These physical effects lead to cell signaling pathways for
enhanced cell survival.
The results were that BES
enhanced cell survival and prevented the apoptosis of NPCs caused by growth factor deprivation.
Loss of PTPN12 Stimulates Progression of ErbB2 - Dependent Breast Cancer by
Enhancing Cell Survival, Migration, and Epithelial - to - Mesenchymal Transition.
Not exact matches
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.
«In animal studies, exercise has been shown to specifically affect the hippocampus, significantly increasing the growth of new neurons and
cell survival,
enhancing memory and learning, and increasing molecules that are involved in the plasticity of the brain,» Chaddock said.
When optimal temperatures are restored, the plant stem
cells can divide at a faster rate, which will in turn
enhance recovery and
survival of the plant.»
In order to learn more about how celecoxib was
enhancing stem
cell survival and wound healing, the researchers conducted experiments to identify the cytokines or enzymes directly or indirectly influencing the process.
The research team, spearheaded by postdoctoral fellow Yajie Liang, Ph.D., wondered whether the
cells»
survival could also be
enhanced with steady doses of a compound called basic fibroblast growth factor (bFGF), an «energy drink» that spurs
cells to grow.
The transcription factor Runx3
enhances the differentiation and
survival of CD8 + resident memory T
cells;
enhancing Runx3 expression in responding T
cells could lead to better therapies for infection and cancer.
The mechanism for this markedly
enhanced effect appears to be increased
cell survival and retention.
Importantly, while the
enhanced presence of Bcl - xL is expected to promote cancer
cell survival in the first place, it may also indicate that the apoptotic machinery (especially the caspases) are still in place, making it necessary for the tumor
cell to maintain a high level of Bcl - xL [10].
Researchers have discovered that inducing quiescence in stem
cells may be an effective means to
enhance stem
cell survival
Strikingly, this cancer
cell subpopulation displayed
enhanced expression of Bcl - xL, strongly suggesting that the upregulation of this antiapoptotic protein also supports the
survival of invasive cancer
cells within patients.
Moreover, the proapoptotic gene products BBC3 / Puma and BCL2L11 / Bim were downregulated in mesenchymal
cells, possibly contributing further to their
enhanced survival.
• Keeping abnormal proteins from building up and potentially shutting down major organs (heart, liver and nervous system, to name a few) • Protecting the brain's functions of learning and memory against neurotransmitter toxicity • Activating or increasing the activity of proteins that promote the initial growth, maintenance and
survival of brain neurons •
Enhancing the movement of proteins, lipids and other
cell parts through the cytoplasm of
cell bodies.
ORAI1 Deficiency Impairs Activated T
Cell Death and
Enhances T
Cell Survival.
Direct Transcriptional Up - regulation of Cyclooxygenase - 2 by Hypoxia - Inducible Factor (HIF)-1 Promotes Colorectal Tumor
Cell Survival and
Enhances HIF - 1 Transcriptional Activity during Hypoxia
Thus apart from direct cytotoxic effect, the exposure of cancer
cells to therapeutic doses of radiation also
enhances the
survival and proliferation of a fraction of
cells which ultimately leads to radiation resistance and therapeutic inefficacy.
Significant advancements have been made in the bioprocessing of hPS
cells including the formulation of new
cell culture media, the development of extracellular and acellular matrices that can replace feeder
cells, the development of new enzymes for passaging and the discovery of small molecules that significantly
enhance the
survival and clonogenicity of dissociated
cells, allowing single
cell cryopreservation.
Vignali and his colleagues used a variety of molecular and cellular techniques to show that Sema4a binding to Nrp1 turns on a biochemical pathway in mouse regulatory T
cells that
enhances their function, stability and
survival.
We then evaluated whether the encapsulation of hPSC - CDH5 +
cells in PA - RGDS could
enhance long - term
cell survival and vascular regenerative effects in a hind - limb ischemia model with laser Doppler perfusion imaging, bioluminescence imaging, real - time reverse transcription - polymerase chain reaction, and histological analysis.
In breast cancer
cells, the ABL kinases activated the transcriptional coactivator TAZ and the transcription factor STAT5, which triggered the transcription of genes encoding factors that activate osteoclasts (
cells that break down bone) and those that
enhance the
survival of breast cancer
cells in the bone microenvironment.