Sentences with phrase «identifies gene in mice»

Olson study identifies gene in mice that may be linked to emotional learning, fear response, risk seeking in humans

Not exact matches

By combining each mouse's genome, phenome, proteome and metabolome, the scientists were able to identify a particular gene, located on their chromosome 2, and whose presence plays an important role in the development of type 2 diabetes «The mice with a high - fat diet are more or less likely to develop diabetes depending on whether this gene is active or not,» said Evan Williams, LISP PhD student and the article's co-first author.

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.

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.

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.

In recent years, clock researchers have uncovered some of the gears and springs that keep this circadian timepiece running, largely by identifying a handful of key genes in organisms from bread mold to micIn recent years, clock researchers have uncovered some of the gears and springs that keep this circadian timepiece running, largely by identifying a handful of key genes in organisms from bread mold to micin organisms from bread mold to mice.

The researchers were trying to identify genes involved in the development of the mouse hypothalamus, the area of the brain that includes the SCN.

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.

Decades of work in developmental biology have provided a start: Biologists have used mutant frogs, flies, mice, chicks, and fish to identify some of the main genes that control a developing cell's decision to become a bone cell or a muscle cell.

2006 Shinya Yamanaka identifies and activates a small number of mouse genes in the cells of connective tissue, showing they can be reprogrammed to behave like immature stem cells.

After eight weeks, they harvested all the viruses in the mice's feces, and identified the viral genes present by comparing them with a large database of known genes.

«We identified that the peculiar look of these naked lizards is due to the disruption of the ectodysplasin - A (EDA), a gene whose mutations in humans and mice are known to generate substantial abnormalities in the development of teeth, glands, nails and hairs», says Michel Milinkovitch.

Using methods for analyzing gene expression in mice, they identified several members of the «BMP» family of proteins from among more than 20,000 possible candidates.

The team screened over 16,000 genes using just 100 litters of mice, and identified about 200 genes that were uniquely important to oncogenic growth in the skin.

The scientists are currently trying to identify exactly where in the skin of the mice the gene expresses itself.

They analyzed which genes were active in different areas of developing mouse brains to identify those that were «turned on» only in the SCN.

We have identified some of the genes in the mouse that are important for both learned fear and instinctive fear.

He and a colleague took samples of both visceral and subcutaneous fat from the mice and, using gene chips, identified the genes in the fat cells as well as in precursor fat cells.

Through DNA microchips, they identified the genes («transcriptome») and the proteins («proteome») which expressed themselves in each of the mice in different phases of the disease.

This allowed them to identify specific genes that are turned on or off by co-regulators of gene function called TAZ and YAP in the nucleus of developing mouse Schwann cells.

A second project, dubbed Eumorphia, will organize more than a dozen labs in nine countries to systematically screen new mouse mutants for interesting characteristics — a key step in determining the function of newly identified genes.

On 18 March, the EC announced the creation of three pan-European projects, including the twin study, a new project to identify the function of genes in mutant mice, and an effort to determine the structures of disease - related proteins.

This gene family was originally identified as important for balance: mice with mutations in otopetrin 1 (Otop1) are called tilted (tlt) because they can not right themselves.

To identify genes whose expression correlated with adiposity, we profiled gene expression in perigonadal adipose tissue from 24 mice in which adiposity varied due to sex, diet, and the obesity - related mutations agouti (Ay) and obese (Lepob).

As described in the journal Genes & Development, the researchers identified a new pathway controlling heterochromatin organisation in mouse embryonic stem cells.

To identify transcriptional patterns that correlate with body mass, we used oligonucleotide microarrays to catalogue gene expression levels in the parametrial or epididymal adipose tissue from two dozen mice whose body mass and adiposity varied due to diet, sex, and mutations in genes affecting energy homeostasis.

Chisholm, D, Devitt, N, Ngam P, Lindquist, I, Schilkey F, Linder, C. Lost in Transcription Using Transcriptomics to Identify Differential Gene Transcription in the Testis of Infertile Golga3repro27 Mice..

Finally, the functional inactivation of our target gene by one identified pharmaceutical agent will be tested in DM1 mouse model in order to monitor its ability to impact in vivo on DM1 molecular and physiological features.

«We have identified the genes and growth factors involved and, thanks to a collaboration with Microsoft Research, we can now computationally model the control circuitry in mouse cells.

