CREB5 Computational Regulation Network Construction and Analysis Between Frontal Cortex of HIV Encephalitis (HIVE) and HIVE-Control Patients

Abstract

CREB5 computational regulation network construction and analysis of frontal cortex of HIV encephalitis (HIVE) is very useful to identify novel markers and potential targets for prognosis and therapy. By integration of gene regulatory network infer and the database for annotation, visualization and integrated discovery we identified and constructed significant molecule CREB5 regulation network from 12 frontal cortex of HIVE-control patients and 16 HIVE in the same GEO Dataset GDS1726. Our result verified CREB5 biological regulation module in the upstream of frontal cortex of HIVE-control patients (MAPKAPK3 activation; DGKG, LY96, TNFRSF11B inhibition) and downstream (ATP6V0E1, CFB, DGKG, MX1, TGFBR3 activation; LGALS3BP, RASGRP3, RDX, STAT1 inhibition), whereas in the upstream of frontal cortex of HIVE (BST2, CFB, LCAT, TNFRSF11B activation; CFHR1, LY96 inhibition) and downstream (GAS1, LCAT, LGALS3BP, NFAT5, VEZF1, ZNF652 activation; DGKG, IFITM1, LY96, TNFRSF11B inhibition). Importantly, we datamined that CREB5 regulation cluster of HIVE was involved in inflammatory response, proteolysis, biological adhesion, and negative regulation of biological process (only in HIVE terms) without positive regulation of cellular process, phosphotransferase, kinase, post-translational protein modification, ATP binding, transmembrane protein, calcium ion binding, acetylation, and hydrolase activity (only in HIVE-control patients terms), the condition was vital to inflammation and cognition impairment of HIVE. Our result demonstrated that common terms in both HIVE-control patients and HIVE included biological regulation, phosphoprotein, metabolic process, zinc, biosynthetic process, organelle, signal transduction, defense response, membrane, secreted, signal peptide, and glycoprotein, and these terms were more relative to inflammation and cognition impairment, therefore we deduced the stronger CREB5 regulation network in HIVE consistent with our number computation. It would be necessary of the stronger CREB5 regulation function to inflammation and cognition impairment of HIVE.

Zika virus infection reprograms global transcription of host cells to allow sustained infection

“…CREB5 (CAMP-responsive element-binding protein 5) is a transcription factor that regulates nucleotide and nucleic acid metabolism, transcription, and signal transduction, and is also highly upregulated in patients with HIV encephalitis and vaccinia virus infections. 43, 44 Because cellular metabolism is often a limiting factor in viral replication, nucleoside/nucleotide-based therapeutics have been developed against a variety of viruses, including HIV, HBV, HCV, HSV and VZV. 26 Indeed, nucleoside analogs including floxuridine, also known to be effective against other flaviviruses such as dengue, displayed dose-dependent inhibition of ZIKV replication.…”

Low BIK outside-inside-out interactive inflammation immune-induced transcription-dependent apoptosis through FUT3-PMM2-SQSTM1-SFN-ZNF384

“…d BIK-activatory different mutualpositive-correlation molecules in low normal adjacent tissues compared with the corresponding high lung adenocarcinoma. Con, human normal adjacent tissues; Ex, lung adenocarcinoma; Act, activation Immunol Res out interactive inflammation immune-induced transcription-dependent apoptosis using SAM [7][8][9][10][11][12]. The GSE7670 raw microarray data were processed by log base 2, two classes were paired, and minimum fold change C2 selected (the false-discovery rate 0 %) [13][14][15][16].…”

BRCA1-Mediated Inflammation and Growth Activated & Inhibited Transition Mechanisms Between No-Tumor Hepatitis/Cirrhotic Tissues and HCC

“…Novel BRCA1 ‐activated (Pearson ≥0.25) and ‐inhibited (Pearson ≤−0.25) different complete (all no positive correlation, Pearson <0.25) and uncomplete (partly no positive correlation except BRCA1 , Pearson <0.25) networks were constructed between lower no‐tumor hepatitis/cirrhotic tissues (HBV or HCV infection) and higher HCC by GRNInfer [Wang et al, ], our articles [Wang et al, ,, ,,,,,, ,,,; Huang et al, 2010, 2011, ; Sun et al, ; Sun et al, ; Lin et al, ] and GVedit tool and our programming, respectively.…”