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OSM — STAT1
Text-mined interactions from Literome
Schaefer et al., Cell Signal 2000
(Brain Neoplasms) :
Of the cytokines tested,
oncostatin M resulted in the most dramatic induction of
Stat1 and Stat3 in all cell lines analysed, as assessed by the formation of protein/DNA complexes
Li et al., J Immunol 2001
:
We demonstrate that
OSM rapidly
stimulated phosphorylation of Janus kinase (JAK) 1, JAK2, JAK3, and
STAT1 as well as extracellular signal regulated kinase ( ERK ) 1/2, p38, and c-Jun N-terminal kinase 1/2 mitogen activated protein kinases in primary bovine and human chondrocytes ... A JAK3-specific inhibitor blocked
OSM stimulated
STAT1 tyrosine phosphorylation, DNA binding activity of STAT1 as well as collagenase-1 ( MMP-1 ), stromelysin-1 ( MMP-3 ), collagenase-3 ( MMP-13 ), and TIMP-3 RNA expression ... Similarly, curcumin ( diferuloylmethane ), an anti-inflammatory agent, suppressed
OSM stimulated
STAT1 phosphorylation, DNA binding activity of STAT1, and c-Jun N-terminal kinase activation without affecting JAK1, JAK2, JAK3, ERK1/2, and p38 phosphorylation
Krona et al., Oncol Rep 2005
(Glioma) :
OSM treatment
induced phosphorylation of STAT3 and
STAT1 indicating presence of a functional JAK/STAT pathway
Song et al., Int J Biochem Cell Biol 2005
(MAP Kinase Signaling System) :
Furthermore, OSM treatment elicited phosphorylation of STAT1 and STAT3, and pretreatment with WHI-P131 specifically prevented the
OSM induced phosphorylation of
STAT1 , without affecting the OSM induced phosphorylation of ERK and STAT3
Dekanty et al., J Biol Chem 2006
:
LIF and
OSM specifically
trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so
Song et al., Int J Biochem Cell Biol 2007
:
OSM induced phosphorylation of STAT1, and treatment of adipocytes with JAK3 inhibitor WHI-P131 or MEK inhibitor U0126, but not with JAK2 inhibitor AG490,
prevented the activation of
STAT1
El Mabrouk et al., J Cell Biochem 2008
:
IL-4 did not affect
OSM stimulated phosphorylation of extracellular signal regulated kinases ( ERKs ), protein 38 (p38), c-Jun N-terminal kinase (JNK) and
Stat1
Pollack et al., American journal of physiology. Renal physiology 2007
(MAP Kinase Signaling System) :
MEK1/2 inhibitor U0126 ( 10 muM ) blocked basal and
OSM induced ERK1/2 phosphorylation but not phosphorylation of either ERK5 or
Stat1/3
Hintzen et al., J Biol Chem 2008
:
Additionally, we show that
OSM induced
STAT1 phosphorylation occurs independently of receptor tyrosine motifs and is mediated directly by Janus kinases, whereas the two C-terminally located tyrosine residues Tyr917/Tyr945 of the OSMR are crucial for STAT3 activation
Kok et al., Arthritis Rheum 2009
(Arthritis) :
AG-490 suppressed
OSM stimulated activation of
STAT-1/3 and synthesis of CCL2 in vitro and diminished the severity of CIA and the number of CCL2 synthesizing osteoblasts in vivo
Kordula et al., J Biol Chem 1998
(Alzheimer Disease) :
When the human ACT gene was cloned, two elements binding
STAT1 and STAT3 ( signal transducer and activator of transcription ) in
response to
OSM or IL-6.sIL-6R complexes could be identified and characterized