◀ Back to JAK2
JAK2 — STAT6
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
STAT6
→
JAK2
(directlyIncreases, JAK2 Activity, STAT6 Activity)
Evidence: ligand-receptor binding activated STAT3, STAT5 and STAT6
-
KEGG Jak-STAT signaling pathway:
JAK1/JAK2/JAK3/TYK2
→
STAT1/STAT2/STAT3/STAT4/STAT5A/STAT5B/STAT6
(protein-protein, phosphorylation)
-
NCI Pathway Database IL12-mediated signaling events:
IL12/IL12R/TYK2/JAK2 complex (IL12A-IL12B-IL12RB1-IL12RB2-TYK2-JAK2)
→
STAT6 (STAT6)
(modification, activates)
Moriggl et al., J Immunol 1998
Evidence: assay
-
NCI Pathway Database IL4-mediated signaling events:
IL4/IL4R/JAK1/IL13RA1/JAK2 complex (IL4-IL4R-JAK1-IL13RA1-JAK2)
→
STAT6 (STAT6)
(modification, activates)
Hou et al., Science 1994, Murata et al., J Immunol 1996
Evidence: mutant phenotype
Text-mined interactions from Literome
Deng et al., Biochem Biophys Res Commun 2000
:
In this report, we provide evidence that interleukin 4 (IL-4) induced
JAK2 mediated
STAT6 tyrosine phosphorylation and DNA binding in 3T3-L1 preadipocytes but not in 3T3-L1 adipocytes
Murata et al., Int J Hematol 1999
:
While JAK3 is required for signal transducer and activator of transcription-6 ( STAT6 ) activation in hematopoietic cells, we recently demonstrated that in nonhematopoietic cells
JAK2 is
required for
STAT6 activation for the alternative form of IL-4R
Yamaura et al., Am J Physiol Heart Circ Physiol 2003
(Myocardial Infarction...) :
Tyrphostin AG490, a
JAK2 inhibitor, or 4-amino-5- ( 4-methylphenyl ) -7- ( t-butyl ) -pyrazolo-3,4-d-pyrimidine ( PPI ), a Src kinase blocker,
blocked STAT5A phosphorylation, whereas
STAT6 phosphorylation was blocked only with tyrphostin
Deszo et al., Cell Signal 2004
:
JAK inhibition with WHI-P154 abrogated IL-4 dependent CD11b and CD86 up-regulation and
inhibited STAT6 tyrosine phosphorylation
Nath et al., J Immunol 2004
(Encephalomyelitis, Autoimmune, Experimental...) :
Lovastatin
induced the expression of GATA3 and the phosphorylation of
STAT6 , whereas it inhibited tyrosine phosphorylation of
Janus kinase 2 , tyrosine kinase 2, and STAT4
Guiter et al., Blood 2004
(Lymphoma, B-Cell...) :
MedB1 treatment with JAK2 inhibitor AG490 partially decreased STAT6 phosphorylation, suggesting that
JAK2 is partially
involved in
STAT6 activation in these cells
Mottok et al., Blood 2007
(Hodgkin Disease) :
Somatic hypermutation of SOCS1 in lymphocyte-predominant Hodgkin lymphoma is accompanied by high
JAK2 expression and
activation of
STAT6
Nishimura et al., Circ J 2008
:
IL-13 has anti-angiogenic activity as a result of activation of
JAK2 and subsequent
activation of
STAT6
Chi et al., Exp Cell Res 2010
(Lung Neoplasms) :
Inhibitors of JAKs, kaempferol and
JAK inhibitor I,
attenuated IL-4 stimulated
STAT6 phosphorylation and 15-PGDH activity in a comparable concentration dependent manner
Bhattacharjee et al., Free Radic Biol Med 2013
:
We further show that
Jak2 is upstream of Stat3 activation and Tyk2
controls Stat1 and
Stat6 activation in response to IL-13 stimulation
Murata et al., Blood 1998
:
Because IL-4 phosphorylates JAK1 and JAK2 tyrosine kinases in nonhematopoietic cells, we investigated whether JAK1 and
JAK2 are
required for IL-4 induced
STAT6 activation in various transfectants ... Cotransfection experiments with different chains of IL-4R and kinase-deficient JAK1 and JAK2 mutants in CHO cells showed that JAK1 and
JAK2 are
required for optimal activation of
STAT6 in the alpha ' beta transfectant but only partially in the beta gammac transfectant ... Taken together, our results show that IL-13Ralpha ' is a novel functional component of the IL-4R system and that JAK1 and
JAK2 mediate IL-4 induced optimal activation of
STAT6 in nonhematopoietic cells