FAT1 interacts with the E3 ligase MIB2. by Rui Li (4631)

ASFV-ΔI7L induces higher immune responses than does ASFV-WT in pigs. by Meilin Li (1832905)

Differential expression profiling in the ASFV-ΔI7L-infected primary porcine alveolar macrophages (PAMs) by RNA sequencing analysis. by Meilin Li (1832905)

The phosphorylation of Mas receptor and its induced-effects in <i>hGRK4</i> <i>γ</i> WT and 142V transgenic mice. by Lin Chen (54305)

Targeting of Vps34 reduces B16F10 tumor growth and working model for Vps34-dependent regulation of eTreg transitional heterogeneity and maintenance. by Erienne G. Norton (9612079)

pI7L suppresses the IFN-γ-triggered JAK-STAT signaling pathway. by Meilin Li (1832905)

The <i>I7L</i> gene is involved in ASFV pathogenicity in pigs. by Meilin Li (1832905)

The biological characteristics of the I7L protein (pI7L). by Meilin Li (1832905)

Mas Receptor Phosphorylation and its-mediated Effects in Renal Cortex of WKY Rats and SHRs. by Lin Chen (54305)

pI7L suppresses the IFN-<i>γ</i>-triggered JAK-STAT signaling pathway. by Meilin Li (1832905)

Vps34 orchestrates Treg function in vivo. by Erienne G. Norton (9612079)

Uvrag in Tregs is dispensable for establishment of immune tolerance and eTreg accumulation. by Erienne G. Norton (9612079)

pI7L inhibits the phosphorylation of STAT1 depending on its tyrosine at position 98. by Meilin Li (1832905)

Targeting of Vps34 or Atg14, but not Uvrag, in Tregs reduces tumor growth in mouse models. by Erienne G. Norton (9612079)

Loss of Vps34 reduces Treg suppressive function and is associated with the development of type-I-dominant inflammatory disease. by Erienne G. Norton (9612079)

Vps34 supports Treg maintenance in lymphoid and non-lymphoid tissues. by Erienne G. Norton (9612079)

“…Two-tailed Student <i>t</i> test (<b>A</b>–<b>D</b>, <b>F</b>–<b>I</b>) or Benjamini–Hochberg test (<b>E</b>); NS, not significant. Data are compiled from 15 (<b>A</b>, <b>F</b>), 12 (<b>B</b>), 5 (<b>C</b>, <b>G</b>, <b>I</b>), 6 (<b>D</b>, lung and liver; <b>H</b>), or 2 (<b>D</b>, colon LP) independent experiments. …”

Atg14 does not contribute to terminal eTreg generation during perinatal life. by Erienne G. Norton (9612079)

Chromatin accessibility analysis of perinatal Vps34-deficient Tregs. by Erienne G. Norton (9612079)

“…Relative (normalized to average control in each experiment) fold-change comparisons between genotypes in each cell type are shown in bold (<b>A</b>, <b>B</b>). Data are shown as mean ±  s.e.m. (<b>A</b>, <b>B</b>). Two-tailed Student <i>t</i> test (<b>A</b>, <b>B</b>, <b>I</b>), Benjamini–Hochberg test (<b>C</b>), Wilcoxon rank-sum test (<b>G</b>), Fisher’s exact tes<i>t</i> (<b>H</b>), or binomial test (<b>J</b>); NS, not significant. …”

Atg14 plays a cell-intrinsic role in orchestrating eTreg survival but not terminal differentiation. by Erienne G. Norton (9612079)

“…Pearson’s correlation (<b>A</b>), Benjamini–Hochberg test (<b>B</b>), two-tailed Student <i>t</i> test (<b>C</b>–<b>E, G</b>–<b>J</b>), or Fisher’s exact test (<b>F</b>); NS, not significant. Data are compiled from ≥2 (<b>C</b>, <b>E</b>) or 4 (<b>D</b>, <b>H</b>–<b>J</b>) independent experiments. …”

Atg14 deficiency in Tregs induces a type-I-dominant lymphoproliferative disease and cell-intrinsic reductions in eTregs. by Erienne G. Norton (9612079)