◀ Back to STAT3
STAT3 — STAT5A
Pathways - manually collected, often from reviews:
-
BioCarta bioactive peptide induced signaling pathway:
STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B)
→
STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B)
(modification, collaborate)
-
BioCarta bioactive peptide induced signaling pathway:
STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B)
→
STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B)
(modification, collaborate)
-
BioCarta bioactive peptide induced signaling pathway:
STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B)
→
STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B)
(modification, collaborate)
-
BioCarta il22 soluble receptor signaling pathway:
STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B)
→
STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B)
(modification, collaborate)
-
BioCarta bioactive peptide induced signaling pathway:
STATs (STAT3/STAT5A/STAT1/STAT5A/STAT5B/STAT5B)
→
STATS/STATS complex (STAT3_STAT5A_STAT1_STAT5A_STAT5B_STAT5B)
(modification, collaborate)
-
NCI Pathway Database CXCR4-mediated signaling events:
STAT1-3-5-active (STAT5A/STAT5B/STAT1/STAT3)
→
STAT1-3-5 (dimer) complex (STAT5A_STAT5B_STAT1_STAT3)
(modification, collaborate)
Vila-Coro et al., FASEB J 1999
-
NCI Pathway Database CXCR4-mediated signaling events:
STAT1-3-5 (STAT5A/STAT5B/STAT1/STAT3)
→
STAT1-3-5-active (STAT5A/STAT5B/STAT1/STAT3)
(modification, collaborate)
Vila-Coro et al., FASEB J 1999, Ahr et al., J Biol Chem 2005
Evidence: assay, physical interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Yamashita et al., J Biol Chem 1999
(Lymphoma, T-Cell) :
Short term incubation ( < 60 min ) of prolactin-responsive Nb2 lymphoma cells at high density selectively blocked prolactin stimulation of p42/p44 mitogen activated protein kinases and transcription factors Stat1 and
Stat3 but not prolactin
activation of
Stat5 or the tyrosine kinase Jak2
Rebsamen et al., J Mol Cell Cardiol 2000
(Cardiomegaly) :
EGF did not activate Stat1 and
Stat3 , but did
induce a rapid and transient activation of
Stat5 , which corresponded mainly to Stat5b DNA binding
Klausen et al., Oncogene 2000
:
All cytokines
induced STAT3 phosphorylation to approximately the same level, but only OSM, and to a lesser extent IL-6, induced
STAT5 phosphorylation
Xue et al., Int Immunol 2002
:
Serine phosphorylation has also been found to occur in a number of STAT proteins, including Stat1, Sat3, Stat4, Stat5a, Stat5b and Stat6, and was shown to be important for maximal transcriptional activation
mediated by Stat1,
Stat3 and Stat4, but not for
Stat5a or Stat5b
Lundin Brockdorff et al., Cytokine 2002
(MAP Kinase Signaling System...) :
However, the constitutive tyrosine phosphorylation of
Stat3 as well as IL-2
induced Stat5 tyrosine phosphorylation and DNA binding were unaffected by the stably transfected wild-type SHP2 as well as the inactive SHP2
Tanabe et al., J Immunol 2005
:
The antiapoptotic response in the absence of STAT1 is predominantly
mediated by
STAT3 , and to a lesser extent by
STAT5A/B ... In contrast, the mitogenic IFN-alphabeta response gained through the absence of STAT1 is only marginally affected when
STAT5A/B expression is also abrogated, but is completely
dependent on
STAT3 activation
Dagvadorj et al., Clin Cancer Res 2008
(Prostatic Neoplasms) :
The
effects of
Stat5a/b on the viability of prostate cancer cells involve Stat5a/b regulation of Bcl-X ( L ) and cyclin D1 protein levels but not the expression or activation of
Stat3
Momose et al., Hum Pathol 2009
(Lymphoma, Large B-Cell, Diffuse...) :
Recently, the essential role of
STAT3 activation as well as
STAT 5 activation in nucleophosmin-ALK fusion protein mediated lymphomagenesis was reported
Barclay et al., Endocrinology 2011
(Fatty Liver) :
Because loss of
STAT5 signaling
results in elevated STAT1 and
STAT3 activity and intracellular lipid accumulation, we have used DN-STAT5a/b, DN-STAT1, constitutively active ( CA ) -STAT3, or addition of oleate/palmitate in the hepatoma line to assign which of these apply to individual targets in STAT5 signaling deficiency
Lee et al., J Immunol 2011
:
Progesterone
enhanced activation of
STAT5 in response to IL-2, whereas it decreased
STAT3 activation in response to IL-6, which is in line with the selective activity of progesterone in generation of Tregs versus Th17 cells
Huang et al., PloS one 2011
(Lupus Erythematosus, Systemic) :
We observed the basal activation of
STAT3 in SLE T cells and monocytes, and the basal
activation of
STAT5 in SLE T cells and B cells
Katsumi et al., Gan To Kagaku Ryoho 2013
(Leukemia, Myeloid, Acute) :
While phosphorylation of
STAT5 was observed in 4 out of 7 patients, phosphorylation of
STAT3 or FLT3 was not
detected in all cases examined
Mu et al., Blood 1995
:
Both MGDF and IL-3
induce tyrosine phosphorylation of
STAT3 ( APRF ) and STAT5 ( MGF ), with MGDF favoring STAT3 while IL-3 predominantly causes
STAT5 phosphorylation
Li et al., Proc Natl Acad Sci U S A 1997
:
PCD coincided with bax induction, decreased expression of milk proteins, block of prolactin signal transduction through
Stat5a and 5b, and
activation of
Stat3
Nelson et al., J Biol Chem 1998
:
Fes also
induced a dramatic increase in
STAT3 DNA binding activity in this system, whereas no activation of
STAT5 was observed