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PRL — STAT5B

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: STAT5B → PRL (increases) Kazansky et al., J Biol Chem 1999*
  Evidence: Similar to prolactin induction, src activation resulted in tyrosine phosphorylation and DNA binding of both STAT5A and STAT5B. However, nuclear translocation of only STAT5B but not STAT5A was observed.
• Reactome Reaction: PRL → STAT5B (reaction)
• Reactome Reaction: PRL → STAT5B (indirect_complex)

Text-mined interactions from Literome

DeVito et al., J Cell Biochem 1999 : We found that PRL specifically increases the tyrosine phosphorylation of JAK2, but not JAK1, JAK3, or Tyk2, and the subsequent phosphorylation of STAT1 alpha, STAT5a, and STAT5b
Kazansky et al., J Biol Chem 1999 : Differential effects of prolactin and src/abl kinases on the nuclear translocation of STAT5B and STAT5A ... Furthermore, overexpression of a dominant negative kinase-inactive mutant of JAK2 prevented prolactin induced tyrosine phosphorylation and nuclear translocation of STAT5A and STAT5B but did not block src kinase activation and nuclear translocation of STAT5B
Briscoe et al., J Mol Endocrinol 2001 (Insulinoma) : Chronic FA treatment also attenuated prolactin stimulated STAT5b tyrosine phosphorylation but not interleukin-6 stimulated STAT3 tyrosine phosphorylation, suggesting that the effect is receptor/ligand specific
Frasor et al., Mol Endocrinol 2001 : These findings indicate that PRL stimulation of ER expression occurs at the level of transcription and that PRL regulation of ERalpha can be mediated by either Stat5a or Stat5b , while regulation of ERbeta appears to be mediated only by Stat5b
Brelje et al., J Histochem Cytochem 2002 (Insulinoma...) : In isolated rat islets of Langerhans, PRL stimulated the nuclear translocation of both STAT5A and STAT5B only in beta-cells
Frasor et al., Trends Endocrinol Metab 2003 : The tyrosine kinase Jak2 is required for PRL activation of Esr1 promoter activity ; however, additional pathways are involved in PRL induced Stat5b phosphorylation, nuclear translocation and DNA binding
Guren et al., J Cell Physiol 2003 : The Src tyrosine kinase inhibitor CGP77675 blocked the EGF induced activation of Stat5b, but did not affect the Stat5b activation by growth hormone (GH) or prolactin (PRL) ... In hepatocytes at 24 h of culturing ( mid/late G ( 1 ) ) with 20,000 cells per cm ( 2 ), EGF induced strong phosphorylation of the EGF receptor, as well as Shc and ERK, and stimulated DNA synthesis, but did not activate Stat5b, although the Stat5b response to GH or PRL was retained
Piekorz et al., Mol Endocrinol 2005 : Moreover, 20alpha-HSD deficiency partially corrected the abortion of pregnancies associated with Stat5b deficiency, supporting the concept that prolactin activation of Stat5b is important in suppressing 20alpha-HSD gene expression and thereby allowing the maintenance of progesterone levels that are required to sustain pregnancy
Ma et al., Endocrinology 2005 : These results extend our previous findings with STAT5b-deficient mice and strongly suggest that in NEDA neurons, prolactin signaling via the JAK/STAT pathway is mediated exclusively by STAT5b
Anderson et al., Endocrinology 2006 : Because prolactin induced activation of dopamine synthesis in these neurons requires the Janus kinase/signal transducer and activator of transcription 5b ( STAT5b ) signaling pathway, we investigated whether prolactin induced STAT5b signaling is reduced during lactation and whether induction of suppressors of cytokine signaling (SOCS) mRNAs occur at this time and in late pregnancy ... During lactation, the ability of exogenous prolactin to induce STAT5 phosphorylation and STAT5b nuclear translocation was markedly reduced when compared with diestrous rats
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
Neilson et al., Mol Endocrinol 2007 (Breast Neoplasms) : Finally, suppression of Jak1 by lentiviral delivery of Jak1 short hairpin RNA blocked PRL activation of ERK and signal transducer and activator of transcription ( Stat ) 3 and suppressed PRL activation of Jak2, Stat5a, Stat5b , and Akt, as well as tyrosine phosphorylation of PRLR
Steyn et al., Endocrinology 2008 : During late pregnancy, these neurons become unresponsive to prolactin, with a loss of prolactin induced activation of STAT5b and decreased dopamine secretion ... We hypothesized that changes in circulating ovarian steroids during late pregnancy might induce expression of SOCS mRNAs, thus disrupting STAT5b mediated prolactin signaling
Perotti et al., Breast Cancer Res 2008 (Breast Neoplasms) : Focusing on HSP90A, we determined that prolactin increased HSP90A mRNA in cancerous human breast SKBR3 cells and that STAT5B preferentially activated the HSP90A promoter in reporter gene assays
Tran et al., Cancer Res 2010 (Breast Neoplasms...) : Prolactin suppression of BCL6 was enhanced by overexpression of Stat5a but not Stat5b , was mimicked by constitutively active Stat5a, but did not require the transactivation domain of Stat5a
Luo et al., J Biol Chem 1997 (Lymphoma, T-Cell) : Unexpectedly, both Stat5b and Stat5a inhibit PRL induction of the IRF-1 promoter, but they mediate PRL stimulation of the beta-casein promoter ... In contrast, both DNA binding and transactivation domains of Stat5b are required to mediate PRL induction of the beta-casein promoter
Rui et al., J Biol Chem 1998 (Lymphoma) : In prolactin (PRL) dependent Nb2 lymphocytes, ATA sustained cell growth in the absence of hormone and mimicked rapid PRL induced tyrosine phosphorylation of Jak2 and activation of Stat5a and Stat5b with tyrosine phosphorylation, heterodimerization, DNA binding, and induction of the Stat5 regulated pim-1 protooncogene
Cella et al., Mol Cell Biol 1998 : In the mammary gland, prolactin activates Stat5a and Stat5b and glucocorticoids activate the glucocorticoid receptor ( GR )
Kanzaki et al., Endocrinology 1998 (Leydig Cell Tumor...) : In MA-10 cells, both GH and PRL mediate tyrosine phosphorylation of Janus kinase (JAK) 2 and Stat5b and induce DNA binding activity of Stat5b ... In primary Leydig cells isolated from 18-day-old rats, GH, but not PRL , activates cytoplasmic Stat5b and induces the binding of translocated nuclear Stat5b to GAS elements ... Although Stat5b protein is expressed in both Percoll- and elutriator purified adult rat Leydig cells, neither GH nor PRL treatment results in Stat5b-DNA binding
Dajee et al., Mol Endocrinol 1998 : Collectively, these results document for the first time that Stat 5b, SF-1, and COUP-TF each exert specific effects on the function of the alpha2M promoter : basal activity is controlled by the balance of SF-1 ( positive ) and COUP-TF ( negative ) activities and PRL inducibility is mediated by activation of Stat 5b
Yamashita et al., J Biol Chem 1998 : Whereas Ser725 of Stat5a was constitutively phosphorylated both in COS-7 cells and Nb2 lymphocytes, phosphorylation of Ser730 of Stat5b was markedly stimulated by prolactin
Zhou et al., J Biol Chem 1999 : Activation of STAT5b signaling by either GH or prolactin inhibited, by up to 80-85 %, ligand induced, PPARalpha dependent reporter gene transcription