Gene interactions and pathways from curated databases and text-mining

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STAT3 — STAT5A

Pathways - manually collected, often from reviews:

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