◀ Back to STAT3
STAT3 — SYK
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Hussain et al., Cancer Res 2007
(Brain Neoplasms...) :
Specifically, the phosphorylation of
Syk ( Tyr352 ) in monocytes and ZAP-70 ( Tyr319 ) in T cells are
enhanced by the
STAT-3 inhibitor in marked contrast to toll-like receptor and T-cell receptor agonists, respectively
Uckun et al., Proc Natl Acad Sci U S A 2010
(Leukemia, B-Cell) :
Induction of
SYK in an ecdysone-inducible mammalian expression system
results in
STAT3 activation, as documented by tyrosine phosphorylation and nuclear translocation of STAT3, as well as amplified expression of several STAT3 target genes ... Thus,
SYK plays an important and indispensable role in OS-induced
STAT3 activation and its catalytic SH1 domain is critical for this previously unknown regulatory function ... In agreement with a prerequisite
role of
SYK in OS-induced
STAT3 activation, OS does not induce tyrosine phosphorylation of STAT3 in SYK-deficient human proB leukemia cells ... Notably, inhibition of
SYK with a small molecule drug candidate
prevents OS-induced activation of
STAT3 and overcomes the resistance of human B-lineage leukemia/lymphoma cells to OS-induced apoptosis
Lyu et al., Biochem Pharmacol 2010
(Lymphoma, Large B-Cell, Diffuse) :
In agreement with these results, we additionally found that rGel/BLyS down-regulated levels of several STAT3 targets ( c-Myc, p21, Mcl-1, and Bcl-x ( L ) ) and
p-SYK , a positive
regulator of
STAT3
Oellerich et al., Blood 2013
(Leukemia, Myeloid, Acute) :
We show in several AML cell line models that tonic signals derived from the Fc-? chain lead to
Syk dependent activation of
STAT3 and STAT5, which in turn induces cell survival and proliferation