Sentences with phrase «cell survival by»

p70S6K, a key element of mTOR pathway, promotes cell growth by inducing protein synthesis and cell survival by phosphorylating (inactivating) the proapoptotic protein BAD (31, 32).

Calorie restriction promotes mammalian cell survival by inducing the SIRT1 deacetylase Science.

Bcl - 2 proteins play a key role in cell survival by protecting against a form of cell suicide known as apoptosis.

Rather, the group speculates that the transplanted cells secreted protective neurotrophins, proteins that promote cell survival by keeping neurons from inducing apoptosis (programmed cell death).

Not exact matches

By discovering more about their survival tricks, the researchers hope to learn more ways to protect human cells from damage.

To ensure survival of the cells, the blood vessels must be manufactured by the printing process.

A Canadian study published this year around the same time titled «Coconut oil protects cortical neurons from amyloid beta toxicity by enhancing signaling of cell survival pathways» observed that coconut oil and its medium chain fatty acids (MCFAs) protect against amyloid beta (Aβ) induced neurotoxicity in primary rat cortical neurons.

Survival: By week 24, your baby has a 25 percent chance of surviving outside the womb, thanks to the production of white blood cells and the partial development of baby's lungs.

Boldrini says that future research on the aging brain will continue to explore how neural cell proliferation, maturation, and survival are regulated by hormones, transcription factors, and other inter-cellular pathways.

Columbia University biologists have revealed a mechanism by which bacterial cells in crowded, oxygen - deprived environments access oxygen for energy production, ensuring survival of the cell.

The work could help make marrow transplants more effective by improving the survival of transplanted cells.

The tumor - cell survival factors uncovered by this study might one day be targeted with drugs to further diminish people's risk of metastasis.

However, as has been discovered by a team of Frankfurt - based researchers, these cells do have a weakness: In the current edition of the high impact journal «Cancer Research,» they report that the enzyme 5 - lipoxygenase (5 - LO) plays a significant role in the survival of leukaemic AML stem cells.

Later, it was learned that the drug actually works by blocking an enzyme (thymidylate synthase) that the cells need for survival.

In the study, exosomes, which are generated by all cells and are naturally present in blood, were modified as «iExosomes,» capable of delivering small RNA to specifically target mutant KRAS, resulting in disease suppression and increased overall survival in mouse models.

Using the same computer - based approach, the team has now been able to target the c - FLIP (cellular FLICE [FADD - like IL - 1β - converting enzyme]- inhibitory) protein, known to play a key role in cancer stem cell maintenance and survival, described in previously published work by the Institute.

By tinkering with the medium in which cells are grown, researchers at the Salk Institute for Biological Studies created a type of stem cell with a survival rate of 30 to 40 percent, vs. 1 percent.

First, it would necessarily involve denying cancerous cells access to some tool that is absolutely indispensable to their survival, so that they couldn't just make up for its loss by tweaking some other gene expression pathway through mutating its other genes.

By assessing the survival of the cells that engulf the particles and measuring the levels of red or green light that they emitted, the researchers determined which formulation of particles performed best, then tested that formulation in mice with human brain cancer derived from their patients.

Among patients with non-small cell lung cancer (NSCLC) fueled by ALK gene alterations who were being treated with crizotinib (Xalkori), a decrease in the number of circulating tumor cells (CTCs) harboring increased copies of the ALK gene over the first two months of treatment was associated with increased progression - free survival.

Rapamycin works by inhibiting mTOR, which is involved in cell survival and proliferation.

It indicates that the interaction with mitochondria is driven by Toxoplasma, rather than the host cell, and it is likely something the parasite does «to enable survival in some particular subset of hosts,» he says.

«This remodeling process of the cell proteome by autophagy is an important immune - suppressive survival mechanism for Ras - driven cancers, and inhibiting autophagy can provide a means to target these aggressive cancers,» notes White, who is also a distinguished professor of molecular biology and biochemistry at Rutgers School of Arts and Sciences.

However, tumor cells can circumvent this immune defense by establishing a surrounding microenvironment that prevents the infiltration of NK cells and thus promotes tumor survival and growth.

Combining their strategy with an existing immunotherapy treatment that works by releasing the «brakes» on immune cells, they found they could shrink melanoma tumors, and prolong survival in preclinical models for melanoma.

