Not exact matches
One blocks
normal cycles by impeding the clock regulator
genes called CLOCK: BMAL1.
Such plants have two mutant copies of a
gene called hothead, which differ from the
normal gene by a single base pair.
Several mutations were found in
genes coding the machinery that makes mitochondrial proteins, and so would probably hinder mitochondria's ability to make the chemical fuel
called ATP, which is used by
normal cells.
He discovered a second clock
gene,
called timeless, that encodes another protein, TIM, which is required for a
normal circadian rhythm.
Fragile X occurs when a segment in the FMR1
gene on the X chromosome
called the CGG triplet repeat is lengthened from the
normal 5 to 40 repeats to 200 repeats in people with full mutation FXS.
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.
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.
The two closely related regulatory
genes are active in the
normal development of mammals and govern how RNAs produced from the
genes are joined to make final versions of the encoded protein, a process
called alternative splicing.
Brains of fish missing the
gene were relatively
normal except there were cells missing from a region
called the hypothalamus.
Researchers used a technique
called CRISPR / Cas9 - mediated genome editing, which can precisely remove a mutation in DNA, allowing the body's DNA repair mechanisms to replace it with a
normal copy of the
gene.
The team reports that the adenomas grow from cells that express a
gene called Lgr5 +, which is also active in
normal intestinal stem cells.
The research suggests that reducing production of the protein,
called myoferlin, affects cancer cells in two primary ways: by changing the activation of many
genes involved in metastasis in favor of
normal cell behavior, and by altering mechanical properties of cancer cells — including their shape and ability to invade — so they are more likely to remain nested together rather than breaking away to travel to other tissues.
The best example of this occurs in what's
called gene imprinting, where for example, females have two X chromosomes and one of those two X chromosomes must be inactivated in a cell in order for the cell's
normal function.
They transplanted either
normal or
gene - corrected macrophages into the respiratory tracts of mice, which were bred to mimic the hereditary form of a human disease
called hereditary pulmonary alveolar proteinosis (hPAP).
In
normal development, all cells turn off
genes they don't need, often by attaching a chemical methyl group to the DNA, a process
called methylation.
It appears to do this by targeting little knots in their DNA,
called quadruplexes, which are very different from
normal DNA and which are especially found in faulty
genes.
In 1993, Poirier and his Montreal - based team co-discovered an important genetic risk factor involved in the most common form of the disease: a defective
gene,
called Apolipoprotein E type 4 (ApoE4), that prevents the
normal transport of cholesterol and phospholipids to the brain.
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.
Now a study has found that the
gene mutation's toxic effects require higher than
normal levels of a protein
called suPAR to trigger the onset and progression of the disease.
Comparing the damaged sites in
normal cells before and after infection with H. pylori revealed that
genes located close to the margins of the chromosomes, the so -
called sub-telomeric regions, are more likely to be damaged after infection, as are
genes that are active in gastric cells.
She and her colleagues found Karma, a mobile piece of DNA known as a transposon, inserted in the middle of an important
gene for
normal oil - palm fruit development
called DEFICIENS.
They found that altering the activity of a
gene called Cdk5 appeared to make the clocks run faster than
normal, and the flies older than their chronological age.
The new research finds that the stiffness of the extracellular matrix and the availability of certain ligands (molecules that bind to cell membranes) can together determine which
genes are actually
called on — and whether
normal epithelial cells begin to exhibit the behaviors characteristic of highly malignant cancer cells.
In oncology terms, this double - hit status is
called «loss of heterozygosity,» or LOH, to signify that both versions (one from mom, one from dad) of the
normal BRCA
gene have been hobbled.
The researchers set out to understand how this drought tolerance came about by comparing the set of expressed
genes (the transcriptome) in the mutants to that in
normal (so -
called wild - type) plants.
Too much p53 in bone - making cells
called osteoblasts dials down a
gene, H19, and a related protein, decorin, that would otherwise help stem cells mature (differentiate) to become
normal osteoblasts.
A group of transcription factors collectively
called the eye field transcription factors or EFTFs (pax6, rx1, tbx3 [or ET], nr2e1 [or tailless], six3, lhx2, and six6 [or optx2]-RRB- and the neural patterning
gene otx2 are essential for
normal eye formation [6].
A drug
called Repoxygen delivers the EPO
gene with some controls, so that when blood oxygen dips below
normal, the body makes enough red blood cells to restore
normal oxygen.
The study team injected patients with a vector, a genetically engineered adeno - associated virus, which carried a
normal version of a
gene called RPE65 that is mutated in one form of LCA.
They discovered that extra chromosome 21 - a genetic state known as trisomy 21 - disturbs a key regulating
gene called NRSF or REST, which in turn disturbs the cascade of other
genes that control
normal development at the embryonic stem cell stage.
We are using a new technique,
called single cell RNA sequencing, to isolate thousands of single neurons from human brain tissue, study all the
genes that are expressed in each individual cell, and make cell - to - cell comparisons between
normal, early stage and late stage AD.
In the study, functional Ikaros protein produced from the one remaining
normal Ikaros
gene was restored with a novel class of drugs that target a specific enzyme
called casein kinase 2 or CK2.
They inserted mutated and
normal human FABP7
genes into star - shaped glial cells
called astrocytes.
One of them, miR - 142, is known to target a
gene called APC that inhibits the renewal of
normal stem cells.
«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 holdings.
Genes are inherited in pairs, and if a cat has two defective (mutated) genes (called a homozygous cat) this increases the risk of HCM further compared with a cat that has just one defective gene (and one normal gene, a heterozygous
Genes are inherited in pairs, and if a cat has two defective (mutated)
genes (called a homozygous cat) this increases the risk of HCM further compared with a cat that has just one defective gene (and one normal gene, a heterozygous
genes (
called a homozygous cat) this increases the risk of HCM further compared with a cat that has just one defective
gene (and one
normal gene, a heterozygous cat).
Since there are so many
genes involved in polygenic traits such as HD, some few dogs with what we
call a
normal genotype (very few defective
genes as evidenced by progeny results, for example) can be «forced» into dysplastic phenotypes if they are overfed and mineral - supplemented during their fast growth period.
American bulldogs that have one mutant and one
normal gene are
called carriers.
Corgi PRA is caused by a mutation in the
gene called PDE6A whose
normal state is essential for
normal vision.
Called «genetically clear», «noncarriers» or, more formally, «homozygous
normals,» such dogs pass the
normal gene on to all their pups with a very high probability - which means that their pups have a very low risk of being affected with prcd.
Dogs that have one mutant and one
normal gene are
called carriers.