3 research outputs found
Profiling of Protein <i>O</i>‑GlcNAcylation in Murine CD8<sup>+</sup> Effector- and Memory-like T Cells
During
an acute infection, antigenic stimulation leads to activation,
expansion, and differentiation of naïve CD8<sup>+</sup> T cells,
first into cytotoxic effector cells and eventually into long-lived
memory cells. T cell antigen receptors (TCRs) detect antigens on antigen-presenting
cells (APCs) in the form of antigenic peptides bound to major histocompatibility
complex I (MHC-I)-encoded molecules and initiate TCR signal transduction
network. This process is mediated by phosphorylation of many intracellular
signaling proteins. Protein <i>O</i>-GlcNAc modification
is another post-translational modification involved in this process,
which often has either reciprocal or synergistic roles with phosphorylation.
In this study, using a chemoenzymatic glycan labeling technique and
proteomics analysis, we compared protein <i>O</i>-GlcNAcylation
of murine effector and memory-like CD8<sup>+</sup> T cells differentiated <i>in vitro</i>. By quantitative proteomics analysis, we identified
445 proteins that are significantly regulated in either effector-
or memory-like T cell subsets. Furthermore, qualitative and quantitative
analysis identified highly regulated protein clusters that suggest
involvement of this post-translational modification in specific cellular
processes. In effector-like T cells, protein <i>O</i>-GlcNAcylation
is heavily involved in transcriptional and translational processes
that drive fast effector T cells proliferation. During the formation
of memory-like T cells, protein <i>O</i>-GlcNAcylation is
involved in a more specific, perhaps more targeted regulation of transcription,
mRNA processing, and translation. Significantly, <i>O</i>-GlcNAc plays a critical role as part of the “histone code”
in both CD8<sup>+</sup> T cells subgroups
Profiling of Protein <i>O</i>‑GlcNAcylation in Murine CD8<sup>+</sup> Effector- and Memory-like T Cells
During
an acute infection, antigenic stimulation leads to activation,
expansion, and differentiation of naïve CD8<sup>+</sup> T cells,
first into cytotoxic effector cells and eventually into long-lived
memory cells. T cell antigen receptors (TCRs) detect antigens on antigen-presenting
cells (APCs) in the form of antigenic peptides bound to major histocompatibility
complex I (MHC-I)-encoded molecules and initiate TCR signal transduction
network. This process is mediated by phosphorylation of many intracellular
signaling proteins. Protein <i>O</i>-GlcNAc modification
is another post-translational modification involved in this process,
which often has either reciprocal or synergistic roles with phosphorylation.
In this study, using a chemoenzymatic glycan labeling technique and
proteomics analysis, we compared protein <i>O</i>-GlcNAcylation
of murine effector and memory-like CD8<sup>+</sup> T cells differentiated <i>in vitro</i>. By quantitative proteomics analysis, we identified
445 proteins that are significantly regulated in either effector-
or memory-like T cell subsets. Furthermore, qualitative and quantitative
analysis identified highly regulated protein clusters that suggest
involvement of this post-translational modification in specific cellular
processes. In effector-like T cells, protein <i>O</i>-GlcNAcylation
is heavily involved in transcriptional and translational processes
that drive fast effector T cells proliferation. During the formation
of memory-like T cells, protein <i>O</i>-GlcNAcylation is
involved in a more specific, perhaps more targeted regulation of transcription,
mRNA processing, and translation. Significantly, <i>O</i>-GlcNAc plays a critical role as part of the “histone code”
in both CD8<sup>+</sup> T cells subgroups
Boron-Doped Graphite for High Work Function Carbon Electrode in Printable Hole-Conductor-Free Mesoscopic Perovskite Solar Cells
Work function of
carbon electrodes is critical in obtaining high open-circuit voltage
as well as high device performance for carbon-based perovskite solar
cells. Herein, we propose a novel strategy to upshift work function
of carbon electrode by incorporating boron atom into graphite lattice
and employ it in printable hole-conductor-free mesoscopic perovskite
solar cells. The high-work-function boron-doped carbon electrode facilitates
hole extraction from perovskite as verified by photoluminescence.
Meanwhile, the carbon electrode is endowed with an improved conductivity
because of a higher graphitization carbon of boron-doped graphite.
These advantages of the boron-doped carbon electrode result in a low
charge transfer resistance at carbon/perovskite interface and an extended
carrier recombination lifetime. Together with the merit of both high
work function and conductivity, the power conversion efficiency of
hole-conductor-free mesoscopic perovskite solar cells is increased
from 12.4% for the pristine graphite electrode-based cells to 13.6%
for the boron-doped graphite electrode-based cells with an enhanced
open-circuit voltage and fill factor