Cytokines induce a variety of biological responses by binding to specific cell surface receptors and activating cytoplasmic signal transduction pathways. Proteins that mediate these signals from the cell surface to the nucleus include Janus kinases, e.g., Janus kinase 1, and the signal transducers and activators of transcription (STATs), such as STAT1. To maintain tight control of these signal transduction pathways, mechanisms for turning off the signals are necessary. The adverse consequences of an imbalance between positive and negative signals is evident in the motheaten mouse, which lacks the phosphatase SHP1. These mice fail to regulate cytokine responses appropriately, resulting in hyperproliferation and accumulation of cells in several hematopoietic lineages and the development of systemic autoimmune disease. SOCS1 represents a family of proteins that regulates responses to cytokines. The SOCS family comprises at least 8 members, SOCS1 to SOCS7 and CIS (cytokine inducible SH2 containing protein). Structurally, the SOCS proteins are composed of an N terminal region of variable length and amino acid composition, a central SH2 domain, and a previously unrecognized C terminal motif named the SOCS box. SOCS1 (also known as Janus kinase binding protein and STAT induced STAT inhibitor 1) was isolated independently by its ability to interact with Janus kinase 2 in a 2 hybrid screen and on the basis of antigenic similarity with the SH2 domain of STAT3. SOCS 1 inhibition of signal transduction appears to occur by binding to and inhibiting the catalytic activity of members of JAK family of cytoplasmic kinases (direct JAK2 kinase inhibition). Biochemical characterization as well as gene disruption studies indicate that SOCS1 is an important negative regulator of JAK-STAT signal pathway.
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