Sentences with phrase «cellular stress in»

«Cellular stress in the brain may contribute to non-alcoholic fatty liver disease: connection between cellular stress in brain and non-alcoholic fatty liver disease.»

The team examined tissues in mice for cellular stress following acute SD, and they also looked for cellular stress in aging mice.

While changes in insulin secretion are unlikely to play a major role in the acute effects of SD, cellular stress in pancreatic tissue suggests that chronic SD may contribute to the loss or dysfunction of endocrine cells, and that these effects may be exacerbated by normal aging, say the researchers.

Not exact matches

For instance, Evan's blue, a dye that stains the cellular protein albumin, penetrates the brain 10 times more efficiently in stressed mice than in unstressed mice.

They showed that ZIKV infection of cortical progenitors (stem cells for cortical neurons) controlling neurogenesis triggers a stress in the endoplasmic reticulum (where some of the cellular proteins and lipids are synthetized) in the embryonic brain, inducing signals in response to incorrect protein con - formation (referred to as «unfolded protein response»).

It's a first step in mechanistically understanding how cellular stress responses are wired in specific contexts.»

In response to cellular stress that can cause cancer, the team found that LC3, chromatin, and laminB1 migrate from the nucleus — via the nuclear blebs — into the cytoplasm and are eventually targeted for disposal.

Pancreas tissue from acutely sleep - deprived aged animals exhibited a marked increase in CHOP, a protein associated with cell death, suggesting a maladaptive response to cellular stress with age that was amplified by sleep deprivation.

«TIA - 1 is known for its ability to regulate gene expression during cellular stress,» says Hewett, who studies the processes that suppress the severe electrical storms in the brain, leading to seizures.

This metabolic demand makes brain cells particularly vulnerable to damage from oxidative stress, in which reactive oxygen species (ROS), sometimes called free radicals, exert toxic effects on cellular components.

However, Violanti stresses that his findings are preliminary, and that cellular phones can be useful in emergencies.

Now scientists have a clearer view of how ISRIB works — by pinning together parts of a protein involved in cellular stress.

In healthy cells constant growth can overwhelm cellular factories like the ER, leading to cell stress and death, but cancer cells manage to keep their factories running at high capacity to fuel non-stop growth.

A previous study by Segev at the laboratory for research of molecular and cellular mechanisms, directed by Prof. Kobi Rosenblum in the Sagol Department of Neurobiology at the University of Haifa, found a connection between a genetic condition known to be a risk factor for sporadic Alzheimer's and premature aging as manifested in ongoing metabolic stress.

In recent years, Blackburn has expanded on that initial work to show that these gauges of cellular health serve as barometers of environmental and emotional stress and predictors of various diseases.

The third parameter — the spatial distribution of NADH in the cells — shows how the mitochondria split and fuse in response to cellular growth and stress.

To the researchers» surprise, the mice subjected to both prenatal infection and stress during puberty showed far greater behavioral deficits and cellular changes in brain regions relevant to schizophrenia than those that had been exposed to infection or stress alone.

But what role does cellular stress play in the production of hemoglobin?

But until he understands how the cells are stressed in the first place, he won't know much: «We frankly don't have a clue as to how much microwave radiation is needed to cause irreversible damage to cellular proteins.

Her research team found that cellular oxidative stress (arising because of reactive oxygen species) increases in mice exposed to THS, damaging proteins, fats and DNA, and leading to hyperglycemia (excess glucose in the blood stream) and insulinemia (excess insulin in the blood)-- a condition also called insulin resistance.

However, excessive generation of ROS and / or a fall in antioxidant defences can lead to indiscriminate damage, resulting in cellular oxidative stress [27].

