GPR68 inhibited nucleus or ER to exosome non-protein based circadian exercise based on Thalamus big data

Abstract

Abstract G protein-coupled receptor (GPR68) is widely distributed in the human body and participates in various physiological and pathological processes. The main GPR68-inhibited and -activated molecular network was constructed in Thalamus from GDS2678 of NCBI by integrating SAM, SPSS Pearson and GRNInfer mutual positive verification based on richness. The main GPR68 inhibited molecular subnetwork composed of upstream ALG8, or MAF, feedback SMA4, and downstream GSTM3_1 with TYMS. GPR68 activated molecular subnetwork contained upstream RAD50, feedback SPAG9, and downstream RFK. The relationship of SMA4 inhibition to SPAG9 -> MAF -> RAD50 -> ALG8 was found in Thalamus for negative main molecular verification. The relationship of ALG8 activation to SMA4 -> GSTM3_1 -> TYMS -> MAF in Thalamus for positive main molecular verification. Our results show GPR68 inhibited SMA4-nucleoplasm RNA splicing coupling ALG8, or MAF-nucleus sequence specific DNA binding, or ER amino acid glycosylation to GSTM3_1 with TYMS-extracellular exosome small molecule-based circadian exercise, and GPR68 activated SPAG9-integral component of membrane kinesin binding coupling RAD50-membrane positive regulation of kinase activity to RFK-mitochondrion apoptotic process for mutual negative knowledge verification. We put forwards GPR68 inhibited nucleus or ER to exosome non-protein based circadian exercise based on Thalamus big data. Our model is positive verified by the other similar and common inhibited and/or activated knowledge in Thalamus. The role and mechanism of our GPR68 inhibited nucleus or ER to exosome non-protein based circadian exercise contributes to better detection, evaluation, intervention, tracking, and other health management of brain diseases.