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.
When researchers deleted
the gene in mice with various liver injuries, they found that the livers replaced tissue mass quicker and showed reduced fibrosis in response to chemical injury.
Yin then delivered that alongside guide RNAs packaged separately in AAV to fix broken
genes in mice with liver disease.
In 2016, the research team spotted mice that sleep for extraordinarily long periods and ones that have extraordinarily short REM sleep in a sample of about 8,000 specimens, and discovered mutations of particular
genes in those mice with unique sleep patterns.
Not exact matches
Bird and his colleagues created mutant
mice with a roadblock
in the Mecp2
gene that prevented it from being expressed.
In experiments with mice, the researchers found that Paneth cells engineered to lack a functional ATG16L1 gene were five times more likely to die in the face of rising TNF - alpha signals than normal cell
In experiments
with mice, the researchers found that Paneth cells engineered to lack a functional ATG16L1
gene were five times more likely to die
in the face of rising TNF - alpha signals than normal cell
in the face of rising TNF - alpha signals than normal cells.
The study coupled
gene therapy that excited visual neurons
in the eyes
with stimulation — a swirling black - and - white grid placed
in front of the
mice.
A new
mouse model of a genetically - linked type of autism reveals more about the role of
genes in the disorder and the underlying brain changes associated
with autism's social and learning problems.
In 1997 Joseph Takaha - shi of the Howard Hughes Medical Institute at Northwestern University and his colleagues isolated a
gene they called Clock that when mutated yielded
mice with no discernible circadian rhythm.
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.
These findings allowed researchers to create a chimera virus: a
mouse virus
with a human viral
gene that can be used to test molecules that inhibit human LANA protein
in an animal model of disease, treating not only human herpes virus infection but also its associated cancers.
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.
These four
genes and their proteins constitute the heart of the biological clock
in flies, and
with some modifications they appear to form a mechanism governing circadian rhythms throughout the animal kingdom, from fish to frogs,
mice to humans.
So Sandra Ryeom at the Children's Hospital
in Boston and colleagues bred
mice with three
genes to find out if an extra copy gave them extra protection against cancer.
When the researchers paired female
mice treated
with the
gene therapy
with males, the females were still able to become pregnant — and have healthy babies — within the first six weeks, because of those follicles that had already started growing
in the ovaries.
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.
Normally, to achieve such a rapid evolutionary shift, a species needs to start
with an alternative version of a
gene already
in circulation, giving natural selection more to work
with, but
in deer
mice the new version of Agouti spread rapidly from a standing start.
In the study, researchers worked
with a
mouse model that has a debilitating mutation on one of the exons of the dystrophin
gene.
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.
Using a novel form of
gene therapy, scientists from Harvard Medical School and the Massachusetts General Hospital have managed to restore partial hearing and balance
in mice born
with a genetic condition that affects both.
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.
Mice born
with extra copies of a human
gene develop learning defects that may resemble those
in Down syndrome.
They started
with pairs of fat yellow
mice known to scientists as agouti
mice, so called because they carry a particular
gene — the agouti
gene — that
in addition to making the rodents ravenous and yellow renders them prone to cancer and diabetes.
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 mic
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 mic
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 mic
in embryonic stem cells of
mice.
Finally,
mice in which the Hand2
gene was specifically deleted
in the endometrium developed precancerous endometrial lesions
with age.
To determine if defects
in the atrial natriuretic peptide (ANP) system can cause hypertension,
mice were generated
with a disruption of the proANP
gene.
Like the per
gene, the new
genes — dubbed RIGUI
in humans and m - rigui
in mice — are turned on and off
in a daily cycle and may work
with other
genes to generate the oscillating mechanism that runs the internal clock.
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.
Since patients (and
mice)
with Usher 1c also have balance problems caused by hair - cell damage
in the vestibular organs, the researchers also tested whether
gene therapy restored balance.
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.
Nadeau stumbled upon one study,
in mice, describing how environmental factors can tag Foxp3
with chemical markers that tell T - cell precursors to switch the
gene on or off.
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.
As expected, the
mice carrying the mutated
gene had far fewer vocalizations,
with longer gaps between «speech» compared
with their unmodified littermates — Gnptab mutant
mice had about 80 vocalizations compared
with 190
in the nonmutant
mice.
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.
«From other studies ***** we know that epigenetic modifications of the DPP4
gene, which are associated
with an increased production of the enzyme, have a negative impact on the liver metabolism already
in young
mice, long before fatty liver disease emerges,» says Baumeier.
Ronald Kahn and his colleagues at Harvard Medical School
in Boston compared
gene expression
in brain samples from
mice with type 1 or type 2 diabetes against those of healthy
mice.
They destroyed the T cells
in 12
mice, five of which received marrow cells from normal
mice while seven received marrow from
mice with a defective Fas - ligand
gene.
Mineral deposits and bone formation around toe joints of
mouse with mutation
in the ank
gene (mutant foot shown on right, normal skeleton on left).
Diamond's lab circumvented this problem by creating female
mice that had a key interferon
gene knocked out;
in a second experiment, they treated pregnant animals
with an anti-interferon antibody.
Even
in mice with working LCN2
genes, infusions of the hormone reduced food intake, improved blood sugar levels and increased insulin sensitivity.
In their study, the researchers showed that already at the age of six weeks in the mice with a rapid weight gain, the DPP4 gene was less methylated at four specific loci, i.e. epigenetically altered, compared to the other mic
In their study, the researchers showed that already at the age of six weeks
in the mice with a rapid weight gain, the DPP4 gene was less methylated at four specific loci, i.e. epigenetically altered, compared to the other mic
in the
mice with a rapid weight gain, the DPP4
gene was less methylated at four specific loci, i.e. epigenetically altered, compared to the other
mice.
Last week, the company reported that it managed to disable the TTR
gene in the livers of
mice, reducing levels of the protein by 97 per cent
with no signs of any ill effects.
Sensory hair cells
in the cochlea of a Beethoven
mouse treated
with TMC2
gene therapy.
The control
mice,
with all
genes intact, should have lost sight as photo - receptors — the light - sensitive cells
in the retina — died.
Global
gene expression studies found that the LPA - treated
mice shared many similar molecular markers as those found
in humans
with schizophrenia.
First author Kim Martinod, a graduate student
in the Immunology Graduate Program at the Harvard University Medical School, found that,
in response to vein constriction, these «rescued»
mice now could function normally, forming clots as efficiently as
mice with a functioning Pad4
gene, demonstrating that the Pad4
gene did produce a functioning PAD4 enzyme
in these white blood cells to regulate blood clotting.
In one of their experiments, team members compared
mice with a normally functioning Pad4
gene to
mice with a defective
gene.
In a study published earlier this year, Jiang and other collaborators at Duke described a mouse model of autism in which they deleted a prominent autism gene called SHANK3, which is mutated in 1 percent of people with the disorde
In a study published earlier this year, Jiang and other collaborators at Duke described a
mouse model of autism
in which they deleted a prominent autism gene called SHANK3, which is mutated in 1 percent of people with the disorde
in which they deleted a prominent autism
gene called SHANK3, which is mutated
in 1 percent of people with the disorde
in 1 percent of people
with the disorder.
When researchers suppressed the ARF
gene in mole - rat cells during the reprogramming process to iPSCs, the cells stopped proliferation
with sign of cellular senescence, while the opposite happens
with mouse cells.
In humans and
mice, the
gene is associated
with height, face development and other traits.