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EPHB2 — IL2

Text-mined interactions from Literome

Brockdorff et al., Eur J Immunol 1999 : SHP1-DeltaSH2 also inhibited events downstream of ZAP-70 and Syk, such as activation of the mitogen activated protein kinase Erk2 and the transcriptional activation of the interleukin-2 gene
Valledor et al., J Biol Chem 2000 : Granulocyte/macrophage colony stimulating factor, interleukin 3, and TPA, all of which induced macrophage proliferation, also induced ERK activity, which was maximal at 5 min poststimulation
Cacalano et al., Nat Cell Biol 2001 : A tyrosine mutant of SOCS-3 still blocks STAT phosphorylation, but also strongly inhibits IL-2 dependent activation of ERK and cell proliferation
Tham et al., J Immunol 2001 (MAP Kinase Signaling System) : Together these results demonstrate that activation of at least ERK and p38 is essential for IL-2 production by CD8 T cells and that up-regulation of these mitogen activated protein kinases, along with Janus kinase, is defective in AINR cells
Stepkowski et al., Blood 2002 (MAP Kinase Signaling System) : Using human T cells, it was found that a recently discovered variant of the undecylprodigiosin family of antibiotics, PNU156804, previously shown to inhibit IL-2 induced cell proliferation, also blocks IL-2 mediated Jak3 auto-tyrosine phosphorylation, activation of Jak3 substrates signal transducers and activators of transcription ( Stat ) 5a and Stat5b, and extracellular regulated kinase 1 (Erk1) and Erk2 ( p44/p42 )
Wang et al., Anticancer Res 2002 (MAP Kinase Signaling System) : 0.12 mM PA inhibited the activation of ERK1/2 induced by IL2 and enhanced the activation of JNK, which was abrogated by IL2 ... PD98059 ( a specific ERK1/2 inhibitor ) inhibited cell growth, led to cell apoptotic death and effectively decreased ODC activity and suppressed ERK1/2 activation induced by IL2
García-Lora et al., Cancer Immunol Immunother 2003 : IL-2 decreased the expression of ERK2, whereas PSK did not, and both agents increased the expression of ERK3
Maggi et al., J Biol Chem 2003 (Cardiovirus Infections...) : ERK activation is required for double stranded RNA- and virus induced interleukin-1 expression by macrophages
MacGillivray et al., J Biol Chem 2003 (MAP Kinase Signaling System) : The protein tyrosine phosphatase SHP-2 regulates interleukin-1 induced ERK activation in fibroblasts
Faubert Kaplan et al., Int Immunopharmacol 2003 : Collectively, these studies suggest that cannabinoid induced inhibition of IL-2 in PMA/Io stimulated splenocytes might be due , in part, to inhibition of ERK MAPK activation
Jiang et al., J Reprod Immunol 2003 : Erk 1-2 phosphorylation was not required for JAR cells to inhibit IL-2 production in activated PBMC
Marks et al., Biochem Biophys Res Commun 2003 : Unexpectedly, dominant negative Ras17N blocked activation of Ras and ERK in response to IL-2R engagement but not TCR/CD3 ligation
Arnaud et al., Biochem J 2004 (Leukemia, Prolymphocytic, T-Cell) : Expression of the Gab2 Tyr-614 -- > Phe ( Y614F ) mutant, defective in SHP-2 association, prevents ERK ( extracellular-signal regulated kinase ) activation and expression of a luciferase reporter plasmid driven by the c-fos SRE ( serum response element ), indicating that interaction of SHP-2 with Gab2 is required for ERK activation in response to IL-2
Tsukamoto et al., J Biol Chem 2004 : The inhibition of sustained ERK activation by either expression of a dominant negative B-Raf or treatment with a MEK inhibitor resulted in a decrease of the TCR stimulated nuclear factor of activated T cells ( NFAT ) activity and IL-2 production
Chang et al., J Biol Chem 2004 (Inflammation...) : The induction of prostaglandin E2 production, interleukin-6 production, cell cycle arrest, and cytotoxicity in primary oral keratinocytes and KB cancer cells by areca nut ingredients is differentially regulated by MEK/ERK activation
Wang et al., J Biol Chem 2005 : SHP-2 modulates interleukin-1 induced Ca2+ flux and ERK activation via phosphorylation of phospholipase Cgamma1
Kawauchi et al., J Immunol 2005 (Leukemia, Lymphocytic, Chronic, B-Cell...) : ERK1/2 and Akt kinase ( Akt ) were activated by IL-2 stimulation
Miranda et al., Leuk Res 2005 (MAP Kinase Signaling System) : Additionally, interleukin-3 , which inhibits G-CSF induced differentiation of 32 Dc l3 cells, also inhibited the ability of G-CSF to stimulate prolonged MEK/ERK activation
Joshi et al., Mol Cell Biochem 2006 (Calcium Signaling) : Our finding demonstrates that Ca2+ influx via CRAC channels, inhibition of ERK1/ERK2 phosphorylation and IL-2 gene transcription may be implicated in immunosuppressive effects of MLSA antigen
Slack et al., Eur J Immunol 2007 : Syk dependent ERK activation regulates IL-2 and IL-10 production by DC stimulated with zymosan
Venkatachalam et al., Am J Physiol Heart Circ Physiol 2008 (Hyperglycemia) : Resveratrol inhibits high glucose induced PI3K/Akt/ERK dependent interleukin-17 expression in primary mouse cardiac fibroblasts
