurons obtained from mice with the most common inherited form of ALS, one caused by mutations in a gene called SODin a gene called SOD1.

Wondering why the third protein, an enzyme called p66, was not, despite being very similar to the other two, Pelicci's team knocked out the piece of the gene that enabled it to code for p66, in order to make mice and mouse embryonic cells that lacked p66.

Liu and colleagues surmised that destroying the mutated copy of the gene, called Beethoven in mice, might preserve some hearing.

In mice, active L1 genes have a type of promoter called «A», whereas inactive genes have a promoter called «F».

Using a specialized gene manipulation technique called chromosome engineering, researchers developed genetically engineered mouse strains in three separate iterations: MYC only, the rest of the region containing PVT1 but without MYC and the pairing of MYC with the regional genes.

The defect in the responsible mouse gene — called klotho, after the goddess in Greek mythology who spins the thread of life — accelerates the onset of disorders such as atherosclerosis and osteoporosis.

After conducting studies in both humans and mice, the researchers said this new schizophrenia risk gene, called C4, appears to be involved in eliminating the connections between neurons — a process called «synaptic pruning,» which, in humans, happens naturally in the teen years.

Eliminating genes in mice is a standard technique for determining their function; the resultant animals are called knockout mice.

Other research has found that this gene, called SLITRK6, is active in the hypothalamus of male mice fetuses a few days before they are born.

In the study, the scientists used a type of mouse, called CVN - AD, that they had created several years ago by swapping out a handful of important genes to make the animal's immune system more similar to a human's.

Then for HARE5, the most active enhancer in an area of the brain called the cortex, they made minigenes containing either the chimp or human version of the enhancer linked to a «reporter» gene that caused the developing mouse embryo to turn blue wherever the enhancer turned the gene on.

The mouse atlas was produced using a method called «in situ hybridisation», in which thin slices of brain tissue are bathed in a solution containing molecular probes that bind to messenger RNA sequences produced by each gene.

Foltz's team has also used the mouse atlas to help home in on two genes, known as BEX1 and BEX2, which seem to be silenced in a form of brain cancer called glioma.