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SOAT1 — SOCS1

Text-mined interactions from Literome

Hanada et al., J Biol Chem 2001 : These data suggested that F59D-JAB up-regulated STAT activity by sustaining JAK activation
Cooney et al., Shock 2002 : The expression of SOCS-1 to -3 and CIS is induced by cytokine or GF stimulation, resulting in the inhibition of JAK/STAT mediated cytokine signaling by what appears to be a classic negative feedback loop
van de Geijn et al., J Leukoc Biol 2004 : We show that SOCS1 and SOCS3, but not CIS and SOCS2, inhibited G-CSF induced STAT activation in human embryo kidney 293 cells
Shi et al., FEBS Lett 2008 : Overexpression of SOCS-1 in HMCs inhibited HG-induced JAK2/STAT activation, c-Fos/c-Jun expression, and increased synthesis of TGF-beta1 and fibronectin
Koelsche et al., Mol Immunol 2009 : Altering the subcellular localization of SOCS1 by mutating clusters of arginine residues within the NLS did not affect the inhibition of interferon mediated STAT1 tyrosine-phosphorylation, but surprisingly led to impaired inhibitory activity of STAT mediated reporter gene induction and IFN-gamma induced CD54 regulation
Mallette et al., Aging 2010 (Cell Transformation, Neoplastic) : However, SOCS1 not only regulates STAT signaling but can also localize to the nucleus and directly interact with the p53 tumor suppressor through its central SH2 domain
Gao et al., Exp Hematol 2013 (Myeloproliferative Disorders) : Moreover, overexpression of SOCS1 and SOCS3 significantly inhibited cell growth and suppressed JAK2/STAT signaling in K562 and HEL cells
Starr et al., Nature 1997 : Expression of SOCS-1 inhibited both interleukin-6 induced receptor phosphorylation and STAT activation