Not exact matches
After determining the proper dosage of tamoxifen — an early trial
resulted in a number of
mouse deaths due to overactivation of Mecp2 — researchers settled on a four - week regimen of ramping up the
gene's function.
This suggested that obesity
in both obese and db
mouse strains
resulted from a mutation
in a single
gene in each case.
Bone marrow transplant cured compulsive behaviour
in mice whose OCD symptom seems to be the
result of a mutation
in a
gene never before linked to behaviour.
So far,
gene therapy attempts have only
resulted in partial improvements of hearing
in mouse models of specific human deafness forms that did not include severe anomalies
in hair cell structure.
With a single local injection of the USH1G
gene just after birth, the scientists observed a restoration of the structure and mechanosensory function of the inner ear hair bundles — profoundly damaged before birth -,
resulting in a long - term partial recovery of hearing, and complete recovery of vestibular function
in these
mice.
In a test of this theory, researchers have demonstrated that mice harboring a human SCN1A gene mutation that results in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deat
In a test of this theory, researchers have demonstrated that
mice harboring a human SCN1A
gene mutation that
results in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances in the heart that culminate in ventricular fibrillation and sudden cardiac deat
in Dravet Syndrome (DS), a severe and intractable genetic epilepsy, have electrical disturbances
in the heart that culminate in ventricular fibrillation and sudden cardiac deat
in the heart that culminate
in ventricular fibrillation and sudden cardiac deat
in ventricular fibrillation and sudden cardiac death.
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.
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 research team found that when the SMAD4
gene is eradicated
in mice, it also
results in depletion of ME2 levels.
In Martin's view, the
result strongly suggested that the patients had inherited the silenced
gene from one of their parents, like the case with agouti
mice.
To find out what BRCA2 does normally, the team reporting the new
results, which includes Allan Bradley of Baylor College of Medicine
in Houston and Paul Hasty of Lexicon Genetics Inc.
in The Woodlands, Texas, created «knockout»
mice in which the
gene was inactivated.
She and her colleagues will be exploring the role of YY1 further, using clinical samples as well as
mouse models, to look at the protein
in diseases like lupus to deepen their understanding of how autoimmunity could
result from the «escape» of immune
genes from X chromosome inactivation.
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.
When his team looked at
gene expression changes
in the
mice, then applied them to humans with early stage cancer, the
results revealed a breakdown of which patients have a high or low chance of survival.
«To our knowledge, our model is the first
in which expression of a single
gene in postnatal hair cells
results in hair cell survival and hearing preservation
in mice that otherwise suffer from age - related and noise - induced hearing loss,» Dr. Chen said.
In this mouse model, mutations in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different color
In this
mouse model, mutations
in Kras and p53 genes resulted in the formation of individual tumor cell populations that were labeled with different color
in Kras and p53
genes resulted in the formation of individual tumor cell populations that were labeled with different color
in the formation of individual tumor cell populations that were labeled with different colors.
«No
gene is truly off, and the off state
in this case
resulted in enough leaky DUX4 expression to kill the
mice.»
Scientists deleted the LZK
gene in astrocytes of one group of injured
mice, which decreased the cells» injury response and
resulted in a larger wound on the spinal cord.
The genetically modified
mice distort the
results because of the human growth hormone, so
in many cases the effect of that
gene was either overvalued or undervalued.
Results showed that naturally healthy macrophages and
gene - corrected macrophages worked equally well
in correcting the disease
in the
mice.
In mice lacking the NDST1 gene, and therefore the NDST1 enzyme, nature substitutes with an NDST1 isoform (NDST2, NDST3, and NDST4), but the results — like substitutions in cooking — are noticeabl
In mice lacking the NDST1
gene, and therefore the NDST1 enzyme, nature substitutes with an NDST1 isoform (NDST2, NDST3, and NDST4), but the
results — like substitutions
in cooking — are noticeabl
in cooking — are noticeable.
In tests on human breast cancer cells and in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cell
In tests on human breast cancer cells and
in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cell
in special immunodeficient
mice with tissue grafts, the scientists found that both agents interfered with
genes involved with breast cancer cell growth,
resulting in more cancer cell
in more cancer cells.
