Additional micro-patterning of the substrate changes the cytoskeleton in the cell and the shape of the nucleus, which
cause the genes in the cell to change.
Not exact matches
Davies and Lineweaver suggest that
genes active
in embryogenesis and switched off later may be reactivated because of damage,
causing the accelerated
cell division of these rogue cancer
cells.
Blakemore argues that a single
gene mutation could
in fact have been the
cause of this increase - for
in fact only one extra
cell - division step would
cause a doubling of brain size.
«If we could use
gene editing to remove the sequences
in an embryo that
cause sickle
cell disease or cystic fibrosis, I would say not only that we may do so, but
in the case of such severe diseases, we have a moral obligation to do so.»
They discovered that
in the young, more immune
cells called monocytes were recruited to the lungs, and that the
gene expression profiles of these
cells had more inflammatory features,
causing greater inflammation and more severe lung injury.
We wanted to understand what types of differences are always there, what is
causing them, and what they mean,» says Juan Carlos Izpisua Belmonte, a professor
in Salk's
Gene Expression Laboratory and co-senior author, with Kelly Frazer of the University of California, San Diego, on the new paper, which was published
in Cell Stem
Cell in April 2017.
In these and other inherited diseases, 10 to 15 percent of the single - base pair mutations that cause the disease create a misplaced, premature «stop» codon in the middle of the gene — causing the machinery of the cell to prematurely halt synthesis of the protein, which destroys its ability to functio
In these and other inherited diseases, 10 to 15 percent of the single - base pair mutations that
cause the disease create a misplaced, premature «stop» codon
in the middle of the gene — causing the machinery of the cell to prematurely halt synthesis of the protein, which destroys its ability to functio
in the middle of the
gene —
causing the machinery of the
cell to prematurely halt synthesis of the protein, which destroys its ability to function.
A team of researchers at the Stanford University School of Medicine has used a
gene - editing tool known as CRISPR to repair the
gene that
causes sickle
cell disease
in human stem
cells, which they say is a key step toward developing a
gene therapy for the disorder.
In humans, Huntington's is an inherited disease
caused by a
gene encoding a toxic protein, called mutant huntingtin, which
causes brain
cells to die.
The researchers used the dead guide RNAs to turn on the Pdx
gene in the mice's livers, which
caused the liver
cells to produce insulin, reversing the mice's diabetes.
People with the transthyretin amyloidosis have mutations
in the DNA of the transthyretin
gene, which
causes abnormal buildup and deposits of a transport protein called transthyretin
in nerve and heart
cells.
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 experiments on cell cultures, both of these inhibitors succeeded in breaking various forms of the TKI resistance: including forms caused by additional mutations of the gene Bcr - Abl as well as those caused by large quantities of the protein Gab
In experiments on
cell cultures, both of these inhibitors succeeded
in breaking various forms of the TKI resistance: including forms caused by additional mutations of the gene Bcr - Abl as well as those caused by large quantities of the protein Gab
in breaking various forms of the TKI resistance: including forms
caused by additional mutations of the
gene Bcr - Abl as well as those
caused by large quantities of the protein Gab2.
Harvard Medical School researcher Melina Claussnitzer and her team found that a single variation
in the FTO
gene caused fat
cells that would normally become healthier beige to turn into white fat
cells instead.
Scientists have known for 20 years that SMN is necessary
in every
cell of the body, since disrupting the
gene in a mouse
causes early embryonic death, before muscle or nerve
cells form.
Vogelstein, Kenneth Kinzler, and other colleagues found a minor change
in the APC
gene, which normally holds
cell growth
in check and can
cause colon cancers when mutated.
In another landmark success, scientists in Italy and the United States cured «bubble» babies who have a malfunctioning gene for the enzyme adenosine deaminase, which causes a buildup of toxic products that destroy immune cell
In another landmark success, scientists
in Italy and the United States cured «bubble» babies who have a malfunctioning gene for the enzyme adenosine deaminase, which causes a buildup of toxic products that destroy immune cell
in Italy and the United States cured «bubble» babies who have a malfunctioning
gene for the enzyme adenosine deaminase, which
causes a buildup of toxic products that destroy immune
cells.
