Sentences with phrase «gene in normal mice»

Not exact matches

In experiments with mice, the researchers found that Paneth cells engineered to lack a functional ATG16L1 gene were five times more likely to die in the face of rising TNF - alpha signals than normal cellIn experiments with mice, the researchers found that Paneth cells engineered to lack a functional ATG16L1 gene were five times more likely to die in the face of rising TNF - alpha signals than normal cellin the face of rising TNF - alpha signals than normal cells.

Both mouse and human males typically die early from the mutation in Mecp2, because their Y chromosome does not supply a normal copy of the gene.

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.

They destroyed the T cells in 12 mice, five of which received marrow cells from normal mice while seven received marrow from mice with a defective Fas - ligand gene.

Mineral deposits and bone formation around toe joints of mouse with mutation in the ank gene (mutant foot shown on right, normal skeleton on left).

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.

However, cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single gene, according to a study that found that restoring normal levels of a human colorectal cancer gene in mice stopped tumor growth and re-established normal intestinal function within only 4 days.

Because mice lacking both genes would not be born alive, the scientists followed up this lead by making «conditional knockout mice,» in which Esrp1 and Esrp2 activity was normal early in fetal development, but then was switched off in skin epithelial cells.

When the researchers then induced stroke in mice either with or without the PARP gene, they found that the resulting tissue damage in the mice without the enzyme was 80 % less than in normal mice.

The researchers also administered a compound to normal mice that blocked TRPV4, and found that inhibiting TRPV4 also led to smaller reductions in bite force, similar to the effects of the mice engineered without the Trpv4 gene.

In an independent effort, they introduced progressively smaller pieces of DNA from the large region known to contain the gene into embryos of the mutant mice, looking for the smallest piece that would correct the mutation in adult mice and restore a normal rhythIn an independent effort, they introduced progressively smaller pieces of DNA from the large region known to contain the gene into embryos of the mutant mice, looking for the smallest piece that would correct the mutation in adult mice and restore a normal rhythin adult mice and restore a normal rhythm.

Knocking out a particular gene in muscle lets mice run twice as far as normal; knocking out the same gene in fat cells allows the animals to put on weight without developing type - 2 diabetes.

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.

Mice generated from embryonic stem cells in which ion channel genes have been mutated by homologous recombination often have a perfectly normal heart.

Longo also knew of research by molecular biologist John Kopchick at Ohio University, which showed that mice with a mutation in their growth hormone receptor gene lived 40 percent longer than normal mice — the equivalent of an average American living to age 110.

A study published January 4th in Cell Stem Cell demonstrates that a gene therapy approach can lead to the long - term survival of functional beta cells as well as normal blood glucose levels for an extended period of time in mice with diabetes.

Last year, though, researchers reported a strain of mouse that can live almost a third longer than normal because of a mutation in one gene.

Intrigued, Turek joined with endocrinologist Joseph Bass, also at Northwestern, to study the effects of regular and high - fat diets in normal mice and mice with a dysfunctional Clock gene.

DNA sequencing of sperm from the grandfather mice and their pups also revealed epigenetic marks on the gene encoding M71 that weren't seen in normal mice.

To investigate, Akhtar deleted the gene for Rac1 in female mice; their first litter of pups survived, but they were smaller than normal — probably because the milk they received contained less fat and protein than normal.

Scientists compared urination patterns, both volume and frequency, in normal mice and in mice genetically engineered without two circadian genes, Cryptochrome - 1 and Cryptochrome - 2, resulting in dysfunctional circadian rhythms.

The researchers looked for genes that were turned on by dHAND in normal mice, but nonfunctioning when dHAND was shut down.

To see if the effect also works in reverse, the team asked whether mice grown in a germ - free environment would express genes encoding complement components differently than mice grown under normal conditions.

In the new study, the researchers said the converted motor neurons compared favorably to normal mouse motor neurons, in terms of the genes that are turned on and off and how they functioIn the new study, the researchers said the converted motor neurons compared favorably to normal mouse motor neurons, in terms of the genes that are turned on and off and how they functioin terms of the genes that are turned on and off and how they function.

The researchers compared mice with a normal glymphatic system to those with a disabled gene that prevented glial cells from assisting in the fluid flow.

The study showed that mice lacking the SNRK gene had a significantly higher concentration of macrophages in white fat tissue compared with normal mice.