Dr. Je and his team analysed signalling activity
in neuronal cultures that either did not have the DTNBP1
gene or had lowered levels of the
gene, because reduced DTNBP1 levels and genetic disruptions of DTNBP1
in mice resulted in schizophrenia - like behaviours.
Petris found that young
mice missing the ATP7A
gene in their intestinal cells were unable to absorb copper from food,
resulting in an overall copper deficiency that mimics symptoms of Menkes disease
in children.
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.
Results of previous studies
in mice of bexarotene's effect on AD have been mixed, and none of those studies were done
in mice that carry a human APOE
gene and also develop progressive, AD - like pathology.
This
gene therapy
resulted in high - fat diet
mice having a reduced body weight, building up less fat, expending more energy, and showing evidence of improved leptin - signalling.
Furthermore, organ cultured cartilage from ACH
mice treated with statin
resulted in increased expression of the aforementioned three
genes and also
in Runx2 and Col10a1, which indicated that statin stimulated both the differentiation and maturation of ACH
mouse chondrocytes.
Consistent with these
results, genetic inactivation of an HR
gene (Fancd2) and Polq
in mice results in embryonic lethality.
PER2: Deletion of the PER2
gene in mice, associated with the mechanisms of circadian rhythm, appears to improve DNA repair
in stem cell populations relevant to the immune system,
resulting in a healhier immune cell population, better immune function
in old age, and a modestly extended life span.
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.
Catalase:
Gene therapy to increase levels of the antioxidant catalase
in the mitochondria
in mice have produced mixed
results, but some studies show improved health and extended life.
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 adulthoo
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 adulthoo
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 adulthoo
in the death of the organism prior to adulthood.
Südhof used genetic engineering to «knock - out» the synaptotagmin
gene in mice, with the
result that synapses from the forebrains of
mice that lacked synaptotagmin lost their capacity for fast calcium - triggered release of neurotransmitter, thus confirming the importance of synaptotagmin
in vivo.
The scientists removed the
gene region containing the risk variant from the
mouse genome, and found that as a
result the
mice were healthy but displayed a small decrease
in the expression of a nearby cancer
gene, called MYC.
Here we present an experimental reannotation of the GENCODE intergenic lncRNA populations
in matched human and
mouse tissues that
resulted in novel transcript models for 3,574 and 561
gene loci, respectively.
To better illustrate
gene expression profiles
in mouse ES cells, we have organized the
results in an interactive database with a number of features and tools.
Results: Here, we profile genome - wide changes
in DNA methylation,
gene expression and lipidomics
in response to DR and aging
in female
mouse liver.
A
gene that naturally occurs on the
mouse's sex chromosome can be moved to another chromosome where it
results in all - male offspring.
The
results implicate GPC6 as a novel determinant of BMD, and also identify abnormal skeletal phenotypes
in knockout
mice associated with a further 100 prioritized
genes.
In one mouse study, the IGF - 1 gene was placed in the animals» glutes and calves, which resulted in up to a 115 % increase in muscle - cross-sectional are
In one
mouse study, the IGF - 1
gene was placed
in the animals» glutes and calves, which resulted in up to a 115 % increase in muscle - cross-sectional are
in the animals» glutes and calves, which
resulted in up to a 115 % increase in muscle - cross-sectional are
in up to a 115 % increase
in muscle - cross-sectional are
in muscle - cross-sectional area.
The researchers noted that the
mouse results may have implications for human health as well, as they also found an E. coli variant with the suspect
genes in high percentages of human patients with colorectal cancer and irritable bowel disease.
Calorie Restriction - like Effects of 30 Days of Resveratrol Supplementation on Energy Metabolism and Metabolic Profile
in Obese Humans Cell Metabolism 2011 (Nov 2); 14 (5): 612 — 622 ~ FULL TEXT The
result of just 30 days on resveratrol were impressive: (1) The same
gene regulators (AMPK, SIRT1 and PGC - 1a) were activated
in this study as are activated by caloric restriction and resveratrol
in mice and endurance training
in humans.