Conrad et al., Cell Signal 2009 : Pharmacologic inhibition of ERK1/2 or JNK activation inhibited Thy-1 induced DNA synthesis and IL-2 production by T-lymphocytes ... Collectively, these results suggest that during Thy-1 induced T-lymphocyte activation, ERK1/2 and JNK promoted IL-2 production whereas p38 MAPK negatively regulated IL-2 expression
Woolson et al., Cell Signal 2009 : Here we demonstrate that elevation of cyclic AMP ( cAMP ) levels in human umbilical vein endothelial cells ( HUVECs ) specifically attenuates ERK1,2 activation in response to either leptin or a soluble interleukin IL-6 receptor-alpha/IL-6 ( sIL-6R alpha/IL-6 ) trans signalling complex but not protein kinase C activator phorbol 12-myristate 13-acetate
Saraiva et al., Immunity 2009 : Interleukin-10 production by Th1 cells requires interleukin-12 induced STAT4 transcription factor and ERK MAP kinase activation by high antigen dose
Cuong et al., Life Sci 2009 (Inflammation...) : Pre-treatment with C-K significantly inhibited zymosan mediated secretion of tumor necrosis factor-alpha, interleukin (IL)-6 , and IL-12 p40, and the activation of ERK1/2 and p38
Kaltenberg et al., Eur J Immunol 2010 (MAP Kinase Signaling System) : In conclusion, an increase of cytoplasmic free zinc is required for IL-2 induced ERK signaling and proliferation of T cells
Pastorino et al., FASEB J 2010 : However, PEA-15 deficient T cells had increased CD3/CD28 induced nuclear translocation of ERK and increased activation of IL-2 transcription and secretion in comparison to control wild-type littermates
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
Pan et al., Blood 2012 (HIV Infections) : Instead, Nef triggers Lck dependent activation of TGN associated Ras-Erk signaling to promote the production of the T lymphocyte survival factor IL-2 and to enhance virus spread
Warnecke et al., EMBO Rep 2012 : Conversely, Grb2/Sos-but not RasGRP1-are required for IL2 mediated Erk activation
Le Gallou et al., J Immunol 2012 (MAP Kinase Signaling System) : Indeed, IL-2 potentiated ERK activation and subsequent BACH2 and IRF8 downregulation, sustaining BLIMP1 expression, the master regulator for PC differentiation
Gentle et al., J Immunol 2012 : Modulation required de novo protein synthesis, and PI3K, JNK, and ERK activity were necessary for enhanced IL-2 expression, whereas modulation of IL-10 required only PI3K activity
Mizota et al., J Anesth 2013 (MAP Kinase Signaling System) : Morphine pretreatment enhanced ERK phosphorylation, but inhibited I?Ba phosphorylation and IL-2 gene expression in activated T cells
Song et al., Immunology 1993 : These observations suggest that concurrent tyrosine phosphorylation of the 42,000 MW ERK and a 100,000 MW protein may be required for IL-2 production
Perkins et al., J Exp Med 1993 : Activation was both rapid, occurring within 5 min of IL-2 addition, and prolonged, remaining elevated for 30 min. Activation of Erk2 appeared to be necessary for IL-2 stimulation of proliferation, as deletion of a region of the cytoplasmic domain of the IL-2 receptor beta chain, essential for IL-2 stimulation of proliferation, abolished Erk2 activation by IL-2 ... These data suggest that IL-2 must stimulate both Erk2 activity and a further pathway ( s ) to trigger cell proliferation
Whitehurst et al., J Immunol 1996 : Therefore, we sought to determine whether MEK1 and ERK activities also stimulate IL-2 gene transcription ... We conclude that the MAP kinase signal transduction pathway consisting of Raf-1, MEK1, and ERK1 and ERK2 functions in the stimulation IL-2 gene transcription in activated T lymphocytes
Crawley et al., Eur J Immunol 1996 : This possibility was supported by studies with the MEK inhibitor PD098059, which had no selective effect on CT6 proliferation induced by IL-2 as compared with IL-7, although the drug completely inhibited MAP/Erk phosphorylation induced by IL-2
Barber et al., Blood 1997 : In addition, EPO, IL-2 , and IL-15 activated Raf1 and ERK2 , demonstrating that the Raf1/MEK/MAP kinase pathway was activated
Han et al., J Autoimmun 1997 (Diabetes Mellitus, Type 1) : On the basis of these observations, we conclude that TGF-beta may interfere with signal transduction via inhibition of the IL-2 induced JAK/STAT pathway and inhibition of the association of STAT proteins with ERK2 in T cells from NOD splenocytes, resulting in the inhibition of IL-2 dependent T cell proliferation
Calvo et al., J Exp Med 1997 : Since activation of the ERK and JNK kinases is required for stimulation of interleukin (IL)-2 transcription, these data provide a molecular explanation for the block in IL-2 production imposed by CTLA-4
Lo et al., J Biol Chem 1998 : Requirements of focal adhesions and calcium fluxes for interleukin-1 induced ERK kinase activation and c-fos expression in fibroblasts
Liu et al., Cell Immunol 1997 : Because the activities of extracellular signal regulated kinases ( ERK ) and c-Jun NH2-terminal kinases (JNK) are important for IL-2 production, the current study evaluated if aberrancies in the expression and activation of ERK2 or JNK might underlie decreased IL-2 production by human T cells during aging