Gene interactions and pathways from curated databases and text-mining

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PRL — STAT3

Pathways - manually collected, often from reviews:

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
Carpenter et al., Endocrinology 2003 (Hyperprolactinemia) : In study four, Western blot analyses indicated that PRL increased levels of phosphorylated STATs 1 and 5, but not STAT 3 , and phosphorylated ERK 1 and 2 MAPKs and c-Jun N-terminal kinase/stress activated protein kinase proteins in explanted PND 28 ovine uteri
Gutzman et al., Oncogene 2007 (Neoplasms) : We found that PRL activation of Stat5a and Stat5b, but not Stat1 or Stat3 , reduced PRL signals to AP-1, without altering estradiol induced AP-1 activity
AnhĂȘ et al., J Endocrinol 2007 : PRL increased SERCA2 and STAT3 expressions and STAT3 serine phosphorylation in RINm5F cells ... Moreover, PRL induced STAT3 serine phosphorylation and SERCA2 expression were inhibited by dexamethasone ( DEX )
Sodhi et al., Cytokine 2008 : It is further shown that p38 MAP kinase, STAT3 and NF-kappaB could play a differential regulatory role in PRL or GH induced production of cytokines by macrophages
Castilla et al., J Vasc Res 2010 : This effect likely involves the upregulation of the short and long PRL receptor isoforms and is independent of PRL induced JAK2/STAT3 signaling
DaSilva et al., Mol Cell Endocrinol 1996 : The present study of prolactin (PRL) receptor mediated recruitment of signal transducers and activators of transcription ( STATs ) demonstrates that PRL activates STAT3 , in addition to STAT1 and STAT5 as previously reported, and that STAT1, STAT3 and STAT5 are mediators of PRL effects in cells whether of lymphoid, myeloid or mammary epithelial origin
Schaber et al., Cancer Res 1998 (Breast Neoplasms) : A similar additive relationship was observed on IFN alpha/beta- and PRL induced Stat3 tyrosine phosphorylation