Sentences with phrase «gene in mice led»

In a mouse model of eczema, loss of the HTR7 gene in mice led to significantly less scratching and less severe skin lesions.

Deletion of the GM - CSF gene in the mouse led to reduction and impaired regulatory function of gut tissue macrophages and dendritic cells which compromised induction of tolerance to food antigens and increased mice susceptibility to IBD.

In addition, loss of the Esrp1 gene in mice leads to changes in the shape of the inner ear that is very similar to the situation with the siblings.

Not exact matches

This study led to the discovery of 18 new imprinted genes, validated some known genes and resolved the disputed status of some others to provide a gold standard list of 93 imprinted genes in mouse.

Researchers led by Xiao - Jiang Li, MD, PhD and Shihua Li, MD, at Emory University School of Medicine, used genetically engineered mice in which the huntingtin gene can be deleted, triggered only when the mice are given the drug tamoxifen.

The team found that humans are equipped with tiny differences in a particular regulator of gene activity, dubbed HARE5, that when introduced into a mouse embryo, led to a 12 % bigger brain than in the embryos treated with the HARE5 sequence from chimpanzees.

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.

An additional study, currently available at bioRxiv, led by the researchers from the CRG and Cold Spring Harbour Laboratory, highlights the fact that a substantial part of human and mice genes have maintained an essentially constant expression throughout evolution, in tissues and various organs.

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.

But researchers have found a mutation in a mouse gene that leads to an arthritis - like condition because it causes the joint's cartilage cells to pump insufficient amounts of pyrophosphate — a natural water softener — into the joint cleft.

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.

Dr. Timothy Cox, a craniofacial researcher at Seattle Children's Research Institute and lead author, found that mice with a gene mutation that causes cleft lip and palate had problems in their salivary glands that affected gum tissue and oral health.

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.

UT Southwestern Medical Center researchers successfully used a new gene editing method to correct a mutation that leads to Duchenne muscular dystrophy (DMD) in a mouse model of the condition.

Unless sufficient cohesin was present in the developing mouse brain, the researchers showed that the regulation of a number of genes was disrupted, leading to neuronal defects and increased anxiety.

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.

«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.»

In this study, the team was able to piece together the biological process that leads to the production of new bone by studying the offspring of mice lacking the Gastric Intrinsic Factor gene, which is active in the stomach and allows the gut to absorb vitamin B1In this study, the team was able to piece together the biological process that leads to the production of new bone by studying the offspring of mice lacking the Gastric Intrinsic Factor gene, which is active in the stomach and allows the gut to absorb vitamin B1in the stomach and allows the gut to absorb vitamin B12.

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.

Deletion of the CXCR4 gene led to sustained T - ALL remission within a month in similar mice, as well as movement of the cancerous blood cells away from the bone marrow.

Researchers find a full 12,000 genes that act differently in male and female mice, a finding that could lead to sex - specific medicine.

The study team, led by neuroscientist Joseph Buxbaum of the Mount Sinai School of Medicine in New York and including coworkers at the University of Pennsylvania Medical Center in Philadelphia and Manhattanville College in Purchase, New York, genetically engineered mice to carry defective versions of the FOXP2 gene.

While previous investigations into the protein's effects have used either mice in which gene expression was knocked out or transgenic animals that expressed human gene variants throughout their lifetimes, the MGH - MIND - led study used a different approach to investigate the effects of introducing the variant forms of the protein into brains in which plaque formation had already begun.

Indeed, exposure of the protein produced by the nanoparticle - based gene therapy to the gut mucosa prevents inhibitor development and restores clotting - factor activity in mouse models of both haemophilia A and B. «This approach really could hold big benefit for patients,» says Jörg Schüttrumpf, a transfusion - medicine specialist who led one of the studies performed at the German Red Cross Blood Donor Service in Frankfurt.

To do so, a team led by neuroscientist David Holtzman of Washington University in St. Louis injected genes for human apoE3 or apoE4, which is about a third as common, into fertilized mouse eggs.

«This is the first study to offer an unbiased profile of novel imprinted genes in a mammal other than mice,» said lead author Xu Wang, a postdoctoral associate in the laboratory of Andrew Clark, professor of molecular biology and genetics and the study's senior author.

A team of developmental biologists led by Hans Schöler and Karen Hübner at the University of Pennsylvania placed densely packed clusters of stem cells from mouse embryos in a petri dish, using fetal calf serum as a growth medium and adding a gene protein that turns green when germ cells form.

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.

But researchers will have to figure out how to eliminate the viral DNA used to introduce the genes, which in Yamanaka's experiments led to cancers in 20 percent of mice grown from blastocysts.

Using molecular scissors wrapped in a greasy delivery package, researchers have disrupted a gene variant that leads to deafness in mice.

In the Rutgers study, Zong and lead author Ji - An Pan, a scientist in his laboratory, looked at liver and heart damage in laboratory mice and found that the mice in which the TRIM21 gene was inactivated suffered little heart or liver damage when put through the same laboratory procedures used to produce tissue damage in mice with the genIn the Rutgers study, Zong and lead author Ji - An Pan, a scientist in his laboratory, looked at liver and heart damage in laboratory mice and found that the mice in which the TRIM21 gene was inactivated suffered little heart or liver damage when put through the same laboratory procedures used to produce tissue damage in mice with the genin his laboratory, looked at liver and heart damage in laboratory mice and found that the mice in which the TRIM21 gene was inactivated suffered little heart or liver damage when put through the same laboratory procedures used to produce tissue damage in mice with the genin laboratory mice and found that the mice in which the TRIM21 gene was inactivated suffered little heart or liver damage when put through the same laboratory procedures used to produce tissue damage in mice with the genin which the TRIM21 gene was inactivated suffered little heart or liver damage when put through the same laboratory procedures used to produce tissue damage in mice with the genin mice with the gene.

