This work highlights some of the molecular modifications contributing to functional defects of human TIL.
Our results show extensive 5-HT signal modifications contributing to the cancer phenotype.
Novel findings implicate a role for epigenetic modifications contributing to the progression of fibrosis by alteration of gene expression profiles.
The most documented modifications contributing to this phenotype involve profound modifications of cell-wall biosynthesis including increased cell-wall thickness, cross-linking, or accumulation of cell-wall components [ 11, 27].
To identify additional modifications contributing to REDD1 maintenance, we selected two human acute T-cell leukemia and chronic myeloid leukemia lines (JA3 and K562, respectively) expressing high endogenous REDD1 levels, and exposed both to pro- and anti-proliferative stimuli.
The achieved high mass-resolving power and high mass accuracy allows for comprehensive, in-depth, and detailed parallel characterization of various modifications, contributing to our understanding of protein functioning in general.