In test tubes, this
gene caused the
cells to produce extra amounts of a chaperone molecule that ordinarily helps a
cell recognize misfolded proteins.
But
in the 1 September issue of the Journal of Clinical Investigation, cardiologist Michael Parmacek and his colleagues at the University of Chicago describe how they deleted two
genes from the common cold virus to make it unable to
cause any sniffling or fever, then replaced them with a marker
gene that turns out an easily detected protein and the SM22 promoter, which turns on expression of
genes in smooth muscle
cells that surround arteries.
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.
This question has been challenging to address experimentally because attempts to restore function to lost or mutated
genes in cancer
cells often trigger excess
gene activity,
causing other problems
in normal
cells.
Mutations
in at least 60
genes are known to
cause the disease, and many people are not diagnosed until after a a substantial proportion of photoreceptor
cells, the eye's rods and cones, have already degenerated and died.
Sickle
cell disease is a recessive genetic disorder
caused by a single mutation
in both copies of a
gene coding for beta - globin, a protein that forms part of the oxygen - carrying molecule hemoglobin.
The researchers found that the blond hair commonly seen
in Northern Europeans is
caused by a single change
in the DNA that regulates the expression of a
gene that encodes a protein called KITLG, also known as stem
cell factor.
But at the time, they thought it might take years to pinpoint the precise position of the
gene, sequence it, and understand how it
causes mutations to accumulate
in tumour
cells (This Week, 15 May).
In sickle cell disease, a mutation in the beta - globin gene causes hemoglobin to polymerize under low - oxygen conditions in body tissues, deforming red blood cell
In sickle
cell disease, a mutation
in the beta - globin gene causes hemoglobin to polymerize under low - oxygen conditions in body tissues, deforming red blood cell
in the beta - globin
gene causes hemoglobin to polymerize under low - oxygen conditions
in body tissues, deforming red blood cell
in body tissues, deforming red blood
cells.
In a report that appears in PLOS BIOLOGY, Dr. Hugo Bellen and his colleagues at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital and BCM, and Dr. Chao Tong, at the Life Sciences Institute and Innovation Center for Cell Biology, Zhejiang University in Hangzhou, China, find that mutations of human homologs (genes that carry out similar functions) of cacophony and its partner straightjacket (Cacna1a and Cacna2d2 respectively) cause defects in autophagy in neuron
In a report that appears
in PLOS BIOLOGY, Dr. Hugo Bellen and his colleagues at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital and BCM, and Dr. Chao Tong, at the Life Sciences Institute and Innovation Center for Cell Biology, Zhejiang University in Hangzhou, China, find that mutations of human homologs (genes that carry out similar functions) of cacophony and its partner straightjacket (Cacna1a and Cacna2d2 respectively) cause defects in autophagy in neuron
in PLOS BIOLOGY, Dr. Hugo Bellen and his colleagues at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital and BCM, and Dr. Chao Tong, at the Life Sciences Institute and Innovation Center for
Cell Biology, Zhejiang University
in Hangzhou, China, find that mutations of human homologs (genes that carry out similar functions) of cacophony and its partner straightjacket (Cacna1a and Cacna2d2 respectively) cause defects in autophagy in neuron
in Hangzhou, China, find that mutations of human homologs (
genes that carry out similar functions) of cacophony and its partner straightjacket (Cacna1a and Cacna2d2 respectively)
cause defects
in autophagy in neuron
in autophagy
in neuron
in neurons.
The researchers conducted genetic tests and found that many of the tumor
cells had a mutation
in a
gene called PPM1D, which
causes cells to proliferate and avoid natural death.
Klingelhutz and his team immortalized immature precursor fat
cells by adding
in two
genes from HPV (the virus that
causes cervical cancer) along with a
gene for part of an enzyme that controls the length of
cells» telomeres — the pieces of DNA that protect chromosome tips from deterioration.
