Acute energy deprivation affects skeletal muscle protein synthesis and associated
intracellular signaling proteins in physically active adults
The study, published in the journal PLOS Genetics, focuses on the large,
intracellular signaling protein RPM - 1 that is expressed in the nervous system.
Not exact matches
«In the case of glycoprotein hormone receptors, the family of
proteins that includes the thyroid receptor, upon binding of the extracellular hormone, the intramolecular activator (p10) induces structural changes of the receptor
protein, triggering activation of the
intracellular signaling cascade.»
Several target molecules have also been identified in
intracellular signalling pathways and in cell survival
proteins.
In the study published in Nucleic Acids Research, the researchers were able to induce and inhibit the expression of genes in mammalian cell cultures and were able to regulate
intracellular protein levels using light
signals.
In a paper published in the Journal of Neuroscience, the OIST Cell
Signal Unit, led by Professor Tadashi Yamamoto, reported that mice lacking an
intracellular trafficking
protein called LMTK3, are hyperactive.
«
Intracellular signaling depends on these
protein modifications — so by doing these analysis, we know not only what's in the cell, but also how the cell organizes and communicates internally.»
Timothy Springer, with colleagues Michael L. Dustin and Charles A. Dinarello, identifies and characterizes adhesion molecules, a class of cell surface
proteins that function in the interactions of immune cells with other cells, including antigen - specific recognition and cell trafficking: integrin LFA - 1 involved in cytoskeleton and
signaling, and
intracellular adhesion molecules (ICAMs), which are binding partners (ligands) for LFA - 1 and are increased in inflammatory and autoimmune disease.
The alpha subunit of the heterotrimeric G -
protein (Galpha) can then interact with
intracellular partners and propagate the
signal into the cell.
Recently, interest has developed regarding the possibility of targeting
intracellular inhibitory
proteins to improve T cell activity against cancer, including diacylglycerol kinase ζ (DGKζ)(9, 10) and Casitas b - lineage proto - oncogene b (Cbl - b)(11), which attenuate
signal transduction events downstream of the TCR and CD28.
At these concentrations, GDF5 promotes neurite growth and activates
intracellular Smad
signalling to a similar order of magnitude through a common bone morphogenetic
protein (BMP) receptor (BMPR)- dependent mechanism in these two cell models.
There is also another mechanism by which cellular amino acid nutrition impacts on mTOR
signalling; this involves the amino acids generated within the lysosomes by
intracellular protein degradation and autophagosomal digestion [23,24].
With similar precision, Professor Bargmann has also identified many of the
intracellular signalling pathways in C. elegans that relay information from cell surface odorant receptors (G
protein - coupled receptors) to the interior of each sensory neuron.
Fluorescence - based assays Fluorescent markers such as EGFP, YFP, mCherry and mTomato or fluorescent biosensors can be used to measure a variety of real - time cell - based activities, including,
intracellular transport,
protein signaling, receptor desensitization, migration, division, apoptosis, metabolism, differentiation, chemotaxis, transcription and translation.
Although a non - essential amino acid in normal cells, the demand for glutamine is dramatically increased throughout malignant transformation to support increased metabolic demands; namely, provision of catabolic substrates for ATP production and anabolic substrates for macromolecule biosynthesis.The
intracellular glutamine pool is also critical for sustained activation of mTORC1
signalling, a master regulator of cell growth and
protein translation, as well as prevention of apoptosis
These include insoluble extracellular plaques made of beta - amyloid peptide (Aβ);
intracellular neurofibrillary tangles (NFTs) resulting from the hyperphosphorylation of tau (a microtubule - associated
protein); loss of hippocampal neurons; a decrease in production of brain acetylcholine; and a marked decline in glucose usage in regions of the brain associated with memory and learning.5,11,20 - 22 All of these changes can be logically explained as the sequelae resulting from long - term dysregulation of insulin
signaling and glucose metabolism.
This response seems to happen because the continued rise of
intracellular amino acid levels
signal to limit the rate of
protein breakdown.4 It is thought that this
signal to decrease breakdown is due to the action of insulin and has no limit, as
protein breakdown will continue to decrease with ever increasing
protein intake.
While it is true that amino acids were long considered simply substrates for
protein synthesis, they have more recently shown to also act as modulators of
intracellular signal transduction pathways that are typically associated with growth - promoting hormones such as insulin and IGF - 1.
Although no changes in AMPK activity were observed, decreased
intracellular signaling occurred with a concomitant decrease in skeletal muscle
protein synthesis.