Prospects of JAK Inhibition in the Framework of Bone Loss

Abstract

Cytokine receptors may possess an intrinsic capability for the transduction of signals upon engagement by the respective cytokine ligand [1]. However, if they lack an own intracellular signaling entity, they rely on other signaling machineries. One of the key intracellular signaling molecules mediating cytokine effects on immune cells are Janus kinases (JAKs), which induce gene expression via signal transducer and activator of transcription proteins (STATs). In mammals, four JAK (JAK1, JAK2, JAK3 and Tyk2) and seven STAT proteins (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B and STAT6) are described, which in varying combinations mediate signal transduction of well over fifty cytokines [2,3]. In the following article the role of JAK and STAT will be summarized.