This call for projects «Mouse models and rare diseases» aims to give a significant boost to the development of mouse models, in order to: ◊ gain a better understanding of the pathophysiological mechanisms involved in rare diseases whose defective genes have been identified ◊ test and validate therapeutic proofs of concept, at the pre-clinical in vivo level Indeed, producing these models meets a key objective in the development of a therapeutic straMouse models and rare diseases» aims to give a significant boost to the development of mouse models, in order to: ◊ gain a better understanding of the pathophysiological mechanisms involved in rare diseases whose defective genes have been identified ◊ test and validate therapeutic proofs of concept, at the pre-clinical in vivo level Indeed, producing these models meets a key objective in the development of a therapeutic stramouse models, in order to: ◊ gain a better understanding of the pathophysiological mechanisms involved in rare diseases whose defective genes have been identified ◊ test and validate therapeutic proofs of concept, at the pre-clinical in vivo level Indeed, producing these models meets a key objective in the development of a therapeutic strategy.

Aug. 8, 2017 — Using bioinformatics approaches, Vanderbilt investigators have identified gene expression networks that are deregulated in mouse and human stomach cancers.

use CRISPR - Cas technology to carry out genome - wide screens of gene - gene, gene - drug and cancer - microenvironment interactions in cells and mice in order to explore fundamental biology and to identify drug targets and drug resistance / sensitisation mechanisms.

Using bioinformatics approaches, they identified transcription (gene expression) networks that were consistently deregulated in both mouse and human lesions.

Whereas 12 of 16 annotations were confirmed by RT - PCR in human tissues, for only seven genes mouse orthologs could be identified and found to be expressed.

Following a Forward Genetics approach, Fleming researchers identified a novel neurological mouse model caused by a functional mutation in the Slc25a46 gene, a new pathogenic target in a wide spectrum of human neurological diseases, including optic atrophy, Charcot - Marie - Tooth type 2, Leigh syndrome, progressive myoclonic ataxia and lethal congenital pontocerebellar hypoplasia.

FINDINGS The researchers identified 32 known imprinted genes, but no new ones, implying that the list of imprinted genes in the mouse — at least in embryonic fibroblasts — is nearly complete, says Morison, who was not involved in the study (Nucleic Acids Res, 42:1772 - 83, 2014).

Using genetic and epigenetic analyses coupled with powerful perturbation technologies to test gene functions in human cells and mouse models, we hope to identify the critical drivers of this disease and the basis for therapeutic responses.

We have identified a mouse containing a single base pair deletion in the Crb1 gene.

Projects restricted to the creation of conventional mouse knockouts in candidate disease genes identified by association studies, or to broadly overexpress those genes, are discouraged.

The researchers, who previously identified NOTCH1 as a genetic culprit in human CAVD, created mice that had shorter telomeres and were also missing one copy of the NOTCH1 gene, since mutation of NOTCH1 alone failed to induce valve disease in mice.

Potential projects include identifying common pathways that modify retinal degenerative disease from a large collection of actively maintained mouse models; determining molecular networks implicated in pathological disruption of the retinal pigment epithelium; identifying molecular pathways that regulate postnatal ocular growth; and using mouse models to assess the pathogenic role of gene variants that increase the risk of age - related macular degeneration as identified by human genome - wide association studies.

I use epigenetic approach to identify the sexually dimorphic genes that control sexual differentiation in the mouse brain structure and behavior.

Led by Karen Reue, the research team first used a mouse model that they had identified previously as having a spontaneous deletion in the Diet1 gene.

Using this process, they identified more than 3,000 genes that regulate more rapidly in mice and found none that regulate faster in human cells.

We use the Cre - loxP recombination system to generate mice with cell type - specific inactivation of the IL - 10 gene in order to identify cellular sources of the cytokine that are relevant in various situations of immune challenge.

Using this, we have identified abnormalities in these structures among 298 embryos from mutant mouse lines carrying embryonic lethal gene mutations produced for the Deciphering the Mechanisms of Developmental Disorders (DMDD) programme.

Here, we performed forward genetic screening in mice using Sleeping Beauty transposon mutagenesis to identify candidate BC driver genes in an unbiased manner, using a stabilized N - terminal truncated β - catenin gene as a sensitizer.

We identify 23 genes that, when disrupted in mouse, modify the ability of tumour cells to establish metastatic foci, with 19 of these genes not previously demonstrated to play a role in host control of metastasis.

In recent years, a number of genome - wide approaches have identified transcripts present in mouse and human ES cells or their differentiated derivatives using a variety of gene expression profiling methods [24], [27]--[32In recent years, a number of genome - wide approaches have identified transcripts present in mouse and human ES cells or their differentiated derivatives using a variety of gene expression profiling methods [24], [27]--[32in mouse and human ES cells or their differentiated derivatives using a variety of gene expression profiling methods [24], [27]--[32].

We are identifying genes that alter atherosclerosis susceptibility in a mouse model and testing whether they play a role in coronary artery disease in humans.