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CA2 — IL1A

Text-mined interactions from Literome

Tonon et al., J Bone Miner Res 2000 (Calcium Signaling) : IL-1 stimulation induced a dose dependent increase of cytosolic Ca2+ and activates protein tyrosine phosphorylation
Tonon et al., Biorheology 2002 : IL-1 stimulation induced a dose dependent increase of cytosolic Ca2+ and activates protein tyrosine phosphorylation
Wang et al., FASEB J 2003 (Calcium Signaling) : IL-1 induced release of Ca2+ from internal stores is dependent on cell-matrix interactions and regulates ERK activation ... We conducted studies to elucidate which steps of cellular Ca2+ handling are affected by focal adhesions and by which mechanisms focal adhesions modulate IL-1 induced Ca2+ signals and ERK activation in human gingival fibroblasts ... Focal adhesions were also required for Ca2+ entry through store operated channels and for IL-1 induced ERK activation
Wang et al., FASEB J 2005 : Here, we examined the impact of cell energetics and mitochondrial function on the regulation of IL-1 induced Ca2+ signals and ERK activation in human gingival fibroblasts, cells that are important targets for IL-1 induced destruction of extracellular matrix in inflamed connective tissues ... Inhibition of cellular energetics by selective depolarization of mitochondria blocked Ca2+ uptake and almost completely abolished IL-1 induced cytosolic Ca2+ signals and ERK activation ... IL-1 caused rapid Ca2+ release from the endoplasmic reticulum ( ER ), concomitant with mitochondrial Ca2+ uptake from ER and non-ER stores ... Thus, in gingival fibroblasts, mitochondrial Ca2+ uptake is essential not only for shaping the kinetics and duration, but also the generation of, IL-1 induced Ca2+ signals
Fujisaki et al., Life Sci 2007 : In the presence of IL-1alpha , expression of CAII , cathepsin K, and MMP-9 was markedly increased in cells cultured with RANKL or M-CSF+RANKL, whereas expression was difficult to detect in cells cultured with IL-1alpha alone and M-CSF ... These results indicate that the expression of CAII , cathepsin K, and MMP-9 in RAW264.7 cells is not induced by M-CSF, but by RANKL in the presence of IL-1alpha
Corkey et al., J Clin Invest 1991 (Reye Syndrome) : To determine whether this disorder involves a genetically determined abnormal response to cytokines, the effects of tumor necrosis factor (TNF) and IL-1 on intracellular free Ca2+ were compared in cultured skin fibroblasts from control subjects and patients with RS ... IL-1 and TNF caused rapid, transient, and concentration dependent increases in cytosolic free Ca2+
Wang et al., J Biol Chem 2009 (Calcium Signaling) : We examined here the role of protein-tyrosine phosphatase (PTP) alpha in regulating IL-1 induced Ca2+ signaling in fibroblasts ... In response to IL-1 , catalytically active PTPalpha was required for Ca2+ release from the ER, Src dependent phosphorylation of IP3R1 and accumulation of IP3R1 in focal adhesions
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
Jules et al., J Biol Chem 2012 : Here we show that although IL-1 can not activate the expression of the osteoclast genes encoding matrix metalloproteinase 9, cathepsin K, tartrate-resistant acid phosphatase, and carbonic anhydrase II in bone marrow macrophages ( BMMs ), RANKL renders these osteoclast genes responsive to IL-1
Arora et al., J Biol Chem 1995 : Incubation with EGTA ( 5 mM ) or thapsigargin ( 1 microM ) caused 75 % and 37 % reductions, respectively, in the IL-1 induced [Ca2+ ] i increase, suggesting that extracellular Ca2+ predominates in IL-1 stimulated calcium flux
Tokumoto et al., Biochim Biophys Acta 1994 : In the presence of extracellular Ca2+ , ionomycin ( 3 mM ), thapsigargin ( 0.3 mM ), bradykinin ( 10 nM ), and interleukin 1 alpha ( 1 ng/ml ) stimulation of arachidonic acid release was blocked by the Ca2+ influx blocker LaCl3 ( 29, 44, 35, and 41 % inhibition, respectively ) ... These results suggest that following B2 receptor activation, cytosolic phospholipase A2 is stimulated by a rise in intracellular Ca2+ levels which are sensitive to the action of EGTA, whereas interleukin 1 alpha stimulation of cytosolic phospholipase A2 is mediated by a rise in intracellular Ca2+ from both EGTA-sensitive and resistant pools
Yu et al., Biochem Biophys Res Commun 1993 : Pre-incubation with indomethacin ( 30 microM ) does not block the IL-1 alpha effect on [Ca2+ ] i
Conti et al., Calcif Tissue Int 1993 (Granuloma) : Moreover, IL-1 is involved in Ca2+ release causing hypercalcemia and bone resorption
Plami et al., Br J Pharmacol 1996 : 5. Perfusion with a Ca ( 2+ ) -free medium obtained by use of excess EGTA ( 3 mM ) or in the presence of the Ca2+ channel blocker, nifedipine ( 3 x 10 ( -8 M ) abolished the potentiating effect of caffeine without affecting the IL-1 induced 45Ca2+ release
Luo et al., Biochem J 1997 : We have determined whether focal adhesions restrict IL-1 induced Ca2+ signalling in primary cultures of bovine chondrocytes ... Cells plated on poly- ( l-lysine ) or suspended cells showed no Ca2+ increases, whereas cells grown on fibronectin exhibited IL-1 induced Ca2+ responses that corresponded temporally to the time dependent cell spreading after plating on fibronectin ... These results indicate that, in chondrocytes, IL-1 induced Ca2+ signalling is dependent on focal adhesion formation and that focal adhesions recruit IL-1 receptors by redistribution in the cell membrane ... There were no IL-1 induced Ca2+ increases when cells on poly- ( l-lysine ) were incubated with fibronectin coated beads for only 15 min at 37 degrees C, in cells maintained for 3 h at 4 degrees C, in cells incubated with BSA beads for 3 h at 37 degrees C, or in cells pretreated with cytochalasin D. Labelling of IL-1 receptors with 125I-IL-1beta showed 3-fold more specific labelling of focal adhesion complexes in cells incubated with fibronectin coated beads compared with cells incubated with BSA coated beads, indicating that IL-1 receptor binding or the number of IL-1 receptors was increased in focal adhesions