# |
PMID |
Sentence |
1 |
27965446
|
C. muridarum, but not C. trachomatis, inclusions attract several markers of cell-autonomous immunity, including the ubiquitin-binding protein p62, the ubiquitin-like protein LC3, and guanylate-binding protein 1.
|
2 |
26043155
|
TNFAIP3 promotes survival of CD4 T cells by restricting MTOR and promoting autophagy.
|
3 |
26043155
|
TNFAIP3/A20 is a ubiquitin-editing enzyme that is thought to be a negative regulator of autophagy in cell lines.
|
4 |
26043155
|
To determine whether TNFAIP3 regulates autophagy in CD4 T cells, we first analyzed Tnfaip3-deficient naïve CD4 T cells in vitro.
|
5 |
26043155
|
We demonstrated that Tnfaip3-deficient CD4 T cells exhibited reduced MAP1LC3/LC3 (microtubule-associated protein 1 light chain 3) puncta formation, increased mitochondrial content, and exaggerated reactive oxygen species (ROS) production.
|
6 |
26043155
|
These results indicate that TNFAIP3 promotes autophagy after T cell receptor (TCR) stimulation in CD4 T cells.
|
7 |
26043155
|
Taken together, our findings illustrate that TNFAIP3 restricts MTOR signaling and promotes autophagy, providing new insight into the manner in which MTOR and autophagy regulate survival in CD4 T cells.
|
8 |
24997049
|
Exposure of cultured microglia and macrophages to IFN-γ abrogated subsequent IL-10 induction by HSPB5, and strongly promoted HSPB5-triggered release of TNF-α, IL-6, IL-12, IL-1β and reactive oxygen and nitrogen species.
|
9 |
24997049
|
In addition, high levels of CXCL9, CXCL10, CXL11, several guanylate-binding proteins and the ubiquitin-like protein FAT10 were induced by combined activation with IFN-γ and HSPB5.
|
10 |
24997049
|
Together, our data suggest that inflammatory demyelination during MS is selectively associated with IFN-γ-induced re-programming of an otherwise protective response of microglia and macrophages to the endogenous TLR2 agonist HSPB5.
|
11 |
24478392
|
Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice.
|
12 |
24478392
|
Synergistic effect of interferon-gamma and tumor necrosis factor-alpha on coxsackievirus and adenovirus receptor expression: an explanation of cell sloughing during testicular inflammation in mice.
|
13 |
24478392
|
Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility.
|
14 |
24478392
|
Interferon-gamma (IFNG) and tumor necrosis factor alpha (TNF) are two major cytokines that are elevated during testicular inflammation and cause reduced fertility.
|
15 |
24478392
|
We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion.
|
16 |
24478392
|
We investigated the mechanism by which IFNG and TNF exert their disruptive effects on testicular cell adhesion.
|
17 |
24478392
|
We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels.
|
18 |
24478392
|
We have demonstrated that combined treatment with IFNG and TNF (IFNG+TNF) exerts a synergistic effect by downregulating CAR mRNA and protein levels.
|
19 |
24478392
|
Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact.
|
20 |
24478392
|
Immunofluorescence staining revealed that IFNG+TNF treatment effectively removes CAR from the site of cell-cell contact.
|
21 |
24478392
|
Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways.
|
22 |
24478392
|
Using inhibitor and co-immunoprecipitation, we confirmed that IFNG+TNF mediates CAR protein degradation via ubiquitin-proteasome and NFKB pathways.
|
23 |
24478392
|
Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact.
|
24 |
24478392
|
Blockage of ubiquitin-proteasome pathway significantly inhibits CAR degradation, as indicated by the reappearance of CAR at the site of cell-cell contact.
|
25 |
24478392
|
Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation.
|
26 |
24478392
|
Additionally, IFNG+TNF reduces CAR mRNA via transcriptional regulation.
|
27 |
24478392
|
Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription.
|
28 |
24478392
|
Mutational studies have shown that IFNG+TNF-induced CAR repression is achieved by suppression of the basal transcription.
|
29 |
24478392
|
Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region.
|
30 |
24478392
|
Electrophoretic mobility shift assay and chromatin immunoprecipitation assays further confirmed that IFNG+TNF treament not only inhibits binding of the basal transcription factors but also promotes binding of NFKB subunits and Sp1 (negative regulators) to the CAR promoter region.
|
31 |
24478392
|
Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation.
|
32 |
24478392
|
Taken together, IFNG+TNF treatment significantly downregulates CAR expression, which provides an explanation of how cell sloughing in the epithelium mediates, by loss of CAR-based cell adhesion, during testicular inflammation.
|