We observed considerable overlap of the identified phosphoproteomes among our study and the mouse tissue study.
Also consistent with our mouse tissue studies, Gpr119 responses in human colon were only blocked by the Y1 receptor antagonist, BIBO3304.
In contrast, Txnip expression was significantly increased by fasting in Gpr50−/− mice in all tissues studied (P <.01, WAT and BAT PP <.001, liver).
Eight genes (Fkbp5, Irak1, Mobp, Dlk1, Plagl1, Ddc, Mllt2h, and Eya2) had significantly stronger expression in KO mice in all the tissues studied.
Remarkably, the gene density heatmaps showed that AC5 KO has a remarkable similarity to CR mice in all four tissues studied, with the best correlations in heart and skeletal muscle.
In summary, we propose a list of 13 genes that constitute a constitutive AHR gene battery, at least in the tissues studied, in mice and rats (Agt, Car3, Creg1, Ctsc, E2f6, Enpp1, Gatm, Gstm4, Kcnj8, Me1, Pdk1, Slc35a3, and Sqrdl).
We studied mouse tissues because the nuclei of all mouse cells have prominent chromocenters which are convenient for the microscopic approach.
In order to examine the function of Dpr1 in adult mouse tissues, in this study, we generated the conditional Dpr1-knockout mice and found that loss of Dpr1 gene in the central nervous system resulted in the neurodegenerative disorder resembling the autophagy-deficient mice.
We identified several phosphorylation sites known to be important to the actions of insulin and growth factor signaling in general, such as the activating T loop phosphorylation site of Akt (T308) and the hydrophobic motif (HM) of Akt1 (S473) not identified in the mouse tissue phosphoproteome study.
After optimizing an ACE2 assay in mouse tissue, this study found that the sex difference in basal ACE2 activity is selective for the kidney; males have higher renal ACE2 activity than females whereas, under normal conditions, no sex differences in ACE2 activity were detected in the heart and lung.
