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CD79A — SOCS1

Text-mined interactions from Literome

Kaneko et al., Immunology 2005 : These results indicate that high IgA levels in the intestine of TLR4 mutated mice are due to up-regulation of TGF-beta and IL-10 and the lack of regulation by SOCS-1
Park et al., Mol Cells 2010 : Further, overexpression of SOCS1 , a JAK inhibitor, diminished the antagonistic effect of IFN-gamma on TGF-beta1 induced GL alpha transcription and IgA secretion
Yang et al., J Cell Physiol 2011 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive) : Promoter deletion and mutation analysis indicate the Tcf-4/ß-catenin and STAT1 binding sites located between the -405/-223 region of the human Jab1 promoter are important for the activation of Jab1 by Bcr-Abl ... Our results also demonstrate that the AKT signaling pathway is involved in the regulation of Jab1 by Bcr-Abl because the AKT inhibitor LY294002 but not the ERK inhibitor PD98059 reduces Jab1 promoter activity and mRNA expression
Qiu et al., Neoplasia (New York, N.Y.) 2012 (Cell Transformation, Neoplastic...) : Bcr-Abl dependent tyrosine phosphorylation of SOCS-1 and SOCS-3 occurs mainly on Tyr 155 and Tyr 204 residues of SOCS-1 and on Tyr 221 residue of SOCS-3