Genome-wide pathway-based quantitative multiple phenotypes analysis.

For complex diseases, genome-wide pathway association studies have become increasingly promising. Currently, however, pathway-based association analysis mainly focus on a single phenotype, which may insufficient to describe the complex diseases and physiological processes. This work proposes a combination model to evaluate the association between a pathway and multiple phenotypes and to reduce the run time based on asymptotic results.

An investigation into the allosteric mechanism of GPCR A adenosine receptor with trajectory-based information theory and complex network model.

G protein-coupled receptors (GPCRs), a large superfamily of transmembrane (TM) proteins, allosterically transduce the signal of ligand binding in the extracellular (EC) domain to couple to effector proteins in the intracellular (IC) domain, therefore forming the largest class of drug targets. The A adenosine receptor (AAR), a class-A GPCR, has been extensively studied as it offers numerous possibilities for therapeutic applications. However, the mechanism of allosteric communication between EC and IC domains is not completely clear.

Exosomes from mesenchymal stromal cells enhance imatinib-induced apoptosis in human leukemia cells via activation of caspase signaling pathway.

Background Aims: Imatinib (IM), a tyrosine kinase inhibitor targeting the BCR-ABL oncoprotein, remains a major therapeutic strategy for patients with chronic myelogenous leukemia (CML). However, IM resistance is still a challenge in the treatment of CML. Recently, it was reported that exosomes (Exo) were involved in drug resistance.