«We studied how the Sox2 gene is turned on in mice, and found the region of the genome that is needed to turn the gene on in embryonic stem cells,» said Professor Jennifer Mitchell of U of T's Department of Cell and Systems Biology, lead invesigator of a study published in the December 15 issue of Genes & Development.

«It's possible that microRNAs go into the bloodstream and affect the potential transcription of these genes in the sperm,» says Brian Dias at Emory University in Atlanta, Georgia, who led the work in mice.

The FAN1 knockout mice that Smogorzewska's lab has generated allow them to investigate the role of FAN1 in DNA repair, and to figure out how mutations in the gene may lead to kidney disease.

In the animal studies, mice containing the gene expressing human resistin and infected with a parasitic worm similar to the human hookworm experienced excessive inflammation, leading to increased weight loss and other symptoms.

In previous research, Quaggin's lab showed that deleting the gene in mouse models led to glaucoma, but the scientists didn't know how mutations impairing the gene affected humanIn previous research, Quaggin's lab showed that deleting the gene in mouse models led to glaucoma, but the scientists didn't know how mutations impairing the gene affected humanin mouse models led to glaucoma, but the scientists didn't know how mutations impairing the gene affected humans.

The researchers, led by Maria Luisa S. Sequeira - Lopez, MD, of UVA's Child Health Research Center, were investigating how the kidney forms when they noted that the deletion of the S1P1 gene in research mice had deadly consequences elsewhere in the body.

In order to understand this contradiction, the research group led by Raúl Estévez and Alejandro Barrallo compared genetically - modified zebrafish and mice models — in other words, knock - out organisms that, in this case, do not express the gene MLC1 — with the brain biopsy from an MLC patienIn order to understand this contradiction, the research group led by Raúl Estévez and Alejandro Barrallo compared genetically - modified zebrafish and mice models — in other words, knock - out organisms that, in this case, do not express the gene MLC1 — with the brain biopsy from an MLC patienin other words, knock - out organisms that, in this case, do not express the gene MLC1 — with the brain biopsy from an MLC patienin this case, do not express the gene MLC1 — with the brain biopsy from an MLC patient.

As in earlier studies, the investigators, led by Ren Hen of Columbia University, first created a line of so - called knockout mice that lacked the gene encoding the receptor protein.

Humans have an ortholog of the murine Nrk gene, and considering that the gene expression pattern in breast tumor in Nrk mutant mice was similar to that in human luminal B breast cancer, the findings of this study may lead to further understanding of the mechanisms of human breast cancer suppression and to advances in its diagnosis and therapy.

They then compared genetic variants that lead to thin corneas in mice, to genes that increase a person's risk of a common type of glaucoma, called primary open angle glaucoma.

In experiments with mice, disruptions in clock genes can lead to obesity, although scientists don't yet understand the mechanisIn experiments with mice, disruptions in clock genes can lead to obesity, although scientists don't yet understand the mechanisin clock genes can lead to obesity, although scientists don't yet understand the mechanism.

Additionally, the study showed that genetic knockdown of RASAL2 gene can lead to reduced metastasis in breast cancer mouse model.

The newly published PLOS ONE study assessed the long - term efficacy of the therapy and demonstrated that a single gene therapy treatment led to prolonged production of VNA in blood and protected the mice from subsequent exposures to C. botulinum toxin for up to several months.

«Autism - linked gene stunts developing dendrites: Genetic variation leads to excessive pruning of dendrites in rats cells and mouse model of autism.»

Increased expression of a gene linked to autism spectrum disorders (ASDs) leads to a remodeling of dendrites during brain development, according to a new study conducted in cultured neurons and an ASD mouse model published in JNeurosci.

However, their initial finding demonstrated that progenitor derived from iPSCs generated using lentiviral gene transduction led to the high incidence of highly aggressive tumors in immunodeficient mice after transplantation under the kidney capsule.

Lead researcher Christoph Lepper, a predoctoral fellow in Carnegie's Chen - Ming Fan's lab and a Johns Hopkins student, for the first time looked at these two genes in promoting stem cells at varying stages of muscle growth in live mice after birth.

However, researchers at the University of Pennsylvania, led by Dr. George Cotsarelis, have regenerated follicles in mice by manipulating a gene called Wnt.

In the second study, a team led by Shahin Rafii at Weill Cornell Medicine in New York City used adult mouse cells as their starting material, and then guided them through several steps — including exposure to some of the same gene - activating proteins — to create mature blood stem cells in a petri disIn the second study, a team led by Shahin Rafii at Weill Cornell Medicine in New York City used adult mouse cells as their starting material, and then guided them through several steps — including exposure to some of the same gene - activating proteins — to create mature blood stem cells in a petri disin New York City used adult mouse cells as their starting material, and then guided them through several steps — including exposure to some of the same gene - activating proteins — to create mature blood stem cells in a petri disin a petri dish.