In the past 27 years, we have found that this cycling sugar modification of proteins — called O - linked N - acetylglucosamine, or O - GlcNAc — is nearly as common as protein phosphorylation and often competes with it at the same or proximal sites on proteins to regulate nearly every cellular process in response to nutrients and stresIn the past 27 years, we have found that this cycling sugar modification of proteins — called O - linked N - acetylglucosamine, or O - GlcNAc — is nearly as common as protein phosphorylation and often competes with it at the same or proximal sites on proteins to regulate nearly every cellular process in response to nutrients and stresin response to nutrients and stress.

«In a stressed intestinal environment,» the authors note, «retinoic acid, which was thought to lessen inflammation in the intestine, acted as an adjuvant that promoted rather than prevented inflammatory cellular and humoral responses to fed antigen.&raquIn a stressed intestinal environment,» the authors note, «retinoic acid, which was thought to lessen inflammation in the intestine, acted as an adjuvant that promoted rather than prevented inflammatory cellular and humoral responses to fed antigen.&raquin the intestine, acted as an adjuvant that promoted rather than prevented inflammatory cellular and humoral responses to fed antigen.»

Transcriptional regulatory networks in cellular responses and tolerance to dehydration and cold stresses.

Based on the previous evidences, it rusults important to maintain cellular NAD + availability especially in mitochondria when stresses induce a major consumption of NAD + and ATP and prone the organism more susceptible to ROS damages.

This work aims to investigate, mechanistically, the molecular processes related to dysregulation of factors that normally protect the eye against oxidative stress, thus impairing RPE and photoreceptor cellular metabolism and their survival in AMD.

Their activity increases in response to heat, toxins, and various other forms of cellular stress, and dialing up the activity of heat shock proteins is involved in a number of methods demonstrated to slow aging in laboratory animals.

Inhibition of c - Abl with STI571 attenuates stress - activated protein kinase activation and apoptosis in the cellular response to 1 - β - d - arabinofuranosylcytosine.

Molecular characterization, expression analysis, and role of ALDH3B1 in the cellular protection against oxidative stress.

In particular, the cAMP signaling cascade directs adaptive cellular responses to a variety of stress stimuli via a combination of acute affects arising from GS - protein coupled receptor (GPCR)- mediated activation of PKA and long - term affects resulting from transcriptional reprogramming directed by CREB and the CREB Regulated Transcription Coactivators (CTRCs).

Current efforts focus on elucidating the role of molecular chaperones compartmentalized in mitochondria in regulating tumor bioenergetics, adaptation to cellular stress and cell survival.

Significantly, cellular pathologies including impaired cellular trafficking and an increase in oxidative stress, were reduced by treatment with the identified compound.

Telomere length predicts both cellular health and disease in rodent models and humans.8 Shorter telomeres predict onset of cardiometabolic diseases of aging.9 Chronic stress is associated with higher inflammation, shorter telomeres, and lower activity levels of telomerase, the cellular enzyme that elongates telomeric DNA.10, 11 Levels of amyloid beta (Aβ) proteins circulating in the blood appear to be stress - related in rodent models12 and may be affected by stress reduction, and greater Aβ42 / Aβ40 ratios are associated with lower risk of dementia.13

Altieri and his team are currently focused on three programs to understand the biology of survivin with respect to cell cycle progression, in particular, mitosis, cell survival and the cellular stress response and how exploiting these pathways may provide new cancer therapeutics.

«Nutrient scavenging by autophagy is a process that tumors hijack to meet their energetic requirements and to provide the necessary cellular building blocks for growth in a stressed tumor micro-environment» said White, «Preclinical models have demonstrated a critical role for autophagy in multiple cancer types.»

Unlike inanimate matter, cells contain molecular force generators that produce active contractile stresses in the cellular material.

of aberrant amyloid and tau in the retina, quantification of any neuronal degeneration, delineation of cellular stress responses of neurons and particularly glial cells, and investigation of oxidative stress.

The Keap1 - Nrf2 system has evolved to respond to intracellular oxidative stress; in particular the generation of reactive electrophiles produced from oxidation of endogenous cellular constituents as well as xenobiotics [2]--[4].

