Sentences with phrase «gene in the mice for»

After four weeks of such training, researchers reactivated the p25 gene in the mice for six weeks and then tested them to see if they recalled their shocking experiences.

Not exact matches

Infant formula continues to evolve and there are patents already for implanting genes for making human milk in mice.

These experiments were complemented by genetic manipulations in which some mice were engineered to lack a gene known as Tap1, which is crucial for the MHC I complex to make its way to the cell surface.

Gene therapy delivered to a specific part of the brain reverses symptoms of depression in a mouse model of the disease — potentially laying the groundwork for a new approach to treating severe cases of human depression in which drugs are ineffective.

When similar analysis was performed on the db mice, it was found that the disrupted db gene was responsible for encoding a protein that functions as a leptin receptor: When it binds circulating leptin at the cell surface, it sets in motion a biochemical cascade inside the cell.

Twelve transgenic piglets endowed with a mouse UCP1 gene were better able to maintain their body temperature than their unmodified counterparts when they were exposed to cold for a 4 - hour period, the authors report today in the Proceedings of the National Academy of Sciences.

Researchers pin down two genes that may be responsible for abnormal neural development in Down's mice embryos.

An exciting prospect for the future involves the recovery of an entire system of clock - regulated genes in organisms such as fruit flies and mice.

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

Jiang said autism researchers worldwide could use the mouse model to study ways to compensate for the gene and improve symptoms in people with autism spectrum disorders and Phelan - McDermid Syndrome, a more profound developmental condition caused by mutations to SHANK3 and other genes in chromosome 22.

The huntingtin gene is essential for embryonic development, and scientists have already shown that if mouse embryos don't have it at conception, they die in utero.

The mice, which move backwards when they try to walk forwards on a smooth surface, have a gene for a mutated protein that prompts neurons in the cerebellum, a brain area that controls movement and balance, to die off.

In the new study, the researchers sequenced the entire genome of mice that had undergone CRISPR gene editing in the team's previous study and looked for all mutations, including those that only altered a single nucleotidIn the new study, the researchers sequenced the entire genome of mice that had undergone CRISPR gene editing in the team's previous study and looked for all mutations, including those that only altered a single nucleotidin the team's previous study and looked for all mutations, including those that only altered a single nucleotide.

To see if any other receptors existed, Rodriguez's team took tissue from the vomeronasal organ — a pheromone - detecting sense organ found in the nasal cavity of mice, and some other mammals — and searched for genes expressing other possible smell receptors.

«Enigmatic gene critical for a healthy brain: New research has shown how an unusual gene is needed for brain development in young mice.»

Base oxidation regulates gene activity In cooperation with colleagues at LMU, as well as researchers based in Berlin, Basel and Utrecht, Carell and his group have now shown, for the first time, that a standard base other than cytosine is also modified in embryonic stem cells of micIn cooperation with colleagues at LMU, as well as researchers based in Berlin, Basel and Utrecht, Carell and his group have now shown, for the first time, that a standard base other than cytosine is also modified in embryonic stem cells of micin Berlin, Basel and Utrecht, Carell and his group have now shown, for the first time, that a standard base other than cytosine is also modified in embryonic stem cells of micin embryonic stem cells of mice.

Since genes for the T - cell receptor beta chain were previously shown to be on mouse chromosome 6, all three of the Ig - like multigene families expressed and rearranged in T cells are located on different chromosomes, just as are the B - cell multigene families for the Ig heavy chain, and the Ig kappa and lambda light chains.

Scientists of the German Center for Diabetes Research (DZD) led by the German Institute of Human Nutrition (DIfE) have shown in a mouse model that the epigenetic * modification of the Igfbp2 ** gene observed in the young animal precedes a fatty liver in the adult animal later in life.

Based on the ribosome profiling data, the researchers looked for genes that were being expressed differently in the trained mice, identifying 104 genes in total.

In Huntington's disease, mice carrying the pathologic genetic variant of the huntingtin gene are being used to understand how this genetic lesion causes degeneration of striatal neurons and to develop novel treatments for the illness.

That means that the approach that worked so well for finding the sweet receptor — identifying a likely gene for the receptor, destroying it in mouse embryos, and proving that the resulting mice are unable to taste sweetness — will not work in the search for the salt receptor.

To find out if this effect on testosterone production might affect mice's fertility, the team knocked out the gene for osteocalcin in a group of the rodents.

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.

For example, mice have been given an extra color vision gene in the lab, and it has been shown that the protein manufactured by that gene expands the scope of their vision by enhancing their ability to see longer - wavelength light without any other changes in the brain.

Scientists had been searching in vain for such a gene since 1994 when Rockefeller University scientist Jeffery Friedman found that lab mice with a specific genetic mutation fail to produce leptin and as a result have uncontrollable appetites, and become huge.

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.

Brueckner's group looked for gene defects in two strains of mice with situs inversus, a mutation in which the heart, lungs, and other organs are inverted, like a mirror image.

And by studying mice lacking the gene for ERRγ (and therefore unable to make the ERRy molecule), the team observed that all brown fat cells resembled white cells in these mice.

One team has found in two children mutations in the gene for the metabolic hormone leptin, which in mice tells the body it's satiated; defects in this gene had not previously been found in obese people.