In a study of mice, they found that they could correct the mutated gene that causes a rare liver disorder, in 6 percent of liver cells — enough to cure the mice of the disease, known as tyrosinemi
In a study of mice, they found that they could correct the mutated
gene that
causes a rare liver disorder,
in 6 percent of liver cells — enough to cure the mice of the disease, known as tyrosinemi
in 6 percent of liver
cells — enough to cure the mice of the disease, known as tyrosinemia.
The aberrant and ongoing activation of ERVs
caused an accumulation of retroviral proteins
in the affected
cells and deregulation of
genes and pathways.
«This is the first study to show the actual
cell behaviors
caused by mutations
in genes causally linked to polycystic kidney disease, an important new step
in the path towards treatment,» said Dr. Robert L. Bacallao, associate professor of medicine at the IU School of Medicine
in Indianapolis.
The body relies on
cells to process and store energy, and changes
in genes that regulate these functions can
cause an imbalance that leads to excessive energy storage and weight gain.
Researchers believe they have learned how mutations
in the
gene that
causes Huntington's disease kill brain
cells, a finding that could open new opportunities for treating the fatal disorder.
Other plans include using CRISPR to reverse blood disorders, such as sickle
cell anemia and beta thalassemia,
caused by mutations
in the hemoglobin
gene.
All of the diseases, which
cause the death of brain
cells involved
in controlling body movements, have recently been traced to specific
genes.
Previously, cancer researchers surmised that since chromosomal ends get swapped
in ALT, mutation of
genes that restrain DNA exchange, a process scientists call recombination, might actually
cause the condition (or, to extend the ping - pong metaphor, make
cells lose paddle control).
But stem
cell biologist and physician Michele De Luca of the University of Modena and Reggio Emilia
in Italy and his colleagues have been developing a way to counteract an EB -
causing mutation by inserting a new
gene into the
cells used for grafts.
Other researchers have long been concerned that using a retrovirus to insert
genes at random points
in cells» genomes might
cause cancer.
A fault
in the CHM
gene causes choroideremia,
in which
cells in the retina stop working and slowly die, leading to blindness.
By activating the Ret receptor, the scientists were able to prevent
in flies and human
cell cultures the degeneration of mitochondria, which is
caused by a
gene defect related to Parkinson's disease.
SMA is
caused by a mutation
in a
gene that is vital for the survival of nerve
cells that connect the brain and spinal cord to the muscles, known as motor neurons.
«You don't want to just turn down methylation globally, which would result
in over-activation of all
genes in the
cell, but demethylating some of these
gene promoter regions selectively could revive an immune system muted by cancer -
causing viruses,» Kuss - Duerkop says.
The transposon inserts itself almost randomly into the host
cell's chromosomes, and thus, it could land
in the middle of a desirable
gene and
cause a harmful mutation.
Myc is a cancer -
causing gene responsible for disrupting the normal 24 - hour internal rhythm and metabolic pathways
in cancer
cells, found a team led by researchers from the Perelman School of Medicine at the University of Pennsylvania.
A single spelling error
in this
gene causes the loss of the inner ear's hair
cells over time.
In this case, the
gene variation has dramatic effects on the fat
cells on women's abdomens and hips,
causing the
cells to become larger but fewer.
Similarly, carriers
in the Jackson study of one copy of the
genes that
cause sickle -
cell disease — a useful trait against malaria
in Africa — appear to be more at risk for kidney disease.
In this study, by using a systemic mtEF4 gene knockout mouse model, researchers found that mtEF4 knockout damages the oxidative phosphorylation function in germ cells of male mice, thus causing male sterilit
In this study, by using a systemic mtEF4
gene knockout mouse model, researchers found that mtEF4 knockout damages the oxidative phosphorylation function
in germ cells of male mice, thus causing male sterilit
in germ
cells of male mice, thus
causing male sterility.
Mutations
in mitochondrial
genes often
cause neurological conditions because nerve
cells need high levels of energy for their function.