Scientists have known that, in organisms ranging in complexity from yeast to humans, different kinds of cellular stress — such as a backlog of unfolded proteins, DNA - damaging UV light, a shortage of the amino acid building blocks needed to make protein, viral infection, iron deficiency — trigger different enzymes to act downstream to switch off eIF2 alpha.

Analytical endpoints included examination... of aberrant amyloid and tau in the retina, quantification of any neuronal degeneration, delineation of cellular stress responses of neurons and particularly glial cells, and investigation of oxidative stress.

Trudu M, Schaeffer C, Riba M, Ikehata M, Brambilla P, Messa P, Martinelli - Boneschi F, Rastaldi MP, Rampoldi L. Early involvement of cellular stress and inflammatory signals in the pathogenesis of tubulointerstitial kidney disease due to UMOD mutations.

The researchers demonstrated that this stabilizes elF2B and helps it maintain protein production in the face of cellular stress.

In the absence of cellular oxidative stress, Nrf2 levels in the cytoplasm are maintained at low basal levels by binding to Keap1 and Cullin 3, which leads to the degradation of Nrf2 by ubiquitination [2], [5]--[9In the absence of cellular oxidative stress, Nrf2 levels in the cytoplasm are maintained at low basal levels by binding to Keap1 and Cullin 3, which leads to the degradation of Nrf2 by ubiquitination [2], [5]--[9in the cytoplasm are maintained at low basal levels by binding to Keap1 and Cullin 3, which leads to the degradation of Nrf2 by ubiquitination [2], [5]--[9].

In a study published March 29, 2018 in Science, UCSF biochemist Peter Walter, PhD, and structural biologist Adam Frost, MD, PhD, showed that the drug, ISRIB (pronounced «iz - rib»), acts like a molecular staple, pinning together parts of a much larger protein involved in cellular stresIn a study published March 29, 2018 in Science, UCSF biochemist Peter Walter, PhD, and structural biologist Adam Frost, MD, PhD, showed that the drug, ISRIB (pronounced «iz - rib»), acts like a molecular staple, pinning together parts of a much larger protein involved in cellular stresin Science, UCSF biochemist Peter Walter, PhD, and structural biologist Adam Frost, MD, PhD, showed that the drug, ISRIB (pronounced «iz - rib»), acts like a molecular staple, pinning together parts of a much larger protein involved in cellular stresin cellular stress.

We have also identified a transcriptional signature of aneuploidy that is associated with cellular stress and slow proliferation, and is found in aneuploid primary and cancer cells across a host of organisms.

Using these orthogonal measures of cellular pathway analysis, we confirmed that HPP - 4382, in contrast to bardoxolone, did not induce significant cellular stress at high doses as measured by HSPA6 expression and that the mechanism of HPP - 4382 activity does not appear dependent on NF - B as ICAM1 expression is not induced by HPP - 4382 (data not shown).

Characterizing the molecular pathways regulating genomic stability at damaged replication forks in HR - deficient cancers will increase our understanding of the cellular response to replicative stress, and in the same time, potentially allow the identification of new predictors (biomarkers) of chemo - sensitivity / resistance in these tumors (Figure 2B).

Previously, Walter's team discovered that ISRIB (short for «integrated stress response inhibitor») blocks this aspect of the cellular stress response by enhancing the activity of a protein called eIF2B, which helps keep a key protein production line operating in stressed cells.

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

Enhanced amyloidogenic processing of APP by the ß - site APP cleaving enzyme (BACE) and the γ - secretase complex and reduced clearance lead to increased intracellular levels of soluble oligomeric Aß, resulting in cellular dysfunction comprising e.g., synaptic failure, mitochondrial dysfunction, enhanced oxidative stress, neurotransmitter and neurotrophin depletion, inflammation, and apoptosis which is reflected in patients as clinical symptoms such as cognitive deficits [2, 3].