◀ Back to STAT1
STAT1 — 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
Yu et al., J Immunol 1999
:
Moreover, the STAT element was shown to bind
STAT5a/b induced by IL-2 as well as
STAT1alpha induced by IL-6 in human NK cells
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
Vidal et al., Eur J Immunol 2001
:
Furthermore,
STAT1 activation but weak or no
activation of STAT3 or
STAT5 respectively, could be detected in MB-stimulated MDM. Using MonoMac6 cells, we observed high C/EBPbeta and AP-1 but weaker and transient NF-kappaB activation by MB.Moreover, the truncated form of C/EBPbeta, known to repress HIV-1 transcription, was detected in extracts from MB-treated THP-1 cells
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
Wellbrock et al., Curr Biol 2005
(Melanoma) :
The overexpressed
STAT5 diminished IFNalpha triggered
STAT1 activation, most evidently through upregulation of the inhibitor of cytokine signaling CIS
Huang et al., J Clin Invest 2007
(Inflammation...) :
Enforced expression of
STAT1 , IRF-1, or GATA-1
enhanced phosphorylation of STAT1, STAT3, and
STAT5 in cultured Gata1-deficient murine megakaryocytes, with concomitant megakaryocyte maturation
Wang et al., Cell cycle (Georgetown, Tex.) 2009
:
Site-specific
Stat1 phosphorylation also
controls the transcriptional activities of Stat3 and
Stat5 and is capable of orchestrating a complex regulatory network that influences the expression of genes involved in cell cycle control, cell-cell adhesion and signal transduction
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
Nishiyama-Fujita et al., Leuk Res 2013
(Leukemia, Myelogenous, Chronic, BCR-ABL Positive) :
Suppression of TC-PTP
induced activation of
STAT5 , leading to imatinib resistance, while prolonged phosphorylation of
STAT1 was induced by IFN-a, triggering cell death in KT-1 cells
Yu et al., J Immunol 1996
:
IL-2 induced less
STAT1 alpha activation and IFN-alpha
induced greater
STAT5 activation in NK3.3 cells compared with preactivated primary NK cells