Oligodendrocytes, the cells that are known to produce the myelin sheaths which enable saltatory conduction of action potentials along the myelinated axons, are modulators of signal transmission along neuronal connections (axons) and also promote neuronal survival by providing metabolic support.

By performing experiments in petri dishes and with mice, they found that panobinostat, a drug designed to change the way cells regulate genes, may be effective at inhibiting DIPG growth and extending survival rates.

Small molecules called metabolites mediate a cell's survival, and metabolite production is fine - tuned by genes that indirectly sense metabolite levels.

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.

Previous studies from these researchers have showed that FL118 induces cancer cell death, or apoptosis, by inhibiting expression of multiple cell - survival proteins (survivin, Mcl - 1, XIAP or cIAP2).

«These findings could lead to a new therapeutic strategy for patients with AML and potentially other diseases by targeting patients whose leukemia cells display activation of a specific survival pathway.»

Following introduction into mammalian hosts (including humans) by the bite of a sand fly, Leishmania parasites undergo extensive changes to adapt to survival and multiplication inside the new host cells and tissues.

An international study led by scientists from the Crick Institute in London and the Hebrew University of Jerusalem revealed a survival mechanism in cancer cells that allows the disease to erupt again even after aggressive treatment.

«By identifying CD151 and its underlying role in cancer cell survival, we hope to develop a therapy to target it.

Cancer tumours manipulate a natural cell process to promote their survival suggesting that controlling this mechanism could stop progress of the disease, according to new research led by the University of Oxford.

Those cells escape from the apoptosis process by activating a cell - survival mechanism called autophagy.

Astrocytes, one type of glial cells are the supporting cells for survival and function of neurons in the brain by secreting many kinds of neuroprotective molecules.

She also noted the targeting Msi in primary tumors significantly changed «the trajectory of progression by halting pancreatic cancer growth and improving survival,» inhibiting both cancer stem cells and other tumor cells.

The results were that BES enhanced cell survival and prevented the apoptosis of NPCs caused by growth factor deprivation.

By identifying the molecular signals emitted through the soil by friendly fungi, the protein enables a plant to «roll out the red carpet» for cell colonisation by the fungi, and all the survival advantages this mutually - beneficial relationship brings — the fungi feeds minerals such as phosphate into plant cells in return for sugar extractioBy identifying the molecular signals emitted through the soil by friendly fungi, the protein enables a plant to «roll out the red carpet» for cell colonisation by the fungi, and all the survival advantages this mutually - beneficial relationship brings — the fungi feeds minerals such as phosphate into plant cells in return for sugar extractioby friendly fungi, the protein enables a plant to «roll out the red carpet» for cell colonisation by the fungi, and all the survival advantages this mutually - beneficial relationship brings — the fungi feeds minerals such as phosphate into plant cells in return for sugar extractioby the fungi, and all the survival advantages this mutually - beneficial relationship brings — the fungi feeds minerals such as phosphate into plant cells in return for sugar extraction.

A major reason for poor survival rates is late diagnoses, by which time the cancer cells have spread to secondary sites.

Hsp90 inhibitors are among several innovative new types of treatment designed to attack cancer indirectly, by destabilising multiple different proteins required for the growth and survival of cancer cells.

He managed to switch on a survival mode in bone cells by inactivating the oxygen sensor PHD2 before implantation.

A new study by a Cornell University researcher found this coating is especially thick and pronounced on cancer cells and is a crucial determinant of the cell's survival.

Myc is a critical gene in governing cell proliferation and survival, activities that it carries out by regulating the expression of other genes involved in cell metabolism.

The human genome contains around 20,000 genes, by refining CRISPR - Cas9 technology and using it to screen the leukemia genome the team uncovered a catalogue of approximately 500 genes that are essential for cancer cell survival, including more than 200 genes for which drugs could be designed.

Scientists from KU Leuven, Belgium, have now improved survival of these bone cells by preconditioning them to withstand the harmful environment before implantation.

Because cancer cells acquire mutations in oncogenes — genes that can transform cells into cancer cells — to support their growth and survival, a great deal of research has focused on identifying oncogenes that could be targeted by cancer drugs.

The research team discovered how the parasite hijacks the host cell to enable its own growth and survival, hibernating for decades by creating its own food reserve.

Using induced pluripotent stem cells (iPSCs), a team led by Mount Sinai researchers has gained new insight into genetic changes that may turn a well known anti-cancer signaling gene into a driver of risk for bone cancers, where the survival rate has not improved in 40 years despite treatment advances.