At any given time, the liver is releasing a constant supply of amino acids to skeletal muscle for maintaining blood sugar levels and supporting
cellular protein homeostasis.
Not exact matches
Therefore, cells have developed another strategy to get rid of faulty mitochondrial
proteins and maintain
cellular homeostasis,» says Park.
Identification of
proteins that regulate
cellular homeostasis of lipids and
proteins (Carvalho group, Science 2014, J Cell Biol 2015, EMBO J 2016).
The
protein may play a role in the regulation of renal and intestinal calcium and phosphate transport, cell metabolism, or
cellular calcium / phosphate
homeostasis.
The researchers found that loss of collagen VII not only affected the composition of the
cellular microenvironment but also led to global changes in cell
homeostasis on mRNA and on
protein level.
Certain particle compounds may directly generate ROS in vivo because of their surface chemistry (eg, metals, organic compounds, and semiquinones) or after bioactivation by cytochrome P450 systems (eg, polycyclic aromatic hydrocarbon conversion to quinones).6, 290 a, 290 b A particle surface or anions present on otherwise more inert particles may disrupt iron
homeostasis in the lung and thereby also generate ROS via Fenton reactions.291 Other PM constituents may do so indirectly by the upregulation of endogenous
cellular sources (eg, nicotinamide adenine dinucleotide phosphate [NADPH]-RRB- oxidase) 292,293 or by perturbing organelle function (eg, mitochondria) by taken - up PM components.261 Particle stimulation of irritant and afferent ANS fibers may also play a role in local and systemic oxidative stress formation.294 Given the rich antioxidant defenses in the lung fluid, secondarily generated oxidization products of endogenous molecules (eg, oxidized phospholipids,
proteins) or a reduction in endogenous antioxidants per se may be responsible at least in part for the state of oxidative stress in the lungs (along with instigating the subsequent
cellular responses) rather than ROS derived directly from PM and its constituents.
''... we hypothesize that repeated stress - related allostatic overload may affect brain function at three basic levels: (a) at the
cellular level, it may compromise proteostasis (e.g. tau
protein), organelles
homeostasis, and induce epigenetic changes in neuronal DNA; (b) at the tissue level it may affect intracellular communication (synaptic contacts), number of cells (reduction of neuronal density), composition of the extracellular matrix (accumulation of amyloid plaques), and neuroinflammation; (c) at the systemic levels it may alter the brain's regulation of behavior (cognitive decline).