Measurements of body mass index (BMI) and adipose deposits. by Jessica C. M. Hui (20370522)

Role of YAP/TAZ in FAT1-regulated HNSCC growth. by Rui Li (4631)

Loss of FAT1 expression results in increased YAP/TAZ protein levels. by Rui Li (4631)

Quantification of fasting glucose, random glucose, and insulin levels. by Jessica C. M. Hui (20370522)

E3 ligase TRIM56 is up-regulated in response to CVB3 infection. by Yao Wang (102387)

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

S1 File - by Kimesh Loganathan Naidoo (19697486)

“…Of the 45 015 admissions analysed, 1237(2·75%) demised with significant decreases in admissions during all the lockdown levels, with the most significant mean monthly decrease of 450(95%, CI = 657·3, -244·3) p<0·001 in level 5 (the most severe) lockdown. …”

FAT1 and MIB2 control tumor growth <i>in vivo.</i> by Rui Li (4631)

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)

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)

TRIM56 promotes the ubiquitination and proteasomal degradation of CVB3 3D. by Yao Wang (102387)

Vps34 orchestrates Treg function in vivo. 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. …”

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

“…AP-1-related transcription factors with predicted decreased activity are labeled. See also <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.3003074#pbio.3003074.s015" target="_blank">S7 Table</a>. …”

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 orchestrates transcriptional and epigenetic remodeling events corresponding to terminal eTreg differentiation during perinatal life. by Erienne G. Norton (9612079)

“…Data are shown as mean ± s.e.m. (<b>D</b>). Wilcoxon rank-sum test (<b>A</b>, <b>B</b>; <b>J</b>, right), Benjamini–Hochbert test (<b>C</b>), two-tailed Student <i>t</i> test (<b>D</b>, <b>I</b>), Fisher’s exact test (<b>F</b>–<b>H</b>), or bionomial test (<b>J</b>, left); NS, not significant. …”

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

Analysis of Tregs from perinatal mice and mixed BM chimeras for transitional and terminal eTreg states. by Erienne G. Norton (9612079)

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

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