Research Perspective Volume 2, Issue 7 pp 445—452

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.