Gene interactions and pathways from curated databases and text-mining

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IL2 — JAK1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Sudarshan et al., J Immunol 1999 : Similarly, but in contrast to previous reports, we found that TGF-beta1 did not inhibit IL-2 induced phosphorylation of JAK1 , JAK3, and STAT5A ... Similarly, but in contrast to previous reports, we found that TGF-beta1 did not inhibit IL-2 induced phosphorylation of JAK1, JAK3 , and STAT5A
Cohney et al., Mol Cell Biol 1999 : In these experiments, SOCS-3 associated with Jak1 and inhibited Jak1 phosphorylation, and this inhibition was markedly enhanced by the presence of IL-2 receptor beta chain (IL-2Rbeta)
Subramaniam et al., Biochem Biophys Res Commun 1999 : Immunoprecipitation with specific antibodies followed by Western blot analysis with antiphosphotyrosine antibody has shown that in U937 cells, interleukin-17 induces time dependent stimulation of tyrosine phosphorylation of JAK 1 , 2 and 3, Tyk 2 and STAT 1, 2, 3 and 4 within 0.5 to 30 min. Interleukin-17 mediated tyrosine phosphorylation of these proteins strongly suggests that the JAK/STAT signaling pathway may play a major role in transducing signals from interleukin-17 receptors to the nucleus
Yu et al., J Immunol 2000 : However, one T cell line bearing a mutant gammac exhibited impaired endocytosis of IL-2, despite normal IL-2 induced Jak/STAT activation
Kulms et al., J Biol Chem 2001 : In contrast, IL-2 induced tyrosine phosphorylation of the kinases Jak1 and Jak3 located upstream of STAT5 was not affected by UV
Bovolenta et al., Clin Immunol 2001 (HIV Infections) : In particular, IL-2 activates the tyrosine kinases JAK1 and JAK3 and the transcription factors STAT3 and STAT5
Tkaczuk et al., Am J Transplant 2002 (MAP Kinase Signaling System) : Effect of anti-IL-2Ralpha antibody on IL-2 induced Jak/STAT signaling ... Under these circumstances, IL-2 mediated Jak/STAT pathway activation might be generated through residual intermediate affinity IL-2Rbetagamma receptors, and this was demonstrated by complete blockade of signaling when anti-IL-2Rbeta monoclonal antibody was added
Kryworuchko et al., Clin Exp Immunol 2003 : Human immunodeficiency virus-1 envelope glycoproteins and anti-CD4 antibodies inhibit interleukin-2 induced Jak/STAT signalling in human CD4 T lymphocytes ... The treatment of CD4 T cells with HIV env or surface ligation of CD4 with anti-CD4 monoclonal antibodies inhibited the IL-2 induced activation of Jak-1 and Jak-3, as well as their targets, STAT5a and STAT5b
Zhang et al., J Immunol 2004 : In this study, we show that adenosine suppressed IL-2 dependent proliferation of CTLL-2 T cells by inhibiting STAT5a/b tyrosine phosphorylation that is associated with IL-2R signaling without affecting IL-2 induced phosphorylation of Jak1 or Jak3
To et al., Br J Cancer 2004 (Cell Transformation, Neoplastic...) : The interleukin mediated Janus kinase ( JAK ) /STAT pathway plays a crucial role in carcinogenesis
Ozawa et al., J Immunol 2004 (Periodontitis) : Pretreatment with anti-IL-15 neutralizing mAb for 24 h completely inhibited the production of MCP-1 induced by IL-2 and IL-15 and IL-2 induced phosphorylation of Jak 1 and 3 in HGF
Anderson et al., J Immunol 2005 : Although IL-2 expression was deficient, stimulation with IL-2 in vitro induced Jak1 and STAT5 activation in PI-T ( Reg ) cells, restored their proliferative response to antigenic stimulation, and abrogated PI-T ( Reg ) -mediated suppression in vitro
Fujii et al., Biochem Biophys Res Commun 2007 : Here, I showed that Jak3 expression is dispensable for IL-2 induced activation of Jak1 and Stat proteins and expression of nuclear proto-oncogenes in the IL-2R reconstituted fibroblast cell line
Gorjão et al., J Lipid Res 2007 : PA, SA, DHA, and EPA decreased JAK1 , JAK3, STAT5, and Akt phosphorylation induced by IL-2 , but OA and LA did not cause any effect ... PA, SA, DHA, and EPA decreased JAK1, JAK3 , STAT5, and Akt phosphorylation induced by IL-2 , but OA and LA did not cause any effect
Lindemann et al., J Biol Chem 2008 : Cells expressing this mutant IL-2Rbeta chain fail to induce phosphorylation of PI3K-p85alpha/beta or activate Akt, but mediate normal IL-2 dependent proliferation and activation of JAK1 and STAT-5A/B. Microarray analyses revealed differential regulation of numerous genes compared with cells expressing a wild-type IL-2Rbeta, including up-regulation of the IL-17 receptor subunit IL-17RA
Ross et al., J Biol Chem 2010 : Moreover, inhibition of PP2A, but not PP1, diminished IL-2 induced tyrosine phosphorylation of IL-2Rbeta, JAK3 , and STAT5, and abolished STAT5 DNA binding activity
Karitskaya et al., Pflugers Arch 2010 : The pharmacological inhibition of IL-2 induced MEK/ERK or JAK/STAT cascades suppressed the IL-2 induced proliferation and reduced the functional and protein expressions of Na, K-ATPase
