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CA2 — IL2

Text-mined interactions from Literome

Liu et al., Proc Soc Exp Biol Med 2000 (Calcium Signaling) : Ca2+ release from intracellular stores was strongly stimulated by acetylcholine (ACh) and ATP, but not by norepinephrine ( NA ), epidermal growth factor (EGF), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNFalpha)
Cao et al., Pflugers Arch 2002 : Opioid receptor mediated effects of interleukin-2 on the [Ca2+ ] i transient and contraction in isolated ventricular myocytes of the rat ... Pretreatment with the universal opioid receptor antagonist naloxone ( 10 nM ), or a specific kappa opioid receptor antagonist, nor-binaltorphimine ( nor-BNI, 10 nM ), abolished the inhibitory effect of IL-2 on contraction and the [Ca2+ ] i transient ; the specific delta-opioid receptor antagonist naltrindole ( 1 microM ) had no effect ... It is concluded that the effects of IL-2 on contraction and the [Ca2+ ] i transient of ventricular myocytes are mediated via the cardiac kappa opioid receptor, and the postreceptor signal transduction pathway includes a PTX-sensitive G protein and phospholipase C
Cao et al., J Pharmacol Exp Ther 2003 : Interleukin-2 increases activity of sarcoplasmic reticulum Ca2+-ATPase , but decreases its sensitivity to calcium in rat cardiomyocytes ... IL-2 did not affect the sarcolemmal L-type Ca2+ channel activity
Wang et al., J Biol Chem 2009 (Calcium Signaling) : Protein-tyrosine phosphatase-alpha and Src functionally link focal adhesions to the endoplasmic reticulum to mediate interleukin-1 induced Ca2+ signaling
Kodama et al., Meikai Daigaku Shigaku Zasshi 1990 (Bone Resorption...) : Among several bioactive substances known as coupling factors, transforming growth factor-beta ( TGF-beta ), interleukin-1 (IL-1), and prostaglandin ( PG ) E1 and E2 increased not only the activity of alkaline phosphatase but also the rate of incorporation of 45Ca2+ into ROS 17/2.8 during a 3-day culture : the former two factors are known to be formed at the site where bone is resorbed, while PG 's are known as one of the factors involved in bone resorption
Kodama et al., Meikai Daigaku Shigaku Zasshi 1989 (Bone Resorption) : The effects of interleukin 1, transforming growth factor-beta ( coupling factors ), prostaglandin E1, and prostaglandin E2 on incorporation of 45Ca2+ and on alkaline phosphatase activity were studied using cultured ROS 17/2.8 cells, one of cell lines derived from rat osteosarcoma
Mills et al., J Immunol 1985 : This suggests that, although increases in [Ca2+ ] i are an integral event in the induction of proliferation by PHA, the increase in [ Ca2+ ] i is required for the production but not the action of IL 2
LeGrue et al., Lymphokine Res 1987 : Conversely, partially purified rat IL 2 did cause an increase in [Ca2+ ] i that was not inhibited by the channel blockers or by chelation of extracellular free Ca2+ ... Thus, contaminating components in the partially purified rat IL 2, and not the IL 2 itself, resulted in increased [Ca2+ ] i by mobilization from intracellular stores
Qiu et al., Biochem Pharmacol 1994 : In the present study, we investigated the effects of lymphokines [interleukin-4 (IL-4), interleukin-2 (IL-2) ] and other pharmacologic agents [ lipopolysaccharide (LPS), phorbol 12-myristate 13-acetate ( PMA ) ] on HTMT induced Ca2+ and IP responses in non rosetted cells
Negulescu et al., Proc Natl Acad Sci U S A 1994 (Second Messenger Systems) : In T lymphocytes, intracellular Ca2+ concentration ([Ca2+]i) rises within seconds of T-cell antigen-receptor stimulation and initiates the synthesis and secretion of interleukin 2 , a cytokine essential for T-cell proliferation and the immune response
Couez et al., Mol Immunol 1994 : In these transfectants, CD28 mAbs, similarly to CD3 mAbs, were able to induce Ca2+ mobilization, IL-2 promoter induction ( measured as beta-galactosidase activity in T cells hybridomas pre transfected with the IL-2-lac Z reporter gene ), IL-2 secretion, TNF alpha production and apoptosis ( observed as growth arrest and genome fragmentation )
Wacholtz et al., J Immunol 1993 : In contrast, cross linking anti-CD3 with a secondary antibody foreshortened the increase in [Ca2+ ] i, and IL-2 production and DNA synthesis were inhibited
Komada et al., Cell Immunol 1996 : These results indicate that IL-2 production required Ca2+ only in the early ( G0 ) stage and that IL-2R expression was dependent on Ca2+ in both the G0 and the G1 stages
Nabata et al., Atherosclerosis 1997 : IL-2 itself did not affect the basal [Ca2+ ] i level or the maximal response of [ Ca2+ ] i increase induced by AII
Nishina et al., J Exp Med 1997 : Although SEK1 ( -/- ) thymocytes failed to induce SAPK/JNK in response to PMA/Ca2+ ionophore, SEK1 ( -/- ) RAG2 ( -/- ) thymocytes proliferated and made IL-2 after PMA/Ca2+ ionophore and CD3/CD28 stimulation, albeit at significantly lower levels compared to SEK1 ( +/+ ) RAG2 ( -/- ) thymocytes, implying that CD28 costimulation and PMA/Ca2+ ionophore triggered signaling pathways exist that can mediate proliferation and IL-2 production independently of SAPK activation
Kumar et al., Int J Immunopharmacol 1997 : Effect of prolactin on nitric oxide and interleukin-1 production of murine peritoneal macrophages : role of Ca2+ and protein kinase C
Gur et al., Cell Immunol 1999 (Calcium Signaling) : By contrast, cross linking intact murine class I MHC molecules induced [Ca2+ ] i, signal and IL-2 production in transfected Jurkat cells