Figure 2.Schematic representation of the cell proliferation control exerted by SOCS1. Following
activation of the receptor by cytokine binding, JAK phosphorylates the
receptor creating a docking site for STATs. JAK then phopshorylates STATs
causing its release from the receptor, allowing dimerization and
translocation to the nucleus to activate the transcription of specific
genes including members of the SOCS family. Subsequently, SOCS terminates
cytokine signaling by blocking JAK activity and STAT recruitment to the
receptor. However, aberrant activation of STAT5 triggered by oncogenic
fusion kinases like TEL-JAK2 might result in sustained levels of SOCS1 that
can activate p53 by forming a complex with ATM and p53.