In the new study, Kuro - o and collaborators created mice overexpressing the gene for Klotho.

Scientists have known for 20 years that SMN is necessary in every cell of the body, since disrupting the gene in a mouse causes early embryonic death, before muscle or nerve cells form.

In one such study by Ronald Evans and colleagues, the gene for rat growth hormone is stably inserted into mouse cells by a retrovirus.

All animals use the same enzyme to create the same methylation mark as a signal for gene repression, and her colleagues who study epigenetics in mice and humans are excited about the new findings, Strome said.

But for mice in which the whole gene cluster was deleted, serotonin axons don't keep their distance from each other.

A screen for mouse genes dependent on dHAND, a transcription factor implicated in neural crest development, identified Ufd1, which maps to human 22q11 and encodes a protein involved in degradation of ubiquitinated proteins.

«Gene therapy restores hearing in deaf mice: Proof - of - principle study takes a step toward precision medicine for genetic hearing loss.»

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.

Inhibiting NF - ƘB in microglia in mice slowed disease progression by 47 percent, says Brian Kaspar, MD, a principal investigator in the Center for Gene Therapy at Nationwide Children's and senior author of the new study.

To do that, they deleted the gene for SIRT1, which encodes the major mammalian sirtuin, in endothelial cells of mice.

In this study, published in the October 31 issue of the Proceedings of the National Academy of Sciences, Sudhir Yadav PhD, a neuroimmunology post-doctoral fellow in the laboratories of Drs. Kouichi Ito, associate professor of neurology, and Suhayl Dhib - Jalbut, professor and chair of neurology, tested mice that were engineered to have a pre-disposition for MS. Because mice would not normally develop MS, researchers used MS - associated risk genes from real patients to genetically engineer mice for this studIn this study, published in the October 31 issue of the Proceedings of the National Academy of Sciences, Sudhir Yadav PhD, a neuroimmunology post-doctoral fellow in the laboratories of Drs. Kouichi Ito, associate professor of neurology, and Suhayl Dhib - Jalbut, professor and chair of neurology, tested mice that were engineered to have a pre-disposition for MS. Because mice would not normally develop MS, researchers used MS - associated risk genes from real patients to genetically engineer mice for this studin the October 31 issue of the Proceedings of the National Academy of Sciences, Sudhir Yadav PhD, a neuroimmunology post-doctoral fellow in the laboratories of Drs. Kouichi Ito, associate professor of neurology, and Suhayl Dhib - Jalbut, professor and chair of neurology, tested mice that were engineered to have a pre-disposition for MS. Because mice would not normally develop MS, researchers used MS - associated risk genes from real patients to genetically engineer mice for this studin the laboratories of Drs. Kouichi Ito, associate professor of neurology, and Suhayl Dhib - Jalbut, professor and chair of neurology, tested mice that were engineered to have a pre-disposition for MS. Because mice would not normally develop MS, researchers used MS - associated risk genes from real patients to genetically engineer mice for this study.

The researchers scoured the already deciphered mouse genome, looking for genes that might encode additional receptor proteins in its olfactory system, the sensory cells that connect the nose to the brain.

One gene, which codes for a powerful growth - stimulating hormone in mice and humans, is expressed only by paternally derived genes.

Mice engineered to express Lin28 in their kidneys developed Wilms tumor, which regressed when Lin28 was withdrawn, indicating that strategies aimed at blocking or deactivating the gene hold therapeutic promise for children with Wilms.

Because genes and the proteins they code for are often highly conserved across species, the researchers suspect their discoveries — boosted by preliminary studies in mice — could lead to new treatments for people whose insomnia or off - hours work schedules keep them awake long after their heads hit the pillow.

If youdisable the gene for a single vomeronasal protein in mice, a male mouseloses his ability to distinguish other males from females and will tryto mate with both.

«Understanding how gene editing works in human embryos will require research in human embryos,» because mouse embryos, for example, have species - specific developmental differences, notes Dana Carroll, a biochemistry professor at the University of Utah who researches CRISPR.

If the mouse fails a hearing test, for example, it suggests the missing gene has a role in hearing.

In research published in the Journal of Bone and Mineral Research, Javed, a professor in the UAB School of Dentistry's Department of Oral and Maxillofacial Surgery, used a mouse model with mutations in both copies of the gene for SpIn research published in the Journal of Bone and Mineral Research, Javed, a professor in the UAB School of Dentistry's Department of Oral and Maxillofacial Surgery, used a mouse model with mutations in both copies of the gene for Spin the Journal of Bone and Mineral Research, Javed, a professor in the UAB School of Dentistry's Department of Oral and Maxillofacial Surgery, used a mouse model with mutations in both copies of the gene for Spin the UAB School of Dentistry's Department of Oral and Maxillofacial Surgery, used a mouse model with mutations in both copies of the gene for Spin both copies of the gene for Sp7.

«Single gene encourages growth of intestinal stem cells, supporting «niche» cells, and cancer: Finding in mice could lead to new therapies for damaged organs, cancer.»

For example, they succeeded in inserting a gene into a predefined position in the genome (knock - in) in more than 60 per cent of all manipulated mouse cells.