Sewgobind et al., Am J Transplant 2010 : In this study, we examined the effect of CP-690,550 on IL-2 mediated Jak/STAT5 phosphorylation by CD4 ( + ) CD25 ( bright ) FoxP3 ( + ) CD127 ( -/low ) T cells ( Treg ) and CD4 ( + ) CD25 ( neg ) effector T cells ( Teff ) in kidney transplant ( KTx ) patients
Forward et al., Biochem Biophys Res Commun 2011 : IL-2 induced phosphorylation of STAT5A and JAK3, but not JAK1 , was diminished in the presence of curcumin, indicating inhibition of critical proximal events in IL-2R signaling
Soth et al., J Med Chem 2013 : Evaluation of this analogue in cellular and in vivo models confirmed functional selectivity for modulation of a JAK3/JAK1 dependent IL-2 stimulated pathway over a JAK1/JAK2/Tyk2 dependent IL-6 stimulated pathway
Brunn et al., J Biol Chem 1995 : Both IL-2 and IL-4 stimulated the rapid activation of JAK1 and JAK3, whereas JAK2 activity was unaffected by either cytokine
Wakao et al., EMBO J 1995 : Analysis of two EPO receptor (EPOR) transfected CTLL-2 cell lines discloses that IL-2 activates JAK1 and JAK3 as well as STAT5, while EPO stimulates STAT5 and JAK2 in EPO-responsive CTLL-2 cells ( ERT/E2 )
Barber et al., Mol Cell Biol 1994 : In contrast, stimulation with IL-2 or the related cytokine IL-4 resulted in the rapid, dose dependent tyrosine phosphorylation of JAK1 and an additional 116-kDa protein ... Immune complex kinase assays confirmed that IL-2 and IL-4 activated JAK1 and EPO activated JAK2
Russell et al., Science 1994 (Severe Combined Immunodeficiency) : IL-2 , IL-4, IL-7 ( whose receptors are known to contain gamma c ), and IL-9 ( whose receptor is shown here to contain gamma c ) induced the tyrosine phosphorylation and activation of the Janus family tyrosine kinases Jak1 and Jak3
Miyazaki et al., Science 1994 : Functional activation of Jak1 and Jak3 by selective association with IL-2 receptor subunits ... Stimulation with IL-2 induces the tyrosine phosphorylation and activation of the Janus kinases Jak1 and Jak3
Beadling et al., EMBO J 1994 : An IL-2 induced increase in JAK1 and JAK3, but not JAK2 or Tyk2, tyrosine phosphorylation was observed ... The observation that IL-2 and IFN alpha activate JAK1 to a comparable degree, but only IFN alpha activates STAT1, indicates that JAK1 activation is not the only determining factor for STAT1 activation
Johnston et al., Nature 1994 : Phosphorylation and activation of the Jak-3 Janus kinase in response to interleukin-2
Taylor et al., Blood 1996 (Severe Combined Immunodeficiency) : IL-2 stimulation of the transduced cell line resulted in appropriate tyrosine phosphorylation of both Jak1 and Jak3
Yu et al., J Immunol 1996 : Finally, IL-2 induced tyrosine phosphorylation of JAK1 and JAK3, while IL-12 induced phosphorylation of JAK2 and TYK2 in both preactivated primary NK and NK3.3 cells
Ferrag et al., Mol Endocrinol 1996 : Otherwise, Jak1 and Jak3 are involved in IL-2 signaling through heterodimerization of the IL-2 receptor-beta (IL-2R beta) and gamma c-chains
Oakes et al., Immunity 1996 (Severe Combined Immunodeficiency) : Although IL-2 induced phosphorylation of IL-2R beta, JAK1 , and STAT5 all required the presence of JAK3, IL-4 mediated phosphorylation of JAK1, STAT6, and insulin receptor substrates 1 and 2 did not ... Although IL-2 induced phosphorylation of IL-2R beta, JAK1 , and STAT5 all required the presence of JAK3, IL-4 mediated phosphorylation of JAK1, STAT6, and insulin receptor substrates 1 and 2 did not
Yu et al., J Biol Chem 1997 : Activation of Jak and STAT proteins by IL-2 is transient and the mechanism for the subsequent down-regulation of their activity is largely unknown
Bright et al., J Immunol 1997 : TGF-beta inhibits IL-2 induced tyrosine phosphorylation and activation of Jak-1 and Stat 5 in T lymphocytes ... We show here that treatment of activated T cells with TGF-beta inhibited IL-2 induced tyrosine phosphorylation and activation of Jak-1 and Stat 5 but not Jak-3 and Stat 3
Liu et al., Curr Biol 1997 (Fibrosarcoma) : Furthermore, the relative roles of JAK1 and JAK3 in the activation of STAT5 by interleukin-2 (IL-2) remain poorly understood
Ferrag et al., FEBS Lett 1998 : Heterotrimeric IL-2R ( alpha, beta, gamma[c ] chains ) activates Jak1 and Jak3, whereas homodimeric PRLR activates Jak2
Zhu et al., J Biol Chem 1998 : Moreover, Jak1 and Jak3 could associate only in the presence of IL-2Rbeta , suggesting that these kinases can simultaneously bind to IL-2Rbeta
Migone et al., Mol Cell Biol 1998 : Instead, we find that Jak1 , which associates with membrane-proximal regions of the IL-2Rbeta cytoplasmic domain, is essential for efficient IL-2Rbeta-p85 interaction, although some IL-2Rbeta-p85 association can be seen in the absence of Jak1