Gene expression patterns in normal adult or the developing retina have been reported for mouse [18 — 23], aged and normal adult human [24 — 26], canine [27], and rabbit [28].

Importantly, 25 of the 115 transcripts, shared by EFTF - expressing pluripotent cells and the EF, encode for 15 genes that are both expressed in retinal stem / progenitor cells and required for normal eye formation in frogs, fish, mice, or humans (Figure 1C; Table S1).

The resulting change in the appearance, behaviour or biochemical characteristics of the mouse then gives an indication of the gene's normal role in the mouse, and perhaps in humans.

The scientists demonstrated this by transferring T cells lacking the Tob1 gene into mice that had no immune systems but had normal Tob1 in all other cells.

In Yeast, Worms, Flies, and Mice, Only About 1 in 3 Genes is Essential for Viability The consequences of some genomic perturbations can not be compensated for by normal epigenetic processes and result in the death of the organism prior to adulthooIn Yeast, Worms, Flies, and Mice, Only About 1 in 3 Genes is Essential for Viability The consequences of some genomic perturbations can not be compensated for by normal epigenetic processes and result in the death of the organism prior to adulthooin 3 Genes is Essential for Viability The consequences of some genomic perturbations can not be compensated for by normal epigenetic processes and result in the death of the organism prior to adulthooin the death of the organism prior to adulthood.

Now, they have investigated gene expression in low - grade dysplastic lesions and normal stomach tissue from mice and in gastric cancer and normal stomach tissue from humans.

The researchers looked at the dentate gyrus, a specific area of the brain that is critical to memory and particularly vulnerable in Alzheimer's disease, and compared the genes that were turned on and off in normal mice and a mouse model of Alzheimer's disease.

One important difference: the Doogie mice had all their normal genes, and were overproducing a NMDA receptor gene involved in helping neurons communicate.

In their experiments the researchers measured acidity in the endosomes of brain cells of normal mice and in mice with mutations in the NHE6 genIn their experiments the researchers measured acidity in the endosomes of brain cells of normal mice and in mice with mutations in the NHE6 genin the endosomes of brain cells of normal mice and in mice with mutations in the NHE6 genin mice with mutations in the NHE6 genin the NHE6 gene.

«Without DMRT3, the neural circuit that contributes to the coordination of the limbs is not formed in a normal way», states PhD student Martin Larhammar, who participated in the characterization of the DMRT3 gene in both horses and in mice.

It is dedicated to the development of KO / KI mice and their extensive and standardised analysis to understand the function of genes involved in immune response in normal and infectious conditions.

Thus, chronically increased p53 activity causes premature aging in mice, whereas transgenic mice with extra copies of p53 and ARF genes under normal regulation show tumor resistance and extended life span.

Interestingly, the number of immature ILC2s in bone marrow was comparable in normal and gene - deleted mice.

Paternally inherited Dp / + (patDp / +) mice showed expected increases in the gene expression in bone, normal postnatal growth and body weight acquisition compared to the littermate controls.

«Low - Calorie Diet Slows Aging in Mice in Study,» claimed a recent headline.17 According to the article, «Putting elderly mice on a very low - calorie diet for as little as four weeks reversed many of the changes in the activity of various genes that had occurred during normal aging...» The resesearchers were not looking at actual signs of disease, nor were they measuring lifespan, but instead focused on the analysis of 11,000 different genes using a method called microarray technology in which Spindler has large financial holdiMice in Study,» claimed a recent headline.17 According to the article, «Putting elderly mice on a very low - calorie diet for as little as four weeks reversed many of the changes in the activity of various genes that had occurred during normal aging...» The resesearchers were not looking at actual signs of disease, nor were they measuring lifespan, but instead focused on the analysis of 11,000 different genes using a method called microarray technology in which Spindler has large financial holdimice on a very low - calorie diet for as little as four weeks reversed many of the changes in the activity of various genes that had occurred during normal aging...» The resesearchers were not looking at actual signs of disease, nor were they measuring lifespan, but instead focused on the analysis of 11,000 different genes using a method called microarray technology in which Spindler has large financial holdings.

The reason for this response, Gordon says, was twofold: Firmicutes bacteria transplanted from the fat mice produced more of the enzymes that helped the animals extract more energy from their food, and the bacteria also manipulated the genes of the normal mice in ways that triggered the storage of fat rather than its